Offspring of streptozotocin diabetic rats: size changes in Langerhans islets with time after birth

Rodríguez, Rosalía; Renauld, A; Celener, D; Perez, Rogelio; Susemihl, M. C.

doi:10.1016/s0168-8227(98)00073-4

Cited by 7 publications

(12 citation statements)

References 16 publications

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“…In contrast to the present results, Rodríguez et al [37] described that on the first day after parturition, the pancreas section areas and islets' size in pups from mildly and severely diabetic mothers were smaller than those in neonates from nondiabetic controls, and that on day 5 after delivery, the areas of islets of Langerhans in offspring from normal mothers decreased and those in pups from diabetic mothers tended to normalize. Those authors attributed these changes in the islets' size to that after parturition; the offspring is no longer exposed to the high blood sugar levels found in diabetic mothers; thereby, no hyperinsulinemia is needed.…”

Section: Discussioncontrasting

confidence: 99%

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: Discussioncontrasting

confidence: 99%

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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“…The chronic hypoxia leads to intrauterine fetal growth restriction. Rodríguez reported that immediately after parturition, pancreatic islets in pups from mildly and severely diabetic mothers were smaller than those in neonates from nondiabetic controls but the size was rapidly normalized when exposure to high blood sugar had disrupted [33]. The similar results were also observed in the Goto-Kakisaki (GK) rat, a well-defined genetic model for type 2 diabetes [34].…”

Section: Discussionmentioning

confidence: 73%

Severe Maternal Hyperglycemia Exacerbates the Development of Insulin Resistance and Fatty Liver in the Offspring on High Fat Diet

Song

Zhao

et al. 2012

Experimental Diabetes Research

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Background. Adverse maternal environments may predispose the offspring to metabolic syndrome in adulthoods, but the underlying mechanism has not been fully understood. Methods. Maternal hyperglycemia was induced by streptozotocin (STZ) injection while control (CON) rats received citrate buffer. Litters were adjusted to eight pups per dam and then weaned to standard diet. Since 13 weeks old, a subset of offspring from STZ and CON dams were switched to high fat diet (HFD) for another 13 weeks. Glucose and insulin tolerance tests (GTT and ITT) and insulin secretion assay were performed; serum levels of lipids and leptin were measured. Hepatic fat accumulation and islet area were evaluated through haematoxylin and eosin staining. Results. STZ offspring exhibited lower survival rate, lower birth weights, and growth inhibition which persisted throughout the study. STZ offspring on HFD showed more severe impairment in GTT and ITT, and more profound hepatic steatosis and more severe hyperlipidemia compared with CON-HFD rats. Conclusions. Offspring from diabetic dams would be prone to exhibit low birth weight and postnatal growth inhibition, but could maintain normal glucose tolerance and insulin sensitivity. HFD accelerates development of insulin resistance in the offspring of diabetic dams mainly via a compensatory response of islets.

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“…In this study, there were no detectable differences between the groups in terms of staining densities of insulin, glucagon and somatostatin receptors in pancreas. In the studies about the effects of GDM on the endocrine pancreas of newborn and 1–2‐week‐old offspring, it has been suggested that the volume and number of Langerhans islet cells (Aref, Ahmed, Ali, & Semmler, ; Rodriguez, Renauld, Celener, Perez, & Susemihl, ) along with insulin receptors decrease, while there is no change in glucagon and somatostatin receptors (Verhaeghe et al., ). However, as the age of offspring of mothers with GDM progress, the damages observed in Langerhans islet cells of newborns show a tendency to normalise due to the fact that pups will no longer be exposed to high glucose levels as during pregnancy (Rodriguez et al., ).…”

Section: Discussionmentioning

confidence: 99%

“…In the studies about the effects of GDM on the endocrine pancreas of newborn and 1–2‐week‐old offspring, it has been suggested that the volume and number of Langerhans islet cells (Aref, Ahmed, Ali, & Semmler, ; Rodriguez, Renauld, Celener, Perez, & Susemihl, ) along with insulin receptors decrease, while there is no change in glucagon and somatostatin receptors (Verhaeghe et al., ). However, as the age of offspring of mothers with GDM progress, the damages observed in Langerhans islet cells of newborns show a tendency to normalise due to the fact that pups will no longer be exposed to high glucose levels as during pregnancy (Rodriguez et al., ). On the other hand, it has also been reported that there is no change in the islet insulin and glucagon staining, islet volume, β‐and α‐cell percentage and β‐cell mass of the pancreas in adult offspring (15‐week‐old) of GDM mothers, but decreased insulin secretion is observed in isolated β‐cells stimulated by high glucose level (Han, Xu, Long, Epstein, & Liu, ).…”

Section: Discussionmentioning

confidence: 99%

Effect of gestational diabetes mellitus on testis and pancreatic tissues of male offspring

et al. 2018

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The purpose of this study was to determine the effect of gestational diabetes mellitus (GDM) on some reproductive characteristics, testicular and pancreatic oxidative status and pancreatic endocrine receptor densities of male offspring at post-pubertal stage. A total of 36 1-day-old Wistar Albino male offspring including 12 pups of nontreated mothers (control group), 14 pups of 40 mg/kg STZ-injected mothers (STZ-40 group) and 10 pups of 60 mg/kg STZ-injected mothers (STZ-60 group) were used. The offspring were euthanised on post-natal day 60, their blood, reproductive organs and pancreatic tissues were obtained and examined. When compared with the control group, there was a significant decrease in body and absolute reproductive organ weights, serum testosterone level, testicular and pancreatic catalase activities, pancreatic glutathione level, epididymal sperm concentration of both STZ-40 and STZ-60 groups as well as in testicular glutathione level of only STZ-60 group. Significant increases were determined in testicular and pancreatic malondialdehyde level and glutathione peroxidase activity in both groups and in fasting serum glucose of only STZ-60 group in comparison with the control group. Although some histopathological damages were observed in testes of both STZ-40 and STZ-60 groups, there were no detectable differences between the groups in density of insulin, glucagon and somatostatin receptors in pancreas. In conclusion, GDM has negative effects on reproductive efficiency and testicular-pancreatic tissue oxidant/antioxidant balance of male offspring at post-pubertal stage.

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Offspring of streptozotocin diabetic rats: size changes in Langerhans islets with time after birth

Cited by 7 publications

References 16 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

Severe Maternal Hyperglycemia Exacerbates the Development of Insulin Resistance and Fatty Liver in the Offspring on High Fat Diet

Effect of gestational diabetes mellitus on testis and pancreatic tissues of male offspring

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