Chronic fetal hypoglycemia inhibits the later steps of stimulus-secretion coupling in pancreatic beta-cells.

Chronic fetal hypoglycemia inhibits the later steps of stimulus-secretion coupling in pancreatic beta-cells. Research Abstract Details 

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Chronic fetal hypoglycemia inhibits the later steps of stimulus-secretion coupling in pancreatic beta-cells. Abstract Text:

Paul J Rozance,Sean W Limesand,Gary O Zerbe,William W Hay,

We measured the impact of chronic late gestation hypoglycemia on pancreatic islet structure and function to determine the cause of decreased insulin secretion in this sheep model of fetal nutrient deprivation. Late gestation hypoglycemia did not decrease pancreas weight, insulin content, beta-cell area, beta-cell mass, or islet size. The pancreatic islet isolation procedure selected a group of islets that were larger and had an increased proportion of beta-cells compared with islets measured in pancreatic sections, but there were no morphologic differences between islets isolated from control and hypoglycemic fetuses. The rates of glucose-stimulated pancreatic islet glucose utilization (126.2 +/- 25.3 pmol glucose.islet(-1).h(-1), hypoglycemic, vs. 93.5 +/- 5.5 pmol glucose.islet(-1).h(-1), control, P = 0.47) and oxidation (10.5 +/- 1.7 pmol glucose.islet(-1).h(-1), hypoglycemic, vs. 10.6 +/- 1.6 pmol glucose.islet(-1).h(-1), control) were not different in hypoglycemic fetuses compared with control fetuses. Chronic late gestation hypoglycemia decreased insulin secretion in isolated pancreatic islets by almost 70% in response to direct nonnutrient membrane depolarization and in response to increased extracellular calcium entry. beta-Cell ultrastructure was abnormal with markedly distended rough endoplasmic reticulum in three of the seven hypoglycemic fetuses studied, but in vitro analysis of hypoglycemic control islets showed no evidence that these changes represented endoplasmic reticulum stress, as measured by transcription of glucose regulatory protein-78 and processing of X-box binding protein-1. In conclusion, these studies show that chronic hypoglycemia in late gestation decreases insulin secretion by inhibiting the later steps of stimulus-secretion coupling after glucose metabolism, membrane depolarization, and calcium entry.

Chronic fetal hypoglycemia inhibits the later steps of stimulus-secretion coupling in pancreatic beta-cells. Publishing Authors By Initials

PJ Rozance,SW Limesand,GO Zerbe,WW Hay,

For similar animals: chordata: vertebrates: mammals: artiodactyla: ruminants: sheep research abstracts see: animals: chordata: vertebrates: mammals: artiodactyla: ruminants: sheep research

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Chronic fetal hypoglycemia inhibits the later steps of stimulus-secretion coupling in pancreatic beta-cells. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: American journal of physiology. Endocrinology and

VOLUME: 292

Page Numbers: E1256-64

Journal Abbreviation:

ISSN: 0193-1849

DAY: 9

MONTH: 01

YEAR: 2007

Chronic fetal hypoglycemia inhibits the later steps of stimulus-secretion coupling in pancreatic beta-cells. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901226

Chronic fetal hypoglycemia inhibits the later steps of stimulus-secretion coupling in pancreatic beta-cells. Keywords Mesh Terms:

KEYWORDS: Sheep

MESH TERMS: pathology

Chemical & Substance for Abstract: Chronic fetal hypoglycemia inhibits the later steps of stimulus-secretion coupling in pancreatic beta-cells. Information

Substance Name: Glucagon

Registry Number: 9007-92-5

Grant and Affiliation Information for Chronic fetal hypoglycemia inhibits the later steps of stimulus-secretion coupling in pancreatic beta-cells.

AFFILIATION: Perinatal Research Center, University of Colorado Health Sciences Center, Aurora, Colorado 80045, USA. Paul.Rozance@uchsc.edu

Country: United States

AGENCY: United States NCRR

GRANT: RR-00069

ACRONYM: RR

MEDLINETA: Am J Physiol Endocrinol Metab

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