Abnormal Development - Maternal Diabetes - Revision history

Z8600021 at 00:37, 29 April 2020

2020-04-29T00:37:58Z

← Older revision		Revision as of 11:37, 29 April 2020
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	* '''Ultrasound assessment of maternal adipose tissue during ~~1st~~ trimester screening for aneuploidies and risk of developing gestational diabetes'''{{#pmid:31898313\|PMID31898313}} "The objective of the present study is to compare the sonographic measurement of subcutaneous adipose thickness and visceral adipose thickness during 1st trimester screening for aneuploidies between non-diabetic pregnant women and patients who develop 1st trimester or 2nd trimester gestational diabetes mellitus (GDM). Adipose thickness was measured by transabdominal ultrasound imaging in pregnant women attending our clinic for screening for fetal aneuploidies between 11 and 13 weeks of gestation. During the 1st trimester all patients were evaluated for fasting glycemia in accordance with the International Association of Diabetes and Pregnancy Study Groups (IADPSG) recommendations. Patients with confirmed fasting glycemia (FPG) ≥92 mg/dL were diagnosed as 1st trimester GDM. Patients with FPG <92 mg/dL underwent a 75-g oral glucose tolerance test between 24 and 28 weeks. ...Sonographic thickness of maternal visceral adipose tissue was greater in women with GDM than in non-diabetic patients, independently of other known risk factors associated with GDM in the 1st and in the 2nd trimester of pregnancy. Thus, this measurement may be considered of clinical use in 1st trimester screening."		* '''{{Ultrasound}} assessment of maternal adipose tissue during {{first trimester}} screening for aneuploidies and risk of developing gestational diabetes'''{{#pmid:31898313\|PMID31898313}} "The objective of the present study is to compare the sonographic measurement of subcutaneous adipose thickness and visceral adipose thickness during 1st trimester screening for aneuploidies between non-diabetic pregnant women and patients who develop 1st trimester or 2nd trimester gestational diabetes mellitus (GDM). Adipose thickness was measured by transabdominal ultrasound imaging in pregnant women attending our clinic for screening for fetal aneuploidies between 11 and 13 weeks of gestation. During the 1st trimester all patients were evaluated for fasting glycemia in accordance with the International Association of Diabetes and Pregnancy Study Groups (IADPSG) recommendations. Patients with confirmed fasting glycemia (FPG) ≥92 mg/dL were diagnosed as 1st trimester GDM. Patients with FPG <92 mg/dL underwent a 75-g oral glucose tolerance test between 24 and 28 weeks. ...Sonographic thickness of maternal visceral adipose tissue was greater in women with GDM than in non-diabetic patients, independently of other known risk factors associated with GDM in the 1st and in the 2nd trimester of pregnancy. Thus, this measurement may be considered of clinical use in 1st trimester screening."

	* [https://www.aihw.gov.au/reports/diabetes/incidence-of-insulin-treated-diabetes/contents/incidence-of-insulin-treated-diabetes-in-australia '''Incidence of insulin-treated diabetes in Australia'''] (AIHW Web report 0 25 Mar 2020) In 2018, about 31,300 people began using insulin to treat their diabetes in Australia, of these 10,800 (34%) females began using insulin to treat {{gestational diabetes}}.		* [https://www.aihw.gov.au/reports/diabetes/incidence-of-insulin-treated-diabetes/contents/incidence-of-insulin-treated-diabetes-in-australia '''Incidence of insulin-treated diabetes in Australia'''] (AIHW Web report 0 25 Mar 2020) In 2018, about 31,300 people began using insulin to treat their diabetes in Australia, of these 10,800 (34%) females began using insulin to treat {{gestational diabetes}}.

Z8600021 at 00:37, 29 April 2020

2020-04-29T00:37:07Z

← Older revision		Revision as of 11:37, 29 April 2020
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			* '''Ultrasound assessment of maternal adipose tissue during 1st trimester screening for aneuploidies and risk of developing gestational diabetes'''{{#pmid:31898313\|PMID31898313}} "The objective of the present study is to compare the sonographic measurement of subcutaneous adipose thickness and visceral adipose thickness during 1st trimester screening for aneuploidies between non-diabetic pregnant women and patients who develop 1st trimester or 2nd trimester gestational diabetes mellitus (GDM). Adipose thickness was measured by transabdominal ultrasound imaging in pregnant women attending our clinic for screening for fetal aneuploidies between 11 and 13 weeks of gestation. During the 1st trimester all patients were evaluated for fasting glycemia in accordance with the International Association of Diabetes and Pregnancy Study Groups (IADPSG) recommendations. Patients with confirmed fasting glycemia (FPG) ≥92 mg/dL were diagnosed as 1st trimester GDM. Patients with FPG <92 mg/dL underwent a 75-g oral glucose tolerance test between 24 and 28 weeks. ...Sonographic thickness of maternal visceral adipose tissue was greater in women with GDM than in non-diabetic patients, independently of other known risk factors associated with GDM in the 1st and in the 2nd trimester of pregnancy. Thus, this measurement may be considered of clinical use in 1st trimester screening."

	* [https://www.aihw.gov.au/reports/diabetes/incidence-of-insulin-treated-diabetes/contents/incidence-of-insulin-treated-diabetes-in-australia '''Incidence of insulin-treated diabetes in Australia'''] (AIHW Web report 0 25 Mar 2020) In 2018, about 31,300 people began using insulin to treat their diabetes in Australia, of these 10,800 (34%) females began using insulin to treat {{gestational diabetes}}.		* [https://www.aihw.gov.au/reports/diabetes/incidence-of-insulin-treated-diabetes/contents/incidence-of-insulin-treated-diabetes-in-australia '''Incidence of insulin-treated diabetes in Australia'''] (AIHW Web report 0 25 Mar 2020) In 2018, about 31,300 people began using insulin to treat their diabetes in Australia, of these 10,800 (34%) females began using insulin to treat {{gestational diabetes}}.
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	* '''Review - Systemic endocrinopathies (thyroid conditions and diabetes): impact on postnatal life of the offspring'''{{#pmid:31155115\|PMID31155115}} "Fetal programming may influence childhood and adult life, determining the risk of specific diseases. During earlier stages of pregnancy, the transfer of maternal thyroid hormones to the fetus is vital for adequate neurologic development. The presence of severe maternal thyroid dysfunction, particularly severe iodine deficiency, is devastating, leading to irreversible neurologic sequelae. Moreover, mild maternal thyroid conditions, such as a mild-to-moderate iodine deficiency, may also lead to milder neurologic and behavioral conditions later during the life of the offspring. Maternal dysglycemia due to pregestational or gestational diabetes mellitus is another common situation in which fetal development encounters a hostile environment. Hyperglycemia in utero may trigger metabolic conditions in the offspring, including abnormalities of glucose tolerance and weight excess. Physicians assisting pregnant women have to be aware about these conditions, because they may go unnoticed if not properly screened. Because an early diagnosis and appropriate management may prevent most of the possible negative consequences for the progeny, the prevention, early diagnosis, and proper management of these endocrine conditions should be offered to all women undergoing pregnancy. Here, we comprehensively review the current evidence about the effects of maternal thyroid dysfunction and maternal dysglycemia on the cognitive function and carbohydrate metabolism in the offspring, two prevalent conditions of utmost importance for the child's health and development."		* '''Review - Systemic endocrinopathies (thyroid conditions and diabetes): impact on postnatal life of the offspring'''{{#pmid:31155115\|PMID31155115}} "Fetal programming may influence childhood and adult life, determining the risk of specific diseases. During earlier stages of pregnancy, the transfer of maternal thyroid hormones to the fetus is vital for adequate neurologic development. The presence of severe maternal thyroid dysfunction, particularly severe iodine deficiency, is devastating, leading to irreversible neurologic sequelae. Moreover, mild maternal thyroid conditions, such as a mild-to-moderate iodine deficiency, may also lead to milder neurologic and behavioral conditions later during the life of the offspring. Maternal dysglycemia due to pregestational or gestational diabetes mellitus is another common situation in which fetal development encounters a hostile environment. Hyperglycemia in utero may trigger metabolic conditions in the offspring, including abnormalities of glucose tolerance and weight excess. Physicians assisting pregnant women have to be aware about these conditions, because they may go unnoticed if not properly screened. Because an early diagnosis and appropriate management may prevent most of the possible negative consequences for the progeny, the prevention, early diagnosis, and proper management of these endocrine conditions should be offered to all women undergoing pregnancy. Here, we comprehensively review the current evidence about the effects of maternal thyroid dysfunction and maternal dysglycemia on the cognitive function and carbohydrate metabolism in the offspring, two prevalent conditions of utmost importance for the child's health and development."

