Effect of maternal high-fat diet on pancreatic beta cells of the offspring

Gulan, Tuohetimulati; Uchida, Toyoyoshi; Toyofuku, Yukiko; Abe, Hiroko; Fujitani, Yoshio; Hirose, Takahisa; Takeda, Satoru; Watada, Hirotaka

doi:10.1007/s13340-012-0081-z

Cited by 12 publications

(10 citation statements)

References 13 publications

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“…The maternal high‐fat/high‐sucrose diet could affect the β‐cell function negatively as found in rat studies with a maternal HFD (Tuohetimulati et al . ) and maternal low‐protein diet (Snoeck et al . , Dahri et al .…”

Section: Discussionmentioning

confidence: 99%

Maternal chocolate and sucrose soft drink intake induces hepatic steatosis in rat offspring associated with altered lipid gene expression profile

et al. 2013

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Section: Discussionmentioning

confidence: 99%

Maternal chocolate and sucrose soft drink intake induces hepatic steatosis in rat offspring associated with altered lipid gene expression profile

et al. 2013

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“… showed that 1‐day‐old neonatal rats exposed to maternal HFD in utero were hyperglycemic and had reduced beta cell volume and number. However, other studies suggest that maternal overnutrition increases the beta cell mass in the offspring early in life with an increased glucose‐induced insulin secretion (GSIS) . However, later in adulthood GSIS was reduced with lower total insulin content in islets, which may suggest declining functional beta cell mass and/or beta cell exhaustion similar to that of T2D in humans .…”

Section: Impact Of Maternal Obesity and Overnutritionmentioning

confidence: 99%

Impact of fetal and neonatal environment on beta cell function and development of diabetes

Nielsen

Haase

Jaksch

et al. 2014

Acta Obstet Gynecol Scand

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The global epidemic of diabetes is a serious threat against health and healthcare expenses. Although genetics is important it does not explain the dramatic increase in incidence, which must involve environmental factors. Two decades ago the concept of the thrifty phenotype was introduced, stating that the intrauterine environment during pregnancy has an impact on the gene expression that may persist until adulthood and cause metabolic diseases like obesity and type 2 diabetes. As the pancreatic beta cells are crucial in the regulation of metabolism this article will describe the influence of normal pregnancy on the beta cells in both the mother and the fetus and how various conditions like diabetes, obesity, overnutrition and undernutrition during and after pregnancy may influence the ability of the offspring to adapt to changes in insulin demand later in life. The influence of environmental factors including nutrients and gut microbiota on appetite regulation, mitochondrial activity and the immune system that may affect beta cell growth and function directly and indirectly is discussed. The possible role of epigenetic changes in the transgenerational transmission of the adverse programming may be the most threatening aspect with regard to the global diabetes epidemics. Finally, some suggestions for intervention are presented.

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“…Consuming high-fat foods is one of the environmental factors threatening the health of the embryo and the newborn. Most pregnant women tend to eat high-calorie and/or high-fat foods that affect not only their own health and pregnancy, but also supplies excessive nutrients to the embryo and may cause many diseases such as metabolic disorders in later life [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

“…Many studies have shown that the mother’s consumption of high-fat food can potentially affect the neuroendocrine programming in newborns and cause glucose metabolism disorders in adulthood [ 2 ]. A chronic high-fat diet in pregnant rats increases insulin levels, impairs glucose tolerance and induces obesity in the adult offspring [ 1 , 3 ]. Another study conducted on rats showed that the offspring of mothers on high-fat diets develop hyperglycemia and hyperinsulinemia and increased plasma triglyceride, body fat, liver weight, hepatic triglyceride content and vascular disorders [ 4 – 6 ].…”

Section: Introductionmentioning

confidence: 99%

“…Nevertheless, there are limited studies on the effect of a maternal high-fat diet on pancreatic beta-cell function. A study in mice showed that a maternal high-fat diet leads to glucose intolerance and reduces glucose-stimulated insulin secretion (GSIS) from the isolated pancreatic islets while increasing glucose transporter 2 (GLUT2) and glucokinase (GK) mRNA expressions [ 1 ]. Another study in rats showed that maternal high-fat feeding during pregnancy and/or lactation decreases plasma insulin concentrations and pancreatic GK and GLUT2 mRNA and protein expressions but increases pancreatic GLUT2 protein in the offspring at postnatal day 21, i.e.…”

Section: Introductionmentioning

confidence: 99%

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Maternal high-fat diet intensifies the metabolic response to stress in male rat offspring

et al. 2017

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BackgroundThe mother’s consumption of high-fat food can affect glucose metabolism and the hypothalamic–pituitary–adrenal axis responsiveness in the offspring and potentially affect the metabolic responses to stress as well. This study examines the effect of maternal high-fat diet on the expression of pancreatic glucose transporter 2 and the secretion of insulin in response to stress in offspring.MethodsFemale rats were randomly divided into normal and high-fat diet groups and were fed in accordance with their given diets from pre-pregnancy to the end of lactation. The offspring were divided into control (NC and HFC) and stress (NS and HFS) groups based on their mothers’ diet and exposure to stress in adulthood. After the two-week stress induction period was over, an intraperitoneal glucose tolerance test (IPGTT) was performed and plasma glucose and insulin levels were assessed. The pancreas was then removed for measuring insulin secretion from the isolated islets as well as glucose transporter 2 mRNA expression and protein levels.ResultsAccording to the results obtained, plasma corticosterone concentrations increased significantly on days 1 and 14 of the stress induction period and were lower on the last day compared to on the first day. In both the NS and HFS groups, stress reduced plasma insulin concentration in the IPGTT without changing the plasma glucose concentration, suggesting an increased insulin sensitivity in the NS and HFS groups, although more markedly in the latter. Stress reduced insulin secretion (at high glucose concentrations) and increased glucose transporter 2 mRNA and protein expression, especially in the HFS group.ConclusionMothers’ high-fat diet appears to intensify the stress response by changing the programming of the neuroendocrine system in the offspring.

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Effect of maternal high-fat diet on pancreatic beta cells of the offspring

Cited by 12 publications

References 13 publications

Maternal chocolate and sucrose soft drink intake induces hepatic steatosis in rat offspring associated with altered lipid gene expression profile

Maternal chocolate and sucrose soft drink intake induces hepatic steatosis in rat offspring associated with altered lipid gene expression profile

Impact of fetal and neonatal environment on beta cell function and development of diabetes

Maternal high-fat diet intensifies the metabolic response to stress in male rat offspring

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