Maternal high-fat diet consumption results in fetal malprogramming predisposing to the onset of metabolic syndrome-like phenotype in adulthood

Abstract

. Maternal high-fat diet consumption results in fetal malprogramming predisposing to the onset of metabolic syndrome-like phenotype in adulthood. Am J Physiol Endocrinol Metab 291: E792-E799, 2006. First published May 23, 2006; doi:10.1152/ajpendo.00078.2006.-Chronic consumption of a high-fat (HF) diet by female rats in their postweaning period resulted in significant increases in body weight and plasma levels of insulin, glucose, and triglycerides during pregnancy compared with female rats consuming a standard rodent laboratory chow (LC). On gestational day 21, plasma insulin levels and the insulin secretory response of islets to various secretogogues were significantly increased in HF fetuses. The HF male progeny weaned onto LC (HF/LC) demonstrated increases in body weight from postnatal day 60 onward. In adulthood, HF/LC male rats were significantly heavier than controls, had increased plasma levels of insulin, glucose, free fatty acids, and triglycerides, and demonstrated glucose intolerance. HF/LC male islets secreted increased amounts of insulin in response to low glucose concentrations, but their response to a high glucose concentration was similar to that of LC/LC islets. In another set of experiments, when the male progeny of HF female rats were weaned onto a high-sucrose diet (HF/HSu), their metabolic profile was further worsened. These results indicate that chronic consumption of a HF diet by female rats malprograms the male progeny for glucose intolerance and development of increased body weight in adulthood. The long-term high-fat feeding to female rats employed in this study bears resemblance to the dietary habits in Western societies. The results of this study implicate dietary practices of women in the etiology of the present epidemic of human obesity and related disorders.fat-enriched diet; intrauterine environment; fetal hyperinsulinemia; adult-onset obesity; glucose intolerance OVER THE PAST TWO TO THREE DECADES, the prevalence of obesity has increased steadily and has now reached epidemic proportions in developed countries. In the US alone, more than two-thirds of the adult population have been classified as overweight, with about one-half of them being obese (27). Obesity is a risk factor for the onset of metabolic diseases in adulthood, including type 2 diabetes and cardiovascular diseases (13). More than 80% of people with diabetes are overweight or obese, indicating a close correlation between being overweight and having diabetes (35). It is now recognized that genetics alone cannot explain the unprecedented increase in the number of overweight/obese individuals worldwide. Several environmental factors have been implicated in the etiology of obesity. Hales and Barker (17) coined the term "fetal programming," which was based on data from several epidemiological studies, to demonstrate that metabolic diseases have their origin in early life nutritional experience during gestation and lactation. A nutritional stress/stimulus occurring during the period of fetal development results in adaptiv...

Hypothalamic alterations in fetuses of high fat diet-fed obese female rats

“…Two rats receiving the same diet were housed per cage from the time of weaning until initiation of breeding. (Srinivasan et al 2006). The energy densities of the diets were 5 .…”

Dietary energy density and the metabolic syndrome among Iranian women

“…Energy-dense diets have been reported to contain higher amounts of fat, refined grains and added sugars, while lower amounts of fruits and vegetables, whole-grains and dietary fiber (Kant and Graubard, 2005;Ledikwe et al, 2006b); such dietary intakes have been related to the high prevalence of the metabolic syndrome and its components in earlier studies (Srinivasan et al, 2006;Radhika et al, 2009;Malik et al, 2010). Furthermore, we are aware of just one report that evaluated dietary energy density in relation to the metabolic syndrome; where Mendoza et al (2007), using cross-sectional data from 1-day 24-h dietary recall in NHANES 1999-2002, found an independent positive association between dietary energy density and the metabolic syndrome among US adults.…”

Maternal high-fat diet inversely affects insulin sensitivity in dams and young adult male rat offspring

“…It is demonstrated that metabolic diseases have their origin in early life nutritional experience such as maternal high-fat (HF) diet consumption during gestation and lactation (Srinivasan et al, 2006). The changes in energy balance and cells' response to insulin are the important metabolic changes in the offspring of HF-fed dams (Sullivan et al, 2015).…”