	* '''Comparative proteomic analysis of maternal peripheral plasma and umbilical venous plasma from normal and gestational diabetes mellitus pregnancies'''{{#pmid:30200149\|PMID30200149}} Gestational diabetes mellitus (GDM) increases many health risks in offspring. The study aims to investigate the underlying mechanism in fetal risk of GDM.We collected maternal peripheral plasma and umbilical venous plasma samples from 4 GDM and 4 control patients during their delivery at a university-based women's hospital. ...We identified 19 up-regulated proteins and 15 down-regulated proteins in GDM peripheral plasma, 29 up-regulated proteins and 69 down-regulated proteins in GDM umbilical venous plasma. Cholesteryl ester transfer protein (CETP) concentration was significantly lower in both GDM peripheral plasma and umbilical venous plasma. Upstream regulator analysis predicted follicle-stimulating hormone ({{FSH}}) as the activated regulator of differentially expressed proteins.The protein profiles in both GDM peripheral plasma and umbilical venous plasma between normal and GDM patients were significantly different. The results indicated that CETP and {{FSH}} might associates with health problem of GDM offspring."

	* [http://collections.plos.org/diabetes-prevention PLoS Collection - Diabetes Prevention] In this Collection, we feature PLOS articles that focus on the prevention of diabetes.		* [http://collections.plos.org/diabetes-prevention PLoS Collection - Diabetes Prevention] In this Collection, we feature PLOS articles that focus on the prevention of diabetes.
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	\| {{Older papers}}		\| {{Older papers}}
			* '''Comparative proteomic analysis of maternal peripheral plasma and umbilical venous plasma from normal and gestational diabetes mellitus pregnancies'''{{#pmid:30200149\|PMID30200149}} Gestational diabetes mellitus (GDM) increases many health risks in offspring. The study aims to investigate the underlying mechanism in fetal risk of GDM.We collected maternal peripheral plasma and umbilical venous plasma samples from 4 GDM and 4 control patients during their delivery at a university-based women's hospital. ...We identified 19 up-regulated proteins and 15 down-regulated proteins in GDM peripheral plasma, 29 up-regulated proteins and 69 down-regulated proteins in GDM umbilical venous plasma. Cholesteryl ester transfer protein (CETP) concentration was significantly lower in both GDM peripheral plasma and umbilical venous plasma. Upstream regulator analysis predicted follicle-stimulating hormone ({{FSH}}) as the activated regulator of differentially expressed proteins.The protein profiles in both GDM peripheral plasma and umbilical venous plasma between normal and GDM patients were significantly different. The results indicated that CETP and {{FSH}} might associates with health problem of GDM offspring."

	* '''Maternal diabetes alters the development of {{ductus venosus}} shunting in the fetus'''{{#pmid:29752712\|PMID29752712}} "Despite adequate glycemic control, the risks of fetal macrosomia and perinatal complications are increased in diabetic pregnancies. Adjustments of the umbilical venous (UV) distribution, including increased ductus venosus (DV) shunting, can be important fetal compensatory mechanisms, but the impact of pregestational diabetes on UV and DV flow is not known. In pregnancies with pregestational diabetes mellitus, prioritized UV distribution to the fetal liver, and lower DV shunt capacity, both reduce the compensatory capability of the fetus and may represent an augmented risk during hypoxic challenges during late pregnancy and birth." {{ductus venosus}}		* '''Maternal diabetes alters the development of {{ductus venosus}} shunting in the fetus'''{{#pmid:29752712\|PMID29752712}} "Despite adequate glycemic control, the risks of fetal macrosomia and perinatal complications are increased in diabetic pregnancies. Adjustments of the umbilical venous (UV) distribution, including increased ductus venosus (DV) shunting, can be important fetal compensatory mechanisms, but the impact of pregestational diabetes on UV and DV flow is not known. In pregnancies with pregestational diabetes mellitus, prioritized UV distribution to the fetal liver, and lower DV shunt capacity, both reduce the compensatory capability of the fetus and may represent an augmented risk during hypoxic challenges during late pregnancy and birth." {{ductus venosus}}

Z8600021 at 23:05, 24 March 2020

2020-03-24T23:05:22Z

← Older revision		Revision as of 10:05, 25 March 2020
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	==Some Recent Findings==		==Some Recent Findings==
			[[File:Australia 2018 - new insulin users.jpg\|thumb\|alt=Australia 2018 - new insulin users\|Australia 2018 - new insulin users]]
	[[File:Australia 2017 - new female insulin users.png\|thumb\|alt=Australia 2017 - new female insulin users\|Australia 2017 - new female insulin users]]		[[File:Australia 2017 - new female insulin users.png\|thumb\|alt=Australia 2017 - new female insulin users\|Australia 2017 - new female insulin users]]
	[[File:Australia - insulin-treated diabetes by type 2015.jpg\|thumb\|200px\|alt=Australia - insulin-treated diabetes by type 2015\|Australia - insulin-treated diabetes by type 2015]]		[[File:Australia - insulin-treated diabetes by type 2015.jpg\|thumb\|200px\|alt=Australia - insulin-treated diabetes by type 2015\|Australia - insulin-treated diabetes by type 2015]]

Z8600021 at 23:01, 24 March 2020

2020-03-24T23:01:54Z

← Older revision		Revision as of 10:01, 25 March 2020
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			* [https://www.aihw.gov.au/reports/diabetes/incidence-of-insulin-treated-diabetes/contents/incidence-of-insulin-treated-diabetes-in-australia '''Incidence of insulin-treated diabetes in Australia'''] (AIHW Web report 0 25 Mar 2020) In 2018, about 31,300 people began using insulin to treat their diabetes in Australia, of these 10,800 (34%) females began using insulin to treat {{gestational diabetes}}.

