Talk:BGDB Gastrointestinal - Fetal

BGD Internal Links 2009 5. Fetal

Development of c-kit immunopositive interstitial cells of Cajal in the human stomach

J Cell Mol Med. 2010 May;14(5):1125-34. doi: 10.1111/j.1582-4934.2009.00725.x.

Radenkovic G, Savic V, Mitic D, Grahovac S, Bjelakovic M, Krstic M. Source Department of Histology and Embryology, Faculty of Medicine, University of Nis, Nis, Serbia. radenkog@scnet.yu

Abstract

Interstitial cells of Cajal (ICC) include several types of specialized cells within the musculature of the gastrointestinal tract (GIT). Some types of ICC act as pacemakers in the GIT musculature, whereas others are implicated in the modulation of enteric neurotransmission. Kit immunohistochemistry reliably identifies the location of these cells and provides information on changes in ICC distribution and density. Human stomach specimens were obtained from 7 embryos and 28 foetuses without gastrointestinal disorders. The specimens were 7-27 weeks of gestational age, and both sexes are represented in the sample. The specimens were exposed to anti-c-kit antibodies to investigate ICC differentiation. Enteric plexuses were immunohistochemically examined by using anti-neuron specific enolase and the differentiation of smooth muscle cells (SMC) was studied with anti-alpha smooth muscle actin and anti-desmin antibodies. By week 7, c-kit-immunopositive precursors formed a layer in the outer stomach wall around myenteric plexus elements. Between 9 and 11 weeks some of these precursors differentiated into ICC. ICC at the myenteric plexus level differentiated first, followed by those within the muscle layer: between SMC, at the circular and longitudinal layers, and within connective tissue septa enveloping muscle bundles. In the fourth month, all subtypes of c-kit-immunoreactivity ICC which are necessary for the generation of slow waves and their transfer to SMC have been developed. These results may help elucidate the origin of ICC and the aetiology and pathogenesis of stomach motility disorders in neonates and young children that are associated with absence or decreased number of these cells. PMID 19298525

Three-dimensional MRI volumetric measurements of the normal fetal colon

AJR Am J Roentgenol. 2009 Mar;192(3):761-5. Rubesova E, Vance CJ, Ringertz HG, Barth RA.

Department of Radiology, Lucile Packard Children's Hospital, Stanford University, 720 Welch Rd., Stanford, CA 94305, USA.

Abstract

OBJECTIVE: The use of fetal MRI markedly improves characterization of abdominal congenital anomalies. Accurate prenatal diagnosis of the level and cause of congenital intestinal obstruction is desired for optimal parental counseling and perinatal care. Because accurate diagnosis would be aided by nomograms of colonic volume, this study was conducted to determine normal colonic volumes at different gestational ages.

MATERIALS AND METHODS: This retrospective study consisted of a review of 83 fetal MRI examinations performed on fetuses with no gastrointestinal abnormalities. MRI was performed with a 1.5-T system. Axial, sagittal, and coronal T1-weighted fast gradient-refocused echo images were acquired at TR/TE, 165/2.6; flip angle, 90 degrees; matrix size, 384 x 192; slice thickness, 5 mm; field of view, 38 cm(2). Two investigators determined the region of interest in the colon by outlining areas of high signal intensity of meconium slice by slice. They then calculated colonic luminal volume in the regions of interest. Colonic luminal volumes were reported relative to gestational age and abdominal circumference. Normative curves were generated, and interobserver and intraobserver analyses were performed.

RESULTS: Seventeen of the 83 fetuses (20%) were excluded because of movement artifacts on the images. Normal colonic luminal volume increased exponentially with gestational age and abdominal circumference. The range of colonic luminal volumes at 20-37 weeks' gestational age was 1.1 - 65 mL. Variation of volume was greater at advanced gestational age. Interobserver and intraobserver correlation was good.

CONCLUSION: This study yielded preliminary volumetric measurements of the normal fetal colon at 20-37 weeks of gestational age that suggest the fetal colon grows exponentially.

Images

Normal fetus at 32 weeks of gestation http://www.ajronline.org/content/vol192/issue3/images/large/03_08_1504_01.jpeg

PMID 19234275

http://www.ajronline.org/cgi/content/full/192/3/761

Prenatal development of gastrointestinal function in the pig and the effects of fetal esophageal obstruction

Pediatr Res. 2002 Sep;52(3):416-24.

