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Aims/hypothesis. Epidemiological evidence suggests that some adult diseases like insulin resistance syndrome and diseases associated with it originate in fetal life. The role of maternal macronutrient malnutrition but not of micronutrients in the fetal origin of adult disease is well studied. We hypothesise that chronic maternal vitamin restriction predisposes the offspring to insulin resistance syndrome. Methods. Female weanling Wistar/NIN rats received a control diet (n=6) or a 50% vitamin-restricted diet (n=14) for 12 weeks and mated with control males. Four dams on the restricted diet were shifted to the control diet from parturition. Pups born to the remaining 10 dams on the restricted diet were weaned on to control diet or continued on the restricted diet. All groups had 8 male pups from weaning onwards.Results. Birthweights of pups were comparable among different groups. Weaning body weights were low in the restricted diet group, but on rehabilitation they caught up with control animals by post-natal day 100. None of the pups had impaired oral glucose tolerance and their insulin resistance status was comparable on days 40, 70, 100 and 180. Compared with offspring on the control diet, offspring on the restricted diet had a significantly higher percentage of body fat and higher plasma triglycerides, as well as lower lean body mass and fat-free mass. They also had increased oxidative stress. Rehabilitation from parturition or weaning prevented the changes in body fat percent, lean body mass, fat-free mass and oxidative stress. Conclusions/interpretation. Since changes in adiposity and fat metabolism are considered forerunners of insulin resistance syndrome, our observations suggest that maternal dietary vitamin restriction predisposes the offspring to insulin resistance syndrome in later life.

OBJECTIVEWe demonstrated previously that chronic maternal micronutrient restriction altered the body composition in rat offspring and may predispose offspring to adult-onset diseases. Chromium (Cr) regulates glucose and fat metabolism. The objective of this study is to determine the long-term effects of maternal Cr restriction on adipose tissue development and function in a rat model.RESEARCH DESIGN AND METHODSFemale weanling WNIN rats received, ad libitum, a control diet or the same with 65% restriction of Cr (CrR) for 3 months and mated with control males. Some pregnant CrR mothers were rehabilitated from conception or parturition and their pups weaned to control diet. Whereas some CrR offspring were weaned to control diet, others continued on CrR diet. Various parameters were monitored in the offspring at three monthly intervals up to 15–18 months of age.RESULTSMaternal Cr restriction significantly increased body weight and fat percentage, especially the central adiposity in both male and female offspring. Further, the expression of leptin and 11 β-hydroxysteroid dehydrogenase 1 genes were significantly increased in CrR offspring of both the sexes. Adipocytokine levels were altered in plasma and adipose tissue; circulating triglyceride and FFA levels were increased, albeit in female offspring only. Rehabilitation regimes did not correct body adiposity but restored the circulating levels of lipids and adipocytokines.CONCLUSIONSChronic maternal Cr restriction increased body adiposity probably due to increased stress and altered lipid metabolism in WNIN rat offspring, which may predispose them to obesity and associated diseases in later life.

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