	* '''Gestational diabetes mellitus affects odontoblastic differentiation of dental papilla cells via Toll-like receptor 4 signaling in offspring'''{{#pmid:31595494\|PMID31595494}} "Gestational diabetes mellitus (GDM) is an important factor involved in the pathogenesis of organ development in the offspring. Here, we analyzed the effects of GDM on odontoblastic differentiation of dental papilla cells (DPCs) and dentin formation in offspring and investigated their underlying mechanisms. A GDM {{rat}} model was induced by intraperitoneal injection of streptozotocin and offspring were collected. The results showed that GDM significantly affected odontoblast differentiation and dentin formation in offspring tooth. GDM activated the toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-ĸB) signaling pathway and inhibited SMAD1/5/9 signaling to modulate the odontoblastic differentiation of DPCs in offspring. Inhibition of TLR4 signaling by treated with TAK-242 significantly reverses the suppression of odonto-differentiation of DPCs in diabetic offspring. Taken together, these data indicate GDM activated the offspring DPCs TLR4/NF-ĸB signaling, which suppressed the SMAD1/5/9 phosphorylation and then inhibited odontoblasts differentiation and dentin formation." {{tooth}}		* '''Gestational diabetes mellitus affects odontoblastic differentiation of dental papilla cells via Toll-like receptor 4 signaling in offspring'''{{#pmid:31595494\|PMID31595494}} "Gestational diabetes mellitus (GDM) is an important factor involved in the pathogenesis of organ development in the offspring. Here, we analyzed the effects of GDM on odontoblastic differentiation of dental papilla cells (DPCs) and dentin formation in offspring and investigated their underlying mechanisms. A GDM {{rat}} model was induced by intraperitoneal injection of streptozotocin and offspring were collected. The results showed that GDM significantly affected odontoblast differentiation and dentin formation in offspring tooth. GDM activated the toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-ĸB) signaling pathway and inhibited SMAD1/5/9 signaling to modulate the odontoblastic differentiation of DPCs in offspring. Inhibition of TLR4 signaling by treated with TAK-242 significantly reverses the suppression of odonto-differentiation of DPCs in diabetic offspring. Taken together, these data indicate GDM activated the offspring DPCs TLR4/NF-ĸB signaling, which suppressed the SMAD1/5/9 phosphorylation and then inhibited odontoblasts differentiation and dentin formation." {{tooth}}

Z8600021 at 04:53, 8 Ocak 2020

2020-01-08T04:53:44Z

← Older revision		Revision as of 15:53, 8 Ocak 2020
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	* '''Comparative proteomic analysis of maternal peripheral plasma and umbilical venous plasma from normal and gestational diabetes mellitus pregnancies'''{{#pmid:30200149\|PMID30200149}} Gestational diabetes mellitus (GDM) increases many health risks in offspring. The study aims to investigate the underlying mechanism in fetal risk of GDM.We collected maternal peripheral plasma and umbilical venous plasma samples from 4 GDM and 4 control patients during their delivery at a university-based women's hospital. ...We identified 19 up-regulated proteins and 15 down-regulated proteins in GDM peripheral plasma, 29 up-regulated proteins and 69 down-regulated proteins in GDM umbilical venous plasma. Cholesteryl ester transfer protein (CETP) concentration was significantly lower in both GDM peripheral plasma and umbilical venous plasma. Upstream regulator analysis predicted follicle-stimulating hormone ({{FSH}}) as the activated regulator of differentially expressed proteins.The protein profiles in both GDM peripheral plasma and umbilical venous plasma between normal and GDM patients were significantly different. The results indicated that CETP and {{FSH}} might associates with health problem of GDM offspring."		* '''Comparative proteomic analysis of maternal peripheral plasma and umbilical venous plasma from normal and gestational diabetes mellitus pregnancies'''{{#pmid:30200149\|PMID30200149}} Gestational diabetes mellitus (GDM) increases many health risks in offspring. The study aims to investigate the underlying mechanism in fetal risk of GDM.We collected maternal peripheral plasma and umbilical venous plasma samples from 4 GDM and 4 control patients during their delivery at a university-based women's hospital. ...We identified 19 up-regulated proteins and 15 down-regulated proteins in GDM peripheral plasma, 29 up-regulated proteins and 69 down-regulated proteins in GDM umbilical venous plasma. Cholesteryl ester transfer protein (CETP) concentration was significantly lower in both GDM peripheral plasma and umbilical venous plasma. Upstream regulator analysis predicted follicle-stimulating hormone ({{FSH}}) as the activated regulator of differentially expressed proteins.The protein profiles in both GDM peripheral plasma and umbilical venous plasma between normal and GDM patients were significantly different. The results indicated that CETP and {{FSH}} might associates with health problem of GDM offspring."

	* '''Maternal diabetes alters the development of {{ductus venosus}} shunting in the fetus'''{{#pmid:29752712\|PMID29752712}} "Despite adequate glycemic control, the risks of fetal macrosomia and perinatal complications are increased in diabetic pregnancies. Adjustments of the umbilical venous (UV) distribution, including increased ductus venosus (DV) shunting, can be important fetal compensatory mechanisms, but the impact of pregestational diabetes on UV and DV flow is not known. In pregnancies with pregestational diabetes mellitus, prioritized UV distribution to the fetal liver, and lower DV shunt capacity, both reduce the compensatory capability of the fetus and may represent an augmented risk during hypoxic challenges during late pregnancy and birth." {{ductus venosus}}

	* [http://collections.plos.org/diabetes-prevention PLoS Collection - Diabetes Prevention] In this Collection, we feature PLOS articles that focus on the prevention of diabetes.		* [http://collections.plos.org/diabetes-prevention PLoS Collection - Diabetes Prevention] In this Collection, we feature PLOS articles that focus on the prevention of diabetes.
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	\|-		\|-
	\| {{Older papers}}		\| {{Older papers}}
			* '''Maternal diabetes alters the development of {{ductus venosus}} shunting in the fetus'''{{#pmid:29752712\|PMID29752712}} "Despite adequate glycemic control, the risks of fetal macrosomia and perinatal complications are increased in diabetic pregnancies. Adjustments of the umbilical venous (UV) distribution, including increased ductus venosus (DV) shunting, can be important fetal compensatory mechanisms, but the impact of pregestational diabetes on UV and DV flow is not known. In pregnancies with pregestational diabetes mellitus, prioritized UV distribution to the fetal liver, and lower DV shunt capacity, both reduce the compensatory capability of the fetus and may represent an augmented risk during hypoxic challenges during late pregnancy and birth." {{ductus venosus}}

