Impact and Mechanisms of Pancreatic Beta-Cell Mass Programming by Maternal Diabetes - Insight from Animal Model Studies

Chavey, Audrey; Movassat, Jamileh; Portha, Bernard

doi:10.5772/23027

Cited by 5 publications

(4 citation statements)

References 178 publications

(189 reference statements)

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“…Insulin secretion has been reported to be abnormal in islets from offspring of diabetic mothers [5, 39], and glucose metabolism was found to be the primary regulator of beta-cell function [40, 41]. Ezenwaka et al [42] also observed that maternal diabetes alters the morphology, number, and size of offspring islets as well as the ability of the offspring islets to respond to the challenge of pregnancy.…”

Section: Discussionmentioning

confidence: 99%

“…Fetal exposure to maternal diabetes in utero increases the risk of obesity/adiposity, glucose intolerance, and type 2 diabetes for offspring in later life [2–5]. Little information is available to explain the mechanism of these actions.…”

Section: Introductionmentioning

confidence: 99%

“…In the case of severe maternal diabetes in the spontaneously diabetic BB rat, this effect has also been associated with a reduction in the pancreatic insulin-positive cell mass [9]. Song et al [10], Xu and Han [11], and Chavey et al [5] demonstrated that maternal diabetes induces many metabolic and functional aberrations in adult offspring pancreatic islets that lead to impaired insulin secretion. They suggested that these aberrations may contribute to the development of NIDDM in later life of the offspring of diabetic mothers.…”

Section: Introductionmentioning

confidence: 99%

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Maternal Rat Diabetes Mellitus Deleteriously Affects Insulin Sensitivity and Beta-Cell Function in the Offspring

Aref

Ahmed

Ali

et al. 2013

Journal of Diabetes Research

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This study was designed to assess the effect of maternal diabetes in rats on serum glucose and insulin concentrations, insulin resistance, histological architecture of pancreas and glycogen content in liver of offspring. The pregnant rat females were allocated into two main groups: normal control group and streptozotocin-induced diabetic group. After birth, the surviving offspring were subjected to biochemical and histological examination immediately after delivery and at the end of the 1st and 2nd postnatal weeks. In comparison with the offspring of normal control dams, the fasting serum glucose level of offspring of diabetic mothers was significantly increased at the end of the 1st and 2nd postnatal weeks. Serum insulin level of offspring of diabetic dams was significantly higher at birth and decreased significantly during the following 2 postnatal weeks, while in normal rat offspring, it was significantly increased with progress of time. HOMA Insulin Resistance (HOMA-IR) was significantly increased in the offspring of diabetic dams at birth and after 1 week than in normal rat offspring, while HOMA insulin sensitivity (HOMA-IS) was significantly decreased. HOMA beta-cell function was significantly decreased at all-time intervals in offspring of diabetic dams. At birth, islets of Langerhans as well as beta cells in offspring of diabetic dams were hypertrophied. The cells constituting islets seemed to have a high division rate. However, beta-cells were degenerated during the following 2 post-natal weeks and smaller insulin secreting cells predominated. Vacuolation and necrosis of the islets of Langerhans were also observed throughout the experimental period. The carbohydrate content in liver of offspring of diabetic dams was at all-time intervals lower than that in control. The granule distribution was more random. Overall, the preexisting maternal diabetes leads to glucose intolerance, insulin resistance, and impaired insulin sensitivity and β-cell function in the offspring at different postnatal periods.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Maternal Rat Diabetes Mellitus Deleteriously Affects Insulin Sensitivity and Beta-Cell Function in the Offspring

Aref

Ahmed

Ali

et al. 2013

Journal of Diabetes Research

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“…Any alteration in the intrauterine environment at this critical stage of fetal development may have serious complications and life-long consequences [1,2]. Maternal diabetes is one of the paramount intrauterine disruptions that have damaging impact on the health of the offspring that can manifest directly and on the long term [3][4][5][6]. The risk for an individual to develop various vascular diseases throughout life is hypothesized to be related to diabetic gestation [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

In-utero Exposure to Maternal Diabetes Increase the Risk of Vascular Diseases in the F1 Offspring in Rats

Kamel¹,

Mahmoud²,

Elfetooh³

2014

Am. J. Biomed. Sci.

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Background: Maternal diabetes is one of the fundamental intrauterine disturbances that have direct and long lasting consequences on the health of the offspring. The risk for an individual to develop various vascular diseases throughout life is hypothesized to be related to diabetic gestation.Aim: The present study aimed to evaluate the postnatal levels of different independent risk factors for vascular diseases including homocysteine (Hcy), nitric oxide (NO), lipid profile, glucose homeostasis and insulin resistance in the rat offspring of diabetic mothers. The effect of postnatal feeding with high caloric diet (HCD) was also assessed.Methods: Two groups of female Wistar rats were used (diabetic and control); diabetes was neonatally induced by STZ injection to 5-day old rats. Pregnancy was induced by mating control or diabetic females with normal healthy males overnight and the pregnancies were completed to term. After delivery the offspring were weaned to control diet (CD) or high-caloric diet (HCD) (Table 1) and followed up for 30 weeks. So the offspring groups were as following: F1 offspring of control mothers under control diet (CF1-CD), F1 offspring of control mothers under HCD (CF1-HCD), F1 offspring of diabetic mothers under control diet (DF1-CD) and F1 offspring of diabetic mothers under HCD (DF1-HCD). Every 5 weeks 0.5 ml blood samples were obtained from the 20 male and female rats for assessment of fasting blood glucose, insulin, triglycerides, cholesterol (total, HDL-C and LDL-C), homocysteine and nitric oxide end products (NOx).Results: The results indicated that maternal diabetes caused an age-dependent alteration in glucose homeostasis and resulted in insulin resistance especially in male offspring. Also, lipid profile showed Am. J. Biomed. Sci. 2014, 6(3), 201-216; doi: 10.5099/aj140300201 © 2014 by NWPII. All rights reserved 202 elevation of triglycerides, cholesterol and LDL-C while HDL-C showed significant decline in the offspring of diabetic mothers. These disturbances in glucose and lipid metabolism were associated with elevated plasma level of Hcy from 25 week age and thereafter. Also, there was an elevation in the level of nitric oxide end products (NOx).Conclusion: Maternal diabetes cause increased risk for vascular diseases in the offspring. The mechanisms of this predisposition involve disturbed lipid profile, insulin resistance, increased circulatory levels of Hcy (independent risk factor for vascular diseases) and nitric oxide end products. Male rat offspring appear to be more sensitive for the development of vascular diseases than female offspring and postnatal diet plays important role in this predisposition as the risk increases with high caloric diet.

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Early environmental factors, alteration of epigenetic marks and metabolic disease susceptibility

et al. 2014

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Impact and Mechanisms of Pancreatic Beta-Cell Mass Programming by Maternal Diabetes - Insight from Animal Model Studies

Cited by 5 publications

References 178 publications

Maternal Rat Diabetes Mellitus Deleteriously Affects Insulin Sensitivity and Beta-Cell Function in the Offspring

Maternal Rat Diabetes Mellitus Deleteriously Affects Insulin Sensitivity and Beta-Cell Function in the Offspring

In-utero Exposure to Maternal Diabetes Increase the Risk of Vascular Diseases in the F1 Offspring in Rats

Early environmental factors, alteration of epigenetic marks and metabolic disease susceptibility

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