Abstract
An adverse endogenous environment during early life predisposes the organism to develop metabolic disorders. We evaluated the impact of intake of an iso-caloric fructose rich diet (FRD) by lactating mothers (LM) on several metabolic functions of their male offspring. On postnatal d 1, ad libitum eating, lactating Sprague-Dawley rats received either 10% F (wt/vol; FRD-LM) or tap water (controls, CTR-LM) to drink throughout lactation. Weaned male offspring were fed ad libitum a normal diet, and body weight (BW) and food intake were registered until experimentation (60 d of age). Basal circulating levels of metabolic markers were evaluated. Both iv glucose tolerance and hypothalamic leptin sensitivity tests were performed. The hypothalamus was dissected for isolation of total RNA and Western blot analysis. Retroperitoneal (RP) adipose tissue was dissected and either kept frozen for gene analysis or digested to isolate adipocytes or for histological studies. FRD rats showed increased BW and decreased hypothalamic sensitivity to exogenous leptin, enhanced food intake (between 49-60 d), and decreased hypothalamic expression of several anorexigenic signals. FRD rats developed increased insulin and leptin peripheral levels and decreased adiponectinemia; although FRD rats normally tolerated glucose excess, it was associated with enhanced insulin secretion. FRD RP adipocytes were enlarged and spontaneously released high leptin, although they were less sensitive to insulin-induced leptin release. Accordingly, RP fat leptin gene expression was high in FRD rats. Excessive fructose consumption by lactating mothers resulted in deep neuroendocrine-metabolic disorders of their male offspring, probably enhancing the susceptibility to develop overweight/obesity during adult life.
Highlights
Endocrinology, September 2010, 151(9):4214 – 4223 endo.endojournals.org 4215. During these critical periods has been used to evaluate some consequences in offspring; nutrient restriction, low protein diet, and high-fat/-carbohydrate diet have been used to identify their contribution on obesity and type 2 diabetes mellitus development in offspring (10 –12)
Food intake and body weight gain are processes regulated by hypothalamic neurons that are still differentiating during the rodent suckling period; altered nutritional status during lactation severely impacts on normal neuron development [13]
Fructose lacks of any short-term stimulatory effect on insulin and leptin production [18], excessive fructose intake through the diet without appropriate pancreatic and adipose tissue responses could lead to long-term detrimental effects on the regulation of energy intake and body adiposity
Summary
Nowadays the individual’s total daily caloric intake rose, the per capita fructose intake (sucrose- and high fructose corn syrup-derived) increased [18] from 64 g/d (during the 1970s) to 81 g/d (in the year 1997), with an additional augment in fructose intake (2.5 g/d) resulted from increased fruit and vegetable consumption. This change in eating behavior due to fructose overload enhanced the prevalence of several metabolic disorders [19].
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