We assessed the biological value of an okara diet and its effects on the hormonal and metabolic profile of rats submitted to protein restriction during intra-uterine life and lactation and recovered after weaning. Male rats from mothers fed either 17% or 6% protein during pregnancy and lactation were maintained on 17% casein (CC, LC), 17% okara (CO, LO) or 6% casein (LL) diets over 60 d. The nutritional quality of the okara protein was similar to that of casein. The okara diet was effective in the nutritional recovery of rats in growing that were malnourished in early life. Furthermore, the okara diet reversed the hypercholesterolemia and the hepatic steatosis observed in the malnutrition and prevented glucose intolerance in an animal model prone to diabetes mellitus.

We evaluated whether protein restriction in fetal life alters food intake and glucose homeostasis in adulthood by interfering with insulin signal transduction through proinflammatory mechanisms in the hypothalamus and peripheral tissues. Rats were divided into the following: a control group (C); a recovered group (R); and a low protein (LP) group. Relative food intake was greater and serum leptin was diminished in LP and R compared to C rats. Proinflammatory genes and POMC mRNA were upregulated in the hypothalamus of R group. Hypothalamic NPY mRNA expression was greater but AKT phosphorylation was diminished in the LP than in the C rats. In muscle, AKT phosphorylation was higher in restricted than in control animals. The HOMA-IR was decreased in R and C compared to the LP group. In contrast, the K itt in R was similar to that in C and both were lower than LP rats. Thus, nutritional recovery did not alter glucose homeostasis but produced middle hyperphagia, possibly due to increased anorexigenic neuropeptide expression that counteracted the hypothalamic inflammatory process. In long term protein deprived rats, hyperphagia most likely resulted from increased orexigenic neuropeptide expression, and glucose homeostasis was maintained, at least in part, at the expense of increased muscle insulin sensitivity.

Nutritional recovery of early malnutrition with soybean diet reduces liver glycogen stores in the fed state and produces liver insulin resistance. We investigated whether nutritional recovery on a soybean flour diet alters hepatic gluconeogenesis in the adult offspring of rats deprived of protein during pregnancy and lactation. Male rats from mothers that were fed either 17% (C) or 6% (L) protein during pregnancy and lactation were maintained on a 17% casein (CC, n=16 and LC, n=17), 17% soybean flour (CS, n=10 and LS, n=10) or 6% casein (LL, n=10) diet after weaning. The soybean diet reduced basal serum glucose (soybean diet=5.6±0.6 mmol/L vs casein diet= 6.2±0.6 mmol/L; p<0.05), but increased alanine aminotransferase mRNA/GAPDH (soybean diet =0.062 ±0.038 vs casein diet= 0.024 ±0.011; p<0.01) and phosphoenolpyruvate carboxykinase mRNA/GAPDH (soybean diet =1.53 ±0.52 vs casein diet= 0.95 ±0.43; p<0.05), and the glycerokinase protein content (soybean diet =0.86 ±0.08 vs casein diet= 0.75 ±0.11; p<0.05). The serum glucose concentration (recovered groups=5.6±0.5mmol/L vs control groups=6.2±0.7mmol/L, p<0.05) and pophosphoenolpyruvate carboxykinase activity (recovered groups=2.8±0.6μU/mg vs control groups=3.6±0.6μU/mg; p<0.05) were decreased in rats subjected to protein restriction in early life. The glucose area under the curve during the pyruvate tolerance test did not differ among the groups, whereas glucose area under the curve after glucagon infusion was reduced by early malnutrition (recovered groups=4210±572mg/dL.40min vs control groups=4493±688mg/dL.40min; p<0.001), and by the soybean diet (soybean diet= 3995±500mg/dL.40min vs casein diet=4686±576 mg/dL.40min, p<0.05). Thus, soybean diet impaired the response to glucagon, but did not alter gluconeogenesis.