	* '''Increased risk of cardiovascular disease in women with prior gestational diabetes'''{{#pmid:29655653\|PMID29655653}} "This study aims to investigate the effect of gestational diabetes mellitus (GDM) on the long-term risk of cardiovascular disease (CVD). PubMed and other databases were searched up to August 31, 2017. ... In the pooled analysis, women with previous GDM had a higher risk of CVD than those without (RR: 1.74, 95%CI: 1.28-2.35, I2=95.7%). Four studies reported the event of coronary artery disease (CAD) and two studies reported stroke. Women with prior GDM have increased risk of CVD."		* '''Increased risk of cardiovascular disease in women with prior gestational diabetes'''{{#pmid:29655653\|PMID29655653}} "This study aims to investigate the effect of gestational diabetes mellitus (GDM) on the long-term risk of cardiovascular disease (CVD). PubMed and other databases were searched up to August 31, 2017. ... In the pooled analysis, women with previous GDM had a higher risk of CVD than those without (RR: 1.74, 95%CI: 1.28-2.35, I2=95.7%). Four studies reported the event of coronary artery disease (CAD) and two studies reported stroke. Women with prior GDM have increased risk of CVD."

Z8600021 at 04:52, 8 Ocak 2020

2020-01-08T04:52:38Z

← Older revision		Revision as of 15:52, 8 Ocak 2020
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	* '''Gestational diabetes mellitus affects odontoblastic differentiation of dental papilla cells via Toll-like receptor 4 signaling in offspring'''{{#pmid:31595494\|PMID31595494}} "Gestational diabetes mellitus (GDM) is an important factor involved in the pathogenesis of organ development in the offspring. Here, we analyzed the effects of GDM on odontoblastic differentiation of dental papilla cells (DPCs) and dentin formation in offspring and investigated their underlying mechanisms. A GDM {{rat}} model was induced by intraperitoneal injection of streptozotocin and offspring were collected. The results showed that GDM significantly affected odontoblast differentiation and dentin formation in offspring tooth. GDM activated the toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-ĸB) signaling pathway and inhibited SMAD1/5/9 signaling to modulate the odontoblastic differentiation of DPCs in offspring. Inhibition of TLR4 signaling by treated with TAK-242 significantly reverses the suppression of odonto-differentiation of DPCs in diabetic offspring. Taken together, these data indicate GDM activated the offspring DPCs TLR4/NF-ĸB signaling, which suppressed the SMAD1/5/9 phosphorylation and then inhibited odontoblasts differentiation and dentin formation." {{tooth}}		* '''Gestational diabetes mellitus affects odontoblastic differentiation of dental papilla cells via Toll-like receptor 4 signaling in offspring'''{{#pmid:31595494\|PMID31595494}} "Gestational diabetes mellitus (GDM) is an important factor involved in the pathogenesis of organ development in the offspring. Here, we analyzed the effects of GDM on odontoblastic differentiation of dental papilla cells (DPCs) and dentin formation in offspring and investigated their underlying mechanisms. A GDM {{rat}} model was induced by intraperitoneal injection of streptozotocin and offspring were collected. The results showed that GDM significantly affected odontoblast differentiation and dentin formation in offspring tooth. GDM activated the toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-ĸB) signaling pathway and inhibited SMAD1/5/9 signaling to modulate the odontoblastic differentiation of DPCs in offspring. Inhibition of TLR4 signaling by treated with TAK-242 significantly reverses the suppression of odonto-differentiation of DPCs in diabetic offspring. Taken together, these data indicate GDM activated the offspring DPCs TLR4/NF-ĸB signaling, which suppressed the SMAD1/5/9 phosphorylation and then inhibited odontoblasts differentiation and dentin formation." {{tooth}}

	* Maternal diabetes during pregnancy and early onset of cardiovascular disease in offspring{{#pmid:31801789\|PMID31801789}} "All 2 432 000 liveborn children without congenital heart disease in Denmark during 1977-2016. Follow-up began at birth and continued until first time diagnosis of CVD, death, emigration, or 31 December 2016, whichever came first. The primary outcome was early onset CVD (excluding congenital heart diseases) defined by hospital diagnosis. Associations between maternal diabetes and risks of early onset CVD in offspring were studied. Cox regression was used to assess whether a maternal history of CVD or maternal diabetic complications affected these associations. Adjustments were made for calendar year, sex, singleton status, maternal factors (parity, age, smoking, education, cohabitation, residence at childbirth, history of CVD before childbirth), and paternal history of CVD before childbirth. The cumulative incidence was averaged across all individuals, and factors were adjusted while treating deaths from causes other than CVD as competing events. Children of mothers with diabetes, especially those mothers with a history of CVD or diabetic complications, have increased rates of early onset CVD from childhood to early adulthood. If maternal diabetes does have a causal association with increased CVD rate in offspring, the prevention, screening, and treatment of diabetes in women of childbearing age could help to reduce the risk of CVD in the next generation."		* '''Maternal diabetes during pregnancy and early onset of cardiovascular disease in offspring'''{{#pmid:31801789\|PMID31801789}} "All 2 432 000 liveborn children without congenital heart disease in Denmark during 1977-2016. Follow-up began at birth and continued until first time diagnosis of CVD, death, emigration, or 31 December 2016, whichever came first. The primary outcome was early onset CVD (excluding congenital heart diseases) defined by hospital diagnosis. Associations between maternal diabetes and risks of early onset CVD in offspring were studied. Cox regression was used to assess whether a maternal history of CVD or maternal diabetic complications affected these associations. Adjustments were made for calendar year, sex, singleton status, maternal factors (parity, age, smoking, education, cohabitation, residence at childbirth, history of CVD before childbirth), and paternal history of CVD before childbirth. The cumulative incidence was averaged across all individuals, and factors were adjusted while treating deaths from causes other than CVD as competing events. Children of mothers with diabetes, especially those mothers with a history of CVD or diabetic complications, have increased rates of early onset CVD from childhood to early adulthood. If maternal diabetes does have a causal association with increased CVD rate in offspring, the prevention, screening, and treatment of diabetes in women of childbearing age could help to reduce the risk of CVD in the next generation."

