High Fat Programming of β-Cell Failure

Cerf, M

doi:10.1007/978-90-481-3271-3_5

Cited by 32 publications

(21 citation statements)

References 48 publications

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“…In this situation, β-cells increase insulin secretion as a compensatory response to insulin resistance [30]. Our data confirm previous demonstrations that critical events during sensitive periods of development may ‘program’ the long-term or lifetime structure or function of the organism [31]. Recently, Cerf et al [32] showed that neonates exposed to a HF diet for the entire duration of pregnancy were hyperglycemic, with reduced β-cell volume and number.…”

Section: Discussionsupporting

confidence: 78%

Maternal High-Fat Diet Programs for Metabolic Disturbances in Offspring despite Leptin Sensitivity

et al. 2012

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A fatty diet during pregnancy in mouse dams causes metabolic abnormalities (similar to metabolic syndrome in humans) in the rodents’ offspring. We tested the hypothesis that the offspring of dams fed a high-fat diet during pregnancy and lactation develop metabolic abnormalities and leptin resistance. Pregnant C57BL/6 mice (n = 20) were fed either standard chow (SC; 19% fat) or a high-fat diet (HF; 49% fat). After weaning, male offspring were divided into four groups, according to the diet of dams and offspring: SC(dams)/SC(offspring), SC/HF, HF/SC and HF/HF (n = 30/group). For a metabolic analysis, we evaluated body mass, fat mass depots, blood plasma and adipocyte structure at 12 weeks of age. To analyse leptin sensitivity, each group was divided into two groups (vehicle or leptin) to identify the feeding response and pSTAT3 expression after acute intracerebroventricular (ICV) treatment. The offspring of mothers fed a high-fat diet presented increased body mass and visceral fat, adipocyte hypertrophy and insulin resistance. This phenotype was not associated with central leptin resistance. Thus, maternal programming by HF predisposes offspring to metabolic abnormalities despite leptin sensitivity.

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Section: Discussionsupporting

confidence: 78%

Maternal High-Fat Diet Programs for Metabolic Disturbances in Offspring despite Leptin Sensitivity

et al. 2012

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“…[1][2][3][4] Paternal programming also influences offspring metabolism. High-fat programming is induced by maternal high saturated fat intake during defined periods of gestation and/or lactation and programs the physiology and metabolism of the offspring 18 but can be extended to include the influence of paternal high-fat feeding on offspring development and health. Hepatic expression of genes involved in proliferation and cholesterol biosynthesis was regulated by a paternal low protein diet, with these changes reflected in levels of several lipid metabolites.…”

Section: Introductionmentioning

confidence: 99%

Parental high-fat programming of offspring development, health and β-cells

Cerf¹

2011

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“…The literature indicates impairment of betacell development in newborns from mothers who received an HF diet during pregnancy (Cerf et al, 2005). These findings may be caused by beta-cell replication inhibition or increased apoptotic mechanisms (Cerf, 2010).…”

Section: Maternal Caloric Restriction and Pancreatic Functionmentioning

confidence: 99%

Animal Models of Nutritional Induction of Type 2 Diabetes Mellitus

Barbosa-da-Silva¹,

Sarmento²,

Bargut³

et al. 2014

Int. J. Morphol.

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SUMMARY:Type 2 diabetes mellitus (DM2) is the most common chronic metabolic disease, affecting approximately 6% of the adult population in the Western world. This condition is a major cause of cardiovascular disease, blindness, renal failure, and amputations, with increasing prevalence worldwide. The influence of obesity on type 2 diabetes risk is determined by the degree of obesity and by body fat localization, with insulin resistance (IR) being the main link between these metabolic diseases. Experimental studies have shown that dietary factors, and particularly lipids, are strongly positively associated with body mass (BM) gain; IR; and, consequently, type 2 diabetes. Similarly, excessive consumption of energy-dense carbohydrate-rich foods can trigger the onset of type 2 diabetes. Additionally, maternal dietary inadequacies at conception and/or during the gestational period have been proposed to lead to developmental programming of excessive BM gain and metabolic disturbances in offspring, such as abnormal glucose homeostasis, reduced wholebody insulin sensitivity, impaired beta-cell insulin secretion and changes in the structure of the pancreas. Metabolic disruption is strongly associated with deleterious effects on beta-cell development and function. However, alterations in the amount and quality of dietary fat can modify glucose metabolism and insulin sensitivity. In this way, certain oils have gained attention in experimental research for their beneficial effects. Olive oil, a source of monounsaturated fatty acids (MUFAs), got attention in the past for its capacity to prevent cardiovascular diseases. Nevertheless, it is currently known that this oil also improves insulin sensitivity and glycemic control. Canola oil, flaxseed oil and especially fish oil (rich in n-3 polyunsaturated fatty acids) were first described as effective dietary nutrients against hypertriglyceridemia but now are known to have positive effects on glucose metabolism as well.

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High Fat Programming of β-Cell Failure

Cited by 32 publications

References 48 publications

Maternal High-Fat Diet Programs for Metabolic Disturbances in Offspring despite Leptin Sensitivity

Maternal High-Fat Diet Programs for Metabolic Disturbances in Offspring despite Leptin Sensitivity

Parental high-fat programming of offspring development, health and β-cells

Animal Models of Nutritional Induction of Type 2 Diabetes Mellitus

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