RL and CR alter systemic and liver glucose metabolism.

Fumonisins (FBs) are mycotoxins produced by Fusarium molds. Several works have shown contamination of maize by this toxin. Fumonisin B1 (FB-1) is found in greatest proportion (about 70%), resistant to several industrialization processes. In that context, the objective of this work was to analyze the effect of administering a diet contaminated with FB-1 on the morphophysiology of the kidneys of 21-day old male Wistar rats. The animals were divided into 2 groups: G0 (with animals receiving feed free of FBs) and G6 (6mg of FB 1 kg-1 of feed). The diet was administered during 42 days. After that period, the animals were placed in metabolic cages for urine collection, blood was collected for analysis of plasma creatinine, and the kidneys were fixed and stained with Masson's trichrome. We observed that FB 1 administration did not affect feed intake, body weight gain and animal growth. The normal levels of plasma creatinine suggest that the toxin did not lead to glomerular lesion. There was also no change in water intake, osmolarity and excretion of sodium in urine. However, there was a significant increase in urine volume and potassium excretion in urine, with mild tubulointerstitial changes in the outer cortex for the group receiving the mycotoxin.

Early life overfeeding in the rat can be experimentally induced by reducing litter size. This investigation assessed the consequences of this manipulation on glucose metabolism in vivo and in isolated hepatocytes in 150-day old rats. Additionally, after body growth, the effects of caloric restriction and refeeding were tested. Adult rats from control (G9) and reduced litters (G3L) did not differ in body and fat weights, glucose tolerance or insulin resistance (insulin-induced hypoglycemia), or hepatocyte glucose release under basal or gluconeogenic conditions. Caloric restriction (G3R) reduced body and fat weights, decreased glucose decay after insulin injection and decreased hepatocyte gluconeogenic glucose release. Refeeding after caloric restriction reversed these parameters to those of the freely-fed groups (G9 and G3L). Taken together, these results suggest that the liver glucose metabolism is not programmed by lactational overfeeding, but rather is responsive to the current nutritional condition of the animal.

BackgroundCaloric restriction since birth changes glucose metabolism by the liver in overnight-fasted rats to a fed-like pattern, in which glucose output is large but gluconeogenesis is negligible. It was investigated whether these changes could be a residual effect of the nutritional condition during lactation and what could be the mechanism of such change.MethodsNewborn Wistar rat pups were arranged in litters of 6 or 12 (G6 and G12). After weaning, the male pups were divided in: G6L and G12 L, fed freely until the age of 90 days (freely-fed groups); G6R and G12R, given 50% of the GL ingestion (food-restricted groups) until 90 days of age; G6RL and G12RL, given 50% of the GL ingestion until 60 days of age and fed freely until 90 days of age (refed groups). The experimental protocols were carried out at the age of 90 days after overnight fasting. Pairs of groups were compared through t test; other statistical comparisons were made with one-way ANOVA with Tukey post hoc text.ResultsCaloric restriction was effective in decreasing body and fat weights, total cholesterol and LDL. These effects were totally or partially reversed after 30 days of refeeding (groups GRL). During liver perfusion, the high glucose output of the GRs was further enhanced by adrenaline (1 μM), but not by lactate infusion. In contrast, in groups G6L, G12 L, G6RL and G12RL glycogenolysis (basal and adrenaline-stimulated glucose output) was low and gluconeogenesis from lactate was significant. A twofold increase in liver content of PKA in group G6R suggests that liver sensitivity to glucagon and adrenaline was higher because of caloric restriction, resulting in enhanced glucose output.ConclusionsAs glucose output was not affected by litter size, liver glucose metabolism in the adult rat, in contrast to other metabolic processes, is not a programmed effect of the nutritional condition during lactation. In addition, the increased expression of PKA points to a higher sensitivity of the animals under caloric restriction to glycogenolytic hormones, a relevant condition for glucose homeostasis during fasting.

The effects of the supplementation with L-glutamine (GLN) or L-alanyl-L-glutamine (GDP) on the progression of the systemic and hepatic metabolic status of rats having untreated type 1 diabetes mellitus (T1DM) were investigated. Male Wistar diabetic rats (streptozotocin, 60 mg/kg) were allotted to four groups supplemented by gavage for thirty days as follows: control and diabetic receiving saline; diabetic receiving GLN (248 mg/kg); and diabetic receiving GDP (400 mg/kg). Body weight, plasmatic parameters and kidney function were analyzed. Isolated hepatocytes were used to assess gluconeogenic capacity. Liver and kidney were used for morphological analyses. T1DM decreased the number and increased the area of the hepatocytes, possibly because of the observed enlargement of glycogen stores. Kidney weight, glomerular area and proteinuria increased, and glomerular filtration rate decreased, in non-supplemented T1DM rats. Glomerular area and proteinuria were reversed by both supplementations. The T1DM hepatocytes released less glucose, which could have been diverted to glycogen synthesis and secondary glycogenosis observed in T1DM; this was partially reversed by the supplementations. The results point to a possible beneficial effect of glutamine on the metabolic and hepatic impairments of T1DM.