. 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...

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Age-associated deficiency of vitamin C contributes to the impaired humoral immune response, which in turn plays a role in the increased risk of illness in old age. Healthy volunteers were given vitamin C supplementation. Neutrophil phagocytic function, complement C3 concen¬ tration, and immunoglobulin status were measured at 30, 60, and 90 days. Neutrophil phago¬ cytic function and levels of serum IgG and IgM and leukocytic ascorbate were considerably lower in the aged humans, but these decreases were attenuated by vitamin C supplementa¬ tion. The level of IgA was not affected by aging. Improved neutrophil phagocytic function and humoral immune response were associated with increased vitamin C status in the aged population and might well contribute to the decreased risk of disease in the aged.

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