	* '''Maternal diabetes induces autism-like behavior by hyperglycemia-mediated persistent oxidative stress and suppression of superoxide dismutase 2'''{{#pmid:31685635\|PMID31685635}} "Epidemiological studies show that maternal diabetes is associated with an increased risk of autism spectrum disorders (ASDs), although the detailed mechanisms remain unclear. The present study aims to investigate the potential effect of maternal diabetes on autism-like behavior in offspring. The results of in vitro study showed that transient hyperglycemia induces persistent reactive oxygen species (ROS) generation with suppressed superoxide dismutase 2 (SOD2) expression. Additionally, we found that SOD2 suppression is due to oxidative stress-mediated histone methylation and the subsequent dissociation of early growth response 1 (Egr1) on the SOD2 promoter. Furthermore, in vivo rat experiments showed that maternal diabetes induces SOD2 suppression in the amygdala, resulting in autism-like behavior in offspring. SOD2 overexpression restores, while SOD2 knockdown mimics, this effect, indicating that oxidative stress and SOD2 expression play important roles in maternal diabetes-induced autism-like behavior in offspring, while prenatal and postnatal treatment using antioxidants permeable to the blood-brain barrier partly ameliorated this effect. We conclude that maternal diabetes induces autism-like behavior through hyperglycemia-mediated persistent oxidative stress and SOD2 suppression. Here we report a potential mechanism for maternal diabetes-induced ASD."		* '''Maternal diabetes induces autism-like behavior by hyperglycemia-mediated persistent oxidative stress and suppression of superoxide dismutase 2'''{{#pmid:31685635\|PMID31685635}} "Epidemiological studies show that maternal diabetes is associated with an increased risk of autism spectrum disorders (ASDs), although the detailed mechanisms remain unclear. The present study aims to investigate the potential effect of maternal diabetes on autism-like behavior in offspring. The results of in vitro study showed that transient hyperglycemia induces persistent reactive oxygen species (ROS) generation with suppressed superoxide dismutase 2 (SOD2) expression. Additionally, we found that SOD2 suppression is due to oxidative stress-mediated histone methylation and the subsequent dissociation of early growth response 1 (Egr1) on the SOD2 promoter. Furthermore, in vivo rat experiments showed that maternal diabetes induces SOD2 suppression in the amygdala, resulting in autism-like behavior in offspring. SOD2 overexpression restores, while SOD2 knockdown mimics, this effect, indicating that oxidative stress and SOD2 expression play important roles in maternal diabetes-induced autism-like behavior in offspring, while prenatal and postnatal treatment using antioxidants permeable to the blood-brain barrier partly ameliorated this effect. We conclude that maternal diabetes induces autism-like behavior through hyperglycemia-mediated persistent oxidative stress and SOD2 suppression. Here we report a potential mechanism for maternal diabetes-induced ASD."

Z8600021 at 04:43, 8 Ocak 2020

2020-01-08T04:43:16Z

← Older revision		Revision as of 15:43, 8 Ocak 2020
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			* '''Gestational diabetes mellitus affects odontoblastic differentiation of dental papilla cells via Toll-like receptor 4 signaling in offspring'''{{#pmid:31595494\|PMID31595494}} "Gestational diabetes mellitus (GDM) is an important factor involved in the pathogenesis of organ development in the offspring. Here, we analyzed the effects of GDM on odontoblastic differentiation of dental papilla cells (DPCs) and dentin formation in offspring and investigated their underlying mechanisms. A GDM {{rat}} model was induced by intraperitoneal injection of streptozotocin and offspring were collected. The results showed that GDM significantly affected odontoblast differentiation and dentin formation in offspring tooth. GDM activated the toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-ĸB) signaling pathway and inhibited SMAD1/5/9 signaling to modulate the odontoblastic differentiation of DPCs in offspring. Inhibition of TLR4 signaling by treated with TAK-242 significantly reverses the suppression of odonto-differentiation of DPCs in diabetic offspring. Taken together, these data indicate GDM activated the offspring DPCs TLR4/NF-ĸB signaling, which suppressed the SMAD1/5/9 phosphorylation and then inhibited odontoblasts differentiation and dentin formation." {{tooth}}

	* Maternal diabetes during pregnancy and early onset of cardiovascular disease in offspring{{#pmid:31801789\|PMID31801789}} "All 2 432 000 liveborn children without congenital heart disease in Denmark during 1977-2016. Follow-up began at birth and continued until first time diagnosis of CVD, death, emigration, or 31 December 2016, whichever came first. The primary outcome was early onset CVD (excluding congenital heart diseases) defined by hospital diagnosis. Associations between maternal diabetes and risks of early onset CVD in offspring were studied. Cox regression was used to assess whether a maternal history of CVD or maternal diabetic complications affected these associations. Adjustments were made for calendar year, sex, singleton status, maternal factors (parity, age, smoking, education, cohabitation, residence at childbirth, history of CVD before childbirth), and paternal history of CVD before childbirth. The cumulative incidence was averaged across all individuals, and factors were adjusted while treating deaths from causes other than CVD as competing events. Children of mothers with diabetes, especially those mothers with a history of CVD or diabetic complications, have increased rates of early onset CVD from childhood to early adulthood. If maternal diabetes does have a causal association with increased CVD rate in offspring, the prevention, screening, and treatment of diabetes in women of childbearing age could help to reduce the risk of CVD in the next generation."		* Maternal diabetes during pregnancy and early onset of cardiovascular disease in offspring{{#pmid:31801789\|PMID31801789}} "All 2 432 000 liveborn children without congenital heart disease in Denmark during 1977-2016. Follow-up began at birth and continued until first time diagnosis of CVD, death, emigration, or 31 December 2016, whichever came first. The primary outcome was early onset CVD (excluding congenital heart diseases) defined by hospital diagnosis. Associations between maternal diabetes and risks of early onset CVD in offspring were studied. Cox regression was used to assess whether a maternal history of CVD or maternal diabetic complications affected these associations. Adjustments were made for calendar year, sex, singleton status, maternal factors (parity, age, smoking, education, cohabitation, residence at childbirth, history of CVD before childbirth), and paternal history of CVD before childbirth. The cumulative incidence was averaged across all individuals, and factors were adjusted while treating deaths from causes other than CVD as competing events. Children of mothers with diabetes, especially those mothers with a history of CVD or diabetic complications, have increased rates of early onset CVD from childhood to early adulthood. If maternal diabetes does have a causal association with increased CVD rate in offspring, the prevention, screening, and treatment of diabetes in women of childbearing age could help to reduce the risk of CVD in the next generation."

Z8600021 at 23:45, 7 Ocak 2020

2020-01-07T23:45:44Z

← Older revision		Revision as of 10:45, 8 Ocak 2020
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	Anencephaly in a fetus (GA week 18) shown by ultrasound (coronal images) complete absence of the cranial vault and brain and enlarged orbits.{{#pmid:21042439\|PMID21042439}}		Anencephaly in a fetus (GA week 18) shown by ultrasound (coronal images) complete absence of the cranial vault and brain and enlarged orbits.{{#pmid:21042439\|PMID21042439}}
	:'''Links:''' [[Neural_System_-_Abnormalities#Anencephaly\|Anencephaly]] \| [[Neural System Development]]		:'''Links:''' [[Neural_System_-_Abnormalities#Anencephaly\|Anencephaly]] \| [[Neural System Development]]

	==Fetal Macrosomia==		==Fetal Macrosomia==
	Fetal macrosomia is a clinical description for a fetus that is too large, condition increases steadily with advancing gestational age and defined by a variety of birthweights. In pregnant women, anywhere between 2 - 15% have birth weights of greater than 4000 grams (4 Kg, 8 lb 13 oz).		Fetal macrosomia is a clinical description for a fetus that is too large, condition increases steadily with advancing gestational age and defined by a variety of birthweights. In pregnant women, anywhere between 2 - 15% have birth weights of greater than 4000 grams (4 Kg, 8 lb 13 oz).
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	:'''Links:''' [[Birth Weight]] \| [[Birth]]		:'''Links:''' [[Birth Weight]] \| [[Birth]]


			==Metabolic Syndrome==
			Obesity and insulin resistance cause Metabolic syndrome (MetS) that acts as a predictor for the risk of type 2 diabetes mellitus and cardiovascular disease.