Sangild PT, Schmidt M, Elnif J, Björnvad CR, Weström BR, Buddington RK. Source Division of Nutrition, Royal Veterinary and Agricultural University, 13 Bulowsvej, DK-1870 Frederiksberg C, Denmark. psa@kvl.dk Abstract Maturation of the fetal gastrointestinal tract (GIT) is influenced by both luminal stimuli (e.g. swallowed fluid) and hormonal factors (e.g. endogenous cortisol release). The aims of the present study were 1) to investigate GIT growth and maturation during the last 20% of gestation in pigs (term = 114 +/- 2 d), and 2) to investigate the effect of esophageal ligation, to prevent fetal swallowing, at 80% to 91% gestation. In normal fetuses, marked increases occurred during late gestation in body weight (+95%), relative intestinal weight (+79%, g kg(-1) body weight), activity of some digestive enzymes (1.5- to 10-fold), and absorption of glucose and intact proteins (3- to 6-fold). Fetuses with ligated esophagi had lowered body weight (-20%), reduced intestinal weight (-43%), aminopeptidase A activity (-24%), and glucose absorption (-27%), while lactase, sucrase, and dipeptidylpeptidase IV activities were increased (+40-50%), compared with sham-operated fetuses (all p < 0.05). Other parameters of GIT function remained unchanged by esophageal obstruction (absorption of amino acids and immunoglobulin, activity of chymosin, amylase, trypsin, chymotrypsin, maltase, aminopeptidase N -- all expressed per gram GIT tissue). Ligated fetuses had elevated cortisol levels, which is known to stimulate fetal GIT maturation. We conclude that the rapid development of GIT function in late gestation is diminished by esophageal obstruction, mainly due to slower GIT growth and not inhibition of normal functional development of enterocytes.

PMID 12193678

The ontogeny of the small intestinal epithelium

JPEN J Parenter Enteral Nutr. 1999 Sep-Oct;23(5 Suppl):S3-6.

Lebenthal A, Lebenthal E. Source Department of Pediatrics, Mt Scopus, Hadassah University Hospital, Jerusalem, Israel.

Abstract

The primary factors in feeding premature infants are dependent on the development and maturation of digestion and absorption. The maturation of digestive and absorptive functions of carbohydrates, proteins, fats, minerals, and vitamins in the young premature infant were determined in relation to availability of hydrolytic enzymes, such as lipases, proteases, amylases, glucosidases, and lactase. The feeding is dependent on the ability of the premature infant to secrete salivary enzymes, gastric acid, pepsin, pancreatic exocrine enzymes, the presence of enterohepatic circulation, and the hydrolytic and absorptive capacity of the entercocyte. To evaluate the complexity of the gut maturation process, we proposed a unified concept where the ontogeny of the gastrointestinal system is the result of the following four major determinants: genetic endowment, intrinsic developmental and biological clock, endogenous regulatory mechanisms, and environmental influences. The developmental clock represents a predetermined temporal sequence of happenings in ontogeny that is inherently controlled. By 20 weeks of gestation, the anatomic differentiation of the fetal gut has progressed to the extent that it resembles that of a newborn. Secretory and absorptive functions, however, develop at different rates; the intestinal absorptive process is only partially available before 26 weeks of gestation, whereas gastric and pancreatic secretion is only basal and can be stimulated only partially even in the full-term newborn period. Regulatory mechanisms control the expression of the genetic endowment at various stages in gastrointestinal development. Neural-hormonal factors play major roles in the ontogeny of the gut. Adrenalectomy, hypophysectomy, and thyroidectomy delay the development of the gut. Administration of glucocorticoids or thyroxine at the critical stage in maturation causes early appearance of enzymes within the intestine. Other hormones that are potentially important in regulating gastrointestinal development include cholecystokinin, gastrin, secretin, which have trophic effects on the gastrointestinal tract, and insulin, insulin-like growth factors, and epidermial growth factor. The development of gastrointestinal secretory function, particularly in response to hormonal stimulation, has received considerable attention. The degree of response of the target cell is determined not only by the amount of effective hormone reaching it but also by the number and affinity of receptors on its surface. Human newborns have high levels of gastrin in their sera, yet have low acid output. Exogenous gastrin is an ineffective stimulant despite the presence of seemingly "anatomically developed" parietal cells. It seems that neither endogenous nor exogenous gastrin has an effect on the target cell. If one accepts the role of circulating gastrin levels in the regulation of its own receptor, one can hypothesize the absence of a regulatory effect of gastrin in the newborn period. It was shown that hormonal regulation of migrating activity by motilin is also absent in the preterm and term infant. Plasma levels of motilin in neonates are comparable to those found in adults, but migrating motor complexes occur in the absence of cycling of plasma concentrations. Interestingly, however, the motilin receptor appears to be present. In conclusion, the feeding mode content, concentration, and volume of the very young premature infant can be assessed by the development of digestive and absorptive capacity and gut motility. The concomitant changes in gut hormones and regulatory peptides during ontogeny and feeding will add a new dimension in the understanding of when, what, and how to feed the very young premature infant. PMID 10483884