Abstract To evaluate the effects in adults rats submitted of a low-protein, high-carbohydrate (LPHC; 6% protein, 74% carbohydrate) diet and reversion (R) to a balanced diet introduced after weaning. Research methods & procedures: Male rats weigting approximately 100g (30 to 32 d old) were treated with control (C; 17% protein, 63% carbohydrate) or LPHC diets for 120 days. The reverse group (R) was treated with the LPHC diet for 15 days, and changed to C diet for another 105 days. Results: The LPHC group showed an increase in serum fasting triglycerides (TAG). Serum adiponectin was increased only in the LPHC group. Lipoprotein lipase (LPL) activity was decreased in the extensor digitorum longus (EDL) and cardiac muscles. The adiponectin receptor 1 content is the same among groups in the cardiac muscle, but it is lower in the EDL muscle in the LPHC group. In animals from the R group, these parameters are the same as the LPHC group. Thus, the LPHC diet administered for a long period, it promotes an increase in TAG. It is possible that there is adiponectin resistance in the EDL muscle, due to the lower LPL activity. The reversal of the LPHC diet did not normalize these parameters.

Abstract: The aim of this study was investigate the effects of a low-protein, high-carbohydrate (LPHC) diet introduced to rats soon after weaning. The animals were distributed in the following groups: LPHC45: fed an LPHC diet (6%-protein, 74%-carbohydrate) for 45 days; C45: fed a control (C) diet (17%-protein, 63%-carbohydrate) for 45 days; R (Reverse): fed with LPHC for 15 days followed by C diet for 30 days. The LPHC45 group showed alterations in the energetic balance with an increase in brown adipose tissue, and in glucose tolerance, and lower final body weight, muscle mass and total protein in blood when compared with C45 group. The HOMA-IR index was similar between LPHC45 and C45 groups, but this parameter was lower in LPHC45 compared with R groups. Serum adiponectin was higher in LPHC45 group than C45 and R groups. The R group presented higher fed insulin than C45 and LPHC45 and higher T4 compared with C45 group. Total cholesterol in R group was higher when compared with LPHC45 group. Thus, the data show that the change of the diet LPHC for a balanced diet led to different metabolic evolution and suggest that the different response can be due to different levels of adiponectin.

Our objective was to establish a diabetes mellitus type 2 (DM2) model in rats using a high-fat diet and streptozotocin (HF-STZ). Male Wistar rats (240-250g) were divided into a control group (commercial feed), and HF-STZ group, (66.5%-commercial feed, 13.5%-lard, and 20%-sugar). STZ (40mg/kg i.p.) or vehicle was administered on the 13th day. An oral glucose tolerance test (OGTT) was performed (2.5mg of glucose/kg v.o.) on both groups. After 39 days of treatment, blood and tissue samples were collected for analyses. The weight gain after STZ administration was lower in the HF-STZ group than in the control group with reductions in muscle mass and adipose tissue. The HF-STZ group showed hyperglycemia after STZ administration (glucose on day 39: HF-STZ: 499 ± 60; control: 134 ± 9mg/dL). Serum glucagon was 23% lower, and insulin levels were unaltered. The HOMA index was 4-times higher in the HF-STZ. The HF-STZ group showed increased post-prandial (330%) and fasting (125%) triglycerides, and while glycogen content in the liver and muscles decreased (70-80%). The area under the curve (OGTT) was 282% higher in the HF-STZ group. The combination of high-fat diet with STZ (i.p) generated rats with hyperglycemia associated with hypertriglyceridemia and introduced many other alterations present in human DM2.