			:'''Links:''' [http://www.ncbi.nlm.nih.gov/pubmed/?term=Metabolic+Syndrome ''Metabolic Syndrome'']
	==Animal Models==		==Animal Models==

Z8600021 at 00:10, 7 December 2019

2019-12-07T00:10:09Z

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			* Maternal diabetes during pregnancy and early onset of cardiovascular disease in offspring{{#pmid:31801789\|PMID31801789}} "All 2 432 000 liveborn children without congenital heart disease in Denmark during 1977-2016. Follow-up began at birth and continued until first time diagnosis of CVD, death, emigration, or 31 December 2016, whichever came first. The primary outcome was early onset CVD (excluding congenital heart diseases) defined by hospital diagnosis. Associations between maternal diabetes and risks of early onset CVD in offspring were studied. Cox regression was used to assess whether a maternal history of CVD or maternal diabetic complications affected these associations. Adjustments were made for calendar year, sex, singleton status, maternal factors (parity, age, smoking, education, cohabitation, residence at childbirth, history of CVD before childbirth), and paternal history of CVD before childbirth. The cumulative incidence was averaged across all individuals, and factors were adjusted while treating deaths from causes other than CVD as competing events. Children of mothers with diabetes, especially those mothers with a history of CVD or diabetic complications, have increased rates of early onset CVD from childhood to early adulthood. If maternal diabetes does have a causal association with increased CVD rate in offspring, the prevention, screening, and treatment of diabetes in women of childbearing age could help to reduce the risk of CVD in the next generation."

	* '''Maternal diabetes induces autism-like behavior by hyperglycemia-mediated persistent oxidative stress and suppression of superoxide dismutase 2'''{{#pmid:31685635\|PMID31685635}} "Epidemiological studies show that maternal diabetes is associated with an increased risk of autism spectrum disorders (ASDs), although the detailed mechanisms remain unclear. The present study aims to investigate the potential effect of maternal diabetes on autism-like behavior in offspring. The results of in vitro study showed that transient hyperglycemia induces persistent reactive oxygen species (ROS) generation with suppressed superoxide dismutase 2 (SOD2) expression. Additionally, we found that SOD2 suppression is due to oxidative stress-mediated histone methylation and the subsequent dissociation of early growth response 1 (Egr1) on the SOD2 promoter. Furthermore, in vivo rat experiments showed that maternal diabetes induces SOD2 suppression in the amygdala, resulting in autism-like behavior in offspring. SOD2 overexpression restores, while SOD2 knockdown mimics, this effect, indicating that oxidative stress and SOD2 expression play important roles in maternal diabetes-induced autism-like behavior in offspring, while prenatal and postnatal treatment using antioxidants permeable to the blood-brain barrier partly ameliorated this effect. We conclude that maternal diabetes induces autism-like behavior through hyperglycemia-mediated persistent oxidative stress and SOD2 suppression. Here we report a potential mechanism for maternal diabetes-induced ASD."		* '''Maternal diabetes induces autism-like behavior by hyperglycemia-mediated persistent oxidative stress and suppression of superoxide dismutase 2'''{{#pmid:31685635\|PMID31685635}} "Epidemiological studies show that maternal diabetes is associated with an increased risk of autism spectrum disorders (ASDs), although the detailed mechanisms remain unclear. The present study aims to investigate the potential effect of maternal diabetes on autism-like behavior in offspring. The results of in vitro study showed that transient hyperglycemia induces persistent reactive oxygen species (ROS) generation with suppressed superoxide dismutase 2 (SOD2) expression. Additionally, we found that SOD2 suppression is due to oxidative stress-mediated histone methylation and the subsequent dissociation of early growth response 1 (Egr1) on the SOD2 promoter. Furthermore, in vivo rat experiments showed that maternal diabetes induces SOD2 suppression in the amygdala, resulting in autism-like behavior in offspring. SOD2 overexpression restores, while SOD2 knockdown mimics, this effect, indicating that oxidative stress and SOD2 expression play important roles in maternal diabetes-induced autism-like behavior in offspring, while prenatal and postnatal treatment using antioxidants permeable to the blood-brain barrier partly ameliorated this effect. We conclude that maternal diabetes induces autism-like behavior through hyperglycemia-mediated persistent oxidative stress and SOD2 suppression. Here we report a potential mechanism for maternal diabetes-induced ASD."

Z8600021 at 23:09, 6 December 2019

2019-12-06T23:09:54Z

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	* '''Maternal diabetes induces autism-like behavior by hyperglycemia-mediated persistent oxidative stress and suppression of superoxide dismutase 2'''{{#pmid:31685635}} "Epidemiological studies show that maternal diabetes is associated with an increased risk of autism spectrum disorders (ASDs), although the detailed mechanisms remain unclear. The present study aims to investigate the potential effect of maternal diabetes on autism-like behavior in offspring. The results of in vitro study showed that transient hyperglycemia induces persistent reactive oxygen species (ROS) generation with suppressed superoxide dismutase 2 (SOD2) expression. Additionally, we found that SOD2 suppression is due to oxidative stress-mediated histone methylation and the subsequent dissociation of early growth response 1 (Egr1) on the SOD2 promoter. Furthermore, in vivo rat experiments showed that maternal diabetes induces SOD2 suppression in the amygdala, resulting in autism-like behavior in offspring. SOD2 overexpression restores, while SOD2 knockdown mimics, this effect, indicating that oxidative stress and SOD2 expression play important roles in maternal diabetes-induced autism-like behavior in offspring, while prenatal and postnatal treatment using antioxidants permeable to the blood-brain barrier partly ameliorated this effect. We conclude that maternal diabetes induces autism-like behavior through hyperglycemia-mediated persistent oxidative stress and SOD2 suppression. Here we report a potential mechanism for maternal diabetes-induced ASD."
			* '''Maternal diabetes induces autism-like behavior by hyperglycemia-mediated persistent oxidative stress and suppression of superoxide dismutase 2'''{{#pmid:31685635\|PMID31685635}} "Epidemiological studies show that maternal diabetes is associated with an increased risk of autism spectrum disorders (ASDs), although the detailed mechanisms remain unclear. The present study aims to investigate the potential effect of maternal diabetes on autism-like behavior in offspring. The results of in vitro study showed that transient hyperglycemia induces persistent reactive oxygen species (ROS) generation with suppressed superoxide dismutase 2 (SOD2) expression. Additionally, we found that SOD2 suppression is due to oxidative stress-mediated histone methylation and the subsequent dissociation of early growth response 1 (Egr1) on the SOD2 promoter. Furthermore, in vivo rat experiments showed that maternal diabetes induces SOD2 suppression in the amygdala, resulting in autism-like behavior in offspring. SOD2 overexpression restores, while SOD2 knockdown mimics, this effect, indicating that oxidative stress and SOD2 expression play important roles in maternal diabetes-induced autism-like behavior in offspring, while prenatal and postnatal treatment using antioxidants permeable to the blood-brain barrier partly ameliorated this effect. We conclude that maternal diabetes induces autism-like behavior through hyperglycemia-mediated persistent oxidative stress and SOD2 suppression. Here we report a potential mechanism for maternal diabetes-induced ASD."

