Passage of Insulin through the Wall of the Gastro-intestinal Tract of the Infant Rat

Mosinger, B; Placer, Z; Koldovský, Otakar

doi:10.1038/1841245a0

Cited by 81 publications

(37 citation statements)

References 4 publications

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“…Neverthe- less, pharmacologic doses of oral insulin (more than 170-fold higher than those used in our study) administered to piglets and human infants less than 24-h-old decreased serum glucose, presumably by having been absorbed (28,29). This response does not occur in older animals (rats), even at pharmacologic doses (30). Such studies indicate that after the immediate newborn period, oral insulin does not induce systemic effects (i.e.…”

Section: Discussionmentioning

confidence: 92%

Oral Insulin Increases Small Intestinal Mass and Disaccharidase Activity in the Newborn Miniature Pig

Shulman

1990

Pediatric Research

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Section: Discussionmentioning

confidence: 92%

Oral Insulin Increases Small Intestinal Mass and Disaccharidase Activity in the Newborn Miniature Pig

Shulman

1990

Pediatric Research

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“…Maternal hyperinsulinemia and hyperglycemia could thus cause fetal hyperglycemia with attendant hyperinsulinemia (235) and later increases in fetal weight in offspring of mothers with gestational diabetes (511). On the other hand, insulin clearly does cross the gut wall in the early postnatal development in rodents (213,349) such that elevations in maternal milk insulin levels can be absorbed by the offspring as potential mediators of obesity development in later life (176).…”

Section: Insulinmentioning

confidence: 99%

Gene-Environment Interactions Controlling Energy and Glucose Homeostasis and the Developmental Origins of Obesity

Bouret

Levin

Ozanne

2015

Physiological Reviews

142

103

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LBouret S, Levin BE, Ozanne SE. Gene-Environment Interactions Controlling Energy and Glucose Homeostasis and the Developmental Origins of Obesity. Physiol Rev 95: 47-82, 2015; doi:10.1152/physrev.00007.2014.-Obesity and type 2 diabetes mellitus (T2DM) often occur together and affect a growing number of individuals in both the developed and developing worlds. Both are associated with a number of other serious illnesses that lead to increased rates of mortality. There is likely a polygenic mode of inheritance underlying both disorders, but it has become increasingly clear that the pre-and postnatal environments play critical roles in pushing predisposed individuals over the edge into a disease state. This review focuses on the many genetic and environmental variables that interact to cause predisposed individuals to become obese and diabetic. The brain and its interactions with the external and internal environment are a major focus given the prominent role these interactions play in the regulation of energy and glucose homeostasis in health and disease.

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“…One of the most striking features of the neonatal rat intestine is its ability to absorb intact macromolecules, including proteins (15)(16)(17), by the process of pinocytosis (18)(19)(20). The capacity for pinocytosis appears in the rat intestine by day 19 or 20 of intrauterine life (21,22), remains high during the first two weeks of suckling, and then decreases markedly towards the end of the third week (18,19,23).…”

Section: Biochemical Development Of the Intestinementioning

confidence: 99%

Biochemistry of Intestinal Development

Henning¹

1979

Environmental Health Perspectives

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In biochemical terms, the rat small intestine is relatively immature at birth and for the first two postnatal weeks. Then during the third week a dramatic array ofenzymic changes begins, and by the end ofthe fourth week the intestine has the digestive and absorptive properties of the adult. Selective examples of these changes are discussed with emphasis on their implications for toxicological studies. The review also includes a detailed consideration of the roles of the dietary change of weaning and of glucocorticoid and thyroid hormones in the regulation of intestinal development.My aim in this paper is to use the rat as a model system for a discussion of the postnatal development of small intestinal function. Factors which affect the developmental process will be reviewed in terms of their implications for toxicological studies. Morphologic Development of the IntestineBy the time of birth, the intestinal mucosa of the rat displays a high level of structural development characterized by villi lined with a single layer of columnar epithelial cells which have well-defined microvilli at their absorptive surface (1-3). After birth, continuous proliferation of epithelial cells occurs only in the lower regions of the crypts (4, 5), and cells migrate from there onto and along the villi, eventually being extruded from the tips into the lumen of the intestine. In adult rats and mice the generation time for the crypt cells is 10-14 hr (6), and the transit time along the length of the villus is approximately 48 hr (7). The characteristics of proliferation and migration of enterocytes in adult animals are dealt with in detail in the review by Lipkin (8). In neonatal rats, generation and migration of the cells is much slower than in adults. Despite the fact that the neonatal villi are shorter, the transit time is at least % hr (7, 9). During the third postnatal week there are significant changes in both cell kinetics and mor-

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Passage of Insulin through the Wall of the Gastro-intestinal Tract of the Infant Rat

Cited by 81 publications

References 4 publications

Oral Insulin Increases Small Intestinal Mass and Disaccharidase Activity in the Newborn Miniature Pig

Oral Insulin Increases Small Intestinal Mass and Disaccharidase Activity in the Newborn Miniature Pig

Gene-Environment Interactions Controlling Energy and Glucose Homeostasis and the Developmental Origins of Obesity

Biochemistry of Intestinal Development

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