			* '''Gestational diabetes associated with incident diabetes in childhood and youth: a retrospective cohort study'''{{#pmid:30988041\|PMID30988041}} "Indicators of childhood- and youth-onset diabetes may be useful for early detection of diabetes; there is a known association between composite exposure of parental type 2 diabetes and gestational diabetes mellitus with childhood- and youth-onset diabetes. We examined associations between gestational diabetes mellitus and incidence of childhood- and youth-onset diabetes in offspring. Using public health insurance administrative databases from Quebec, Canada, we randomly selected singleton live births with maternal gestational diabetes mellitus (1990-2007) and matched them 1:1 with singleton live births without gestational diabetes mellitus. Follow-up was to Mar. 31, 2012. We examined associations of diabetes in offspring with maternal gestational diabetes mellitus through unadjusted and adjusted Cox proportional hazards models. In secondary analyses, we separately considered age groups ranging from birth to age 12 years, and age 12 to 22 years. Gestational diabetes mellitus is associated with incident diabetes in offspring during childhood and adolescence. Future studies are needed to examine longer-term outcomes in patients with pediatric diabetes with a maternal history of gestational diabetes mellitus, to ascertain how they compare with other patients with childhood- or youth-onset diabetes, in terms of disease severity and outcomes."

	* '''Report - Incidence of insulin-treated diabetes in Australia'''<ref name=AIHW-2019_Diabetes>{{Ref-AIHW-2019_Diabetes}}</ref> "In Australia 2017 there were 29,797 people who began using insulin to treat their diabetes, of these 9,053 (30%) women began using insulin to treat {{gestational diabetes}}."		* '''Report - Incidence of insulin-treated diabetes in Australia'''<ref name=AIHW-2019_Diabetes>{{Ref-AIHW-2019_Diabetes}}</ref> "In Australia 2017 there were 29,797 people who began using insulin to treat their diabetes, of these 9,053 (30%) women began using insulin to treat {{gestational diabetes}}."
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	* '''Comparative proteomic analysis of maternal peripheral plasma and umbilical venous plasma from normal and gestational diabetes mellitus pregnancies'''{{#pmid:30200149\|PMID30200149}} Gestational diabetes mellitus (GDM) increases many health risks in offspring. The study aims to investigate the underlying mechanism in fetal risk of GDM.We collected maternal peripheral plasma and umbilical venous plasma samples from 4 GDM and 4 control patients during their delivery at a university-based women's hospital. ...We identified 19 up-regulated proteins and 15 down-regulated proteins in GDM peripheral plasma, 29 up-regulated proteins and 69 down-regulated proteins in GDM umbilical venous plasma. Cholesteryl ester transfer protein (CETP) concentration was significantly lower in both GDM peripheral plasma and umbilical venous plasma. Upstream regulator analysis predicted follicle-stimulating hormone ({{FSH}}) as the activated regulator of differentially expressed proteins.The protein profiles in both GDM peripheral plasma and umbilical venous plasma between normal and GDM patients were significantly different. The results indicated that CETP and {{FSH}} might associates with health problem of GDM offspring."		* '''Comparative proteomic analysis of maternal peripheral plasma and umbilical venous plasma from normal and gestational diabetes mellitus pregnancies'''{{#pmid:30200149\|PMID30200149}} Gestational diabetes mellitus (GDM) increases many health risks in offspring. The study aims to investigate the underlying mechanism in fetal risk of GDM.We collected maternal peripheral plasma and umbilical venous plasma samples from 4 GDM and 4 control patients during their delivery at a university-based women's hospital. ...We identified 19 up-regulated proteins and 15 down-regulated proteins in GDM peripheral plasma, 29 up-regulated proteins and 69 down-regulated proteins in GDM umbilical venous plasma. Cholesteryl ester transfer protein (CETP) concentration was significantly lower in both GDM peripheral plasma and umbilical venous plasma. Upstream regulator analysis predicted follicle-stimulating hormone ({{FSH}}) as the activated regulator of differentially expressed proteins.The protein profiles in both GDM peripheral plasma and umbilical venous plasma between normal and GDM patients were significantly different. The results indicated that CETP and {{FSH}} might associates with health problem of GDM offspring."

	* '''Maternal diabetes alters the development of ductus venosus shunting in the fetus'''{{#pmid:29752712\|PMID29752712}} "Despite adequate glycemic control, the risks of fetal macrosomia and perinatal complications are increased in diabetic pregnancies. Adjustments of the umbilical venous (UV) distribution, including increased ductus venosus (DV) shunting, can be important fetal compensatory mechanisms, but the impact of pregestational diabetes on UV and DV flow is not known. In pregnancies with pregestational diabetes mellitus, prioritized UV distribution to the fetal liver, and lower DV shunt capacity, both reduce the compensatory capability of the fetus and may represent an augmented risk during hypoxic challenges during late pregnancy and birth." {{ductus venosus}}		* '''Maternal diabetes alters the development of {{ductus venosus}} shunting in the fetus'''{{#pmid:29752712\|PMID29752712}} "Despite adequate glycemic control, the risks of fetal macrosomia and perinatal complications are increased in diabetic pregnancies. Adjustments of the umbilical venous (UV) distribution, including increased ductus venosus (DV) shunting, can be important fetal compensatory mechanisms, but the impact of pregestational diabetes on UV and DV flow is not known. In pregnancies with pregestational diabetes mellitus, prioritized UV distribution to the fetal liver, and lower DV shunt capacity, both reduce the compensatory capability of the fetus and may represent an augmented risk during hypoxic challenges during late pregnancy and birth." {{ductus venosus}}

	* [http://collections.plos.org/diabetes-prevention PLoS Collection - Diabetes Prevention] In this Collection, we feature PLOS articles that focus on the prevention of diabetes.		* [http://collections.plos.org/diabetes-prevention PLoS Collection - Diabetes Prevention] In this Collection, we feature PLOS articles that focus on the prevention of diabetes.

← Older revision		Revision as of 15:52, 8 Ocak 2020
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	* '''Gestational diabetes mellitus affects odontoblastic differentiation of dental papilla cells via Toll-like receptor 4 signaling in offspring'''{{#pmid:31595494\|PMID31595494}} "Gestational diabetes mellitus (GDM) is an important factor involved in the pathogenesis of organ development in the offspring. Here, we analyzed the effects of GDM on odontoblastic differentiation of dental papilla cells (DPCs) and dentin formation in offspring and investigated their underlying mechanisms. A GDM {{rat}} model was induced by intraperitoneal injection of streptozotocin and offspring were collected. The results showed that GDM significantly affected odontoblast differentiation and dentin formation in offspring tooth. GDM activated the toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-ĸB) signaling pathway and inhibited SMAD1/5/9 signaling to modulate the odontoblastic differentiation of DPCs in offspring. Inhibition of TLR4 signaling by treated with TAK-242 significantly reverses the suppression of odonto-differentiation of DPCs in diabetic offspring. Taken together, these data indicate GDM activated the offspring DPCs TLR4/NF-ĸB signaling, which suppressed the SMAD1/5/9 phosphorylation and then inhibited odontoblasts differentiation and dentin formation." {{tooth}}		* '''Gestational diabetes mellitus affects odontoblastic differentiation of dental papilla cells via Toll-like receptor 4 signaling in offspring'''{{#pmid:31595494\|PMID31595494}} "Gestational diabetes mellitus (GDM) is an important factor involved in the pathogenesis of organ development in the offspring. Here, we analyzed the effects of GDM on odontoblastic differentiation of dental papilla cells (DPCs) and dentin formation in offspring and investigated their underlying mechanisms. A GDM {{rat}} model was induced by intraperitoneal injection of streptozotocin and offspring were collected. The results showed that GDM significantly affected odontoblast differentiation and dentin formation in offspring tooth. GDM activated the toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-ĸB) signaling pathway and inhibited SMAD1/5/9 signaling to modulate the odontoblastic differentiation of DPCs in offspring. Inhibition of TLR4 signaling by treated with TAK-242 significantly reverses the suppression of odonto-differentiation of DPCs in diabetic offspring. Taken together, these data indicate GDM activated the offspring DPCs TLR4/NF-ĸB signaling, which suppressed the SMAD1/5/9 phosphorylation and then inhibited odontoblasts differentiation and dentin formation." {{tooth}}

	* Maternal diabetes during pregnancy and early onset of cardiovascular disease in offspring{{#pmid:31801789\|PMID31801789}} "All 2 432 000 liveborn children without congenital heart disease in Denmark during 1977-2016. Follow-up began at birth and continued until first time diagnosis of CVD, death, emigration, or 31 December 2016, whichever came first. The primary outcome was early onset CVD (excluding congenital heart diseases) defined by hospital diagnosis. Associations between maternal diabetes and risks of early onset CVD in offspring were studied. Cox regression was used to assess whether a maternal history of CVD or maternal diabetic complications affected these associations. Adjustments were made for calendar year, sex, singleton status, maternal factors (parity, age, smoking, education, cohabitation, residence at childbirth, history of CVD before childbirth), and paternal history of CVD before childbirth. The cumulative incidence was averaged across all individuals, and factors were adjusted while treating deaths from causes other than CVD as competing events. Children of mothers with diabetes, especially those mothers with a history of CVD or diabetic complications, have increased rates of early onset CVD from childhood to early adulthood. If maternal diabetes does have a causal association with increased CVD rate in offspring, the prevention, screening, and treatment of diabetes in women of childbearing age could help to reduce the risk of CVD in the next generation."		* '''Maternal diabetes during pregnancy and early onset of cardiovascular disease in offspring'''{{#pmid:31801789\|PMID31801789}} "All 2 432 000 liveborn children without congenital heart disease in Denmark during 1977-2016. Follow-up began at birth and continued until first time diagnosis of CVD, death, emigration, or 31 December 2016, whichever came first. The primary outcome was early onset CVD (excluding congenital heart diseases) defined by hospital diagnosis. Associations between maternal diabetes and risks of early onset CVD in offspring were studied. Cox regression was used to assess whether a maternal history of CVD or maternal diabetic complications affected these associations. Adjustments were made for calendar year, sex, singleton status, maternal factors (parity, age, smoking, education, cohabitation, residence at childbirth, history of CVD before childbirth), and paternal history of CVD before childbirth. The cumulative incidence was averaged across all individuals, and factors were adjusted while treating deaths from causes other than CVD as competing events. Children of mothers with diabetes, especially those mothers with a history of CVD or diabetic complications, have increased rates of early onset CVD from childhood to early adulthood. If maternal diabetes does have a causal association with increased CVD rate in offspring, the prevention, screening, and treatment of diabetes in women of childbearing age could help to reduce the risk of CVD in the next generation."

	* '''Maternal diabetes induces autism-like behavior by hyperglycemia-mediated persistent oxidative stress and suppression of superoxide dismutase 2'''{{#pmid:31685635\|PMID31685635}} "Epidemiological studies show that maternal diabetes is associated with an increased risk of autism spectrum disorders (ASDs), although the detailed mechanisms remain unclear. The present study aims to investigate the potential effect of maternal diabetes on autism-like behavior in offspring. The results of in vitro study showed that transient hyperglycemia induces persistent reactive oxygen species (ROS) generation with suppressed superoxide dismutase 2 (SOD2) expression. Additionally, we found that SOD2 suppression is due to oxidative stress-mediated histone methylation and the subsequent dissociation of early growth response 1 (Egr1) on the SOD2 promoter. Furthermore, in vivo rat experiments showed that maternal diabetes induces SOD2 suppression in the amygdala, resulting in autism-like behavior in offspring. SOD2 overexpression restores, while SOD2 knockdown mimics, this effect, indicating that oxidative stress and SOD2 expression play important roles in maternal diabetes-induced autism-like behavior in offspring, while prenatal and postnatal treatment using antioxidants permeable to the blood-brain barrier partly ameliorated this effect. We conclude that maternal diabetes induces autism-like behavior through hyperglycemia-mediated persistent oxidative stress and SOD2 suppression. Here we report a potential mechanism for maternal diabetes-induced ASD."		* '''Maternal diabetes induces autism-like behavior by hyperglycemia-mediated persistent oxidative stress and suppression of superoxide dismutase 2'''{{#pmid:31685635\|PMID31685635}} "Epidemiological studies show that maternal diabetes is associated with an increased risk of autism spectrum disorders (ASDs), although the detailed mechanisms remain unclear. The present study aims to investigate the potential effect of maternal diabetes on autism-like behavior in offspring. The results of in vitro study showed that transient hyperglycemia induces persistent reactive oxygen species (ROS) generation with suppressed superoxide dismutase 2 (SOD2) expression. Additionally, we found that SOD2 suppression is due to oxidative stress-mediated histone methylation and the subsequent dissociation of early growth response 1 (Egr1) on the SOD2 promoter. Furthermore, in vivo rat experiments showed that maternal diabetes induces SOD2 suppression in the amygdala, resulting in autism-like behavior in offspring. SOD2 overexpression restores, while SOD2 knockdown mimics, this effect, indicating that oxidative stress and SOD2 expression play important roles in maternal diabetes-induced autism-like behavior in offspring, while prenatal and postnatal treatment using antioxidants permeable to the blood-brain barrier partly ameliorated this effect. We conclude that maternal diabetes induces autism-like behavior through hyperglycemia-mediated persistent oxidative stress and SOD2 suppression. Here we report a potential mechanism for maternal diabetes-induced ASD."