Hypoadiponectinaemia in nonalcoholic fatty liver disease obese women is associated with infrequent intake of dietary sucrose and fatty foods.

BACKGROUND: The present study aimed to investigate the relationship between adiponectinaemia and food intake among obese women with nonalcoholic fatty liver disease (NAFLD). METHODS: In total, 60 obese women were examined by abdominal ultrasound for liver steatosis and subcutaneous and visceral adiposity. A standard interview (including questions about alcohol intake, medical history and physical activity), a physical examination (including height, weight, body mass index, waist and hip circumferences, waist-to-hip ratio, and body composition) and biochemical and clinical parameters (including serum glucose and insulin, homeostatic model assessment insulin resistance, lipid profile, aminotransferases, C-reactive protein, adiponectin, leptin, resistin, tumour necrosis factor-α, interleukin-6 levels and blood pressure) were performed. Food intake was evaluated by a qualitative food frequency questionnaire. RESULTS: Twenty-four NAFLD patients and thirty-six controls were analysed. The Mann-Whitney test showed lower adiponectin levels in the liver disease group compared to controls (P < 0.05). The Pearson correlation coefficient indicated that adiponectinaemia was negatively correlated with lipid profile and serum tumour necrosis factor-α (P = 0.05) and was positively associated with adiposity measures and serum leptin (P < 0.05). By simple linear regression, all of these variables predicted serum adiponectin levels. Chi-squared and Fisher's exact tests indicated that, in both groups, food intake showed no differences, although sucrose and fatty foods were associated with lower adiponectin levels in the liver disease group (P < 0.05 and P < 0.05, respectively), as well as in the control group (P = 0.05 and P < 0.05, respectively). CONCLUSIONS: Hypoadiponectinaemia in NAFLD was associated with dietary sucrose and fatty food intake, emphasising the important role of diet in the occurrence of this disease.

Rice bran supplementation during nutritional recovery period of malnourished rats improves colon development.

OBJECTIVE: To investigate the colon's development in rats subjected to protein energy malnutrition followed by supplementation with rice bran. MATERIALS AND METHODS: Weaned Wistar male rats (21 days old), weight (40-50 g) were divided into two groups: diet with 17% protein (C; control group) or an aproteic diet (A; aproteic group), for 12 days. After this, 50% of the rats from each group were sacrificed. The remaining rats were further distributed in the three groups for a recovery (21 days): control (C) continued to receive the control diet whereas the aproteic group (A) received either a control diet (AC) or a control diet supplemented with 5% of rice bran (ARB). RESULTS: The A group showed alterations in the colon and cecum, excreted dry feces mass and fecal nitrogen, compared with C rats. In the proximal colon of A rats, the external muscularis and the width of the colon wall were higher whereas in the distal colon they were lower than C. After the recovery period, the relative cecum mass, colon mass and colon length of the recovered groups (AC and ARB) were higher than in the C group. Dry feces and fecal nitrogen excreted of the rats from recovered groups were lower than C group. Colon length of the AC group was lower than in the C group. Only the crypt's depth from ARB group was higher than in the C group. CONCLUSION: Control diet supplemented with 5% rice bran, reestablished the large intestine of aproteic rats. The recovery in the ARB group was even better than in the AC rats.

Colorectal cancer: lifestyle and dietary factors.

INTRODUCTION: Colorectal cancer is the most common tumor in the developed countries, and the number of new cases annualy is aproximately equal for men and women. Several environmental factors can interact in all steps of carcinogenesis. Lately the balance between genetic predisposition and these factors, including nutritional components and lifestyle behaviors, determines individual susceptibility to develop colorectal cancer. The aim of this study is to revise the references about lifestyle include diet, physical exercise, tobacco smoking and use of alcohol, and the risk of colorectal cancer in databases published during 1994-2004. DIETARY FACTORS: According to the reports high intake of red meat, and particularly of processed meat and positive energetic balance (high intake of total fat and carbohydrate) was associated with a moderate but significant increase in colorectal cancer risk. Convincing preventive factors include increase consumption of a wide variety of fruit and vegetable, particularly, dark-green leafy, cruciferous, a deep-yellow on tones, and fibre. LIFESTYLE: Physical activity as a means for the primary prevention of colorectal cancer. There is a probable synergic effect among physical inactivity, high energy intake and obesity and incidence of colorectal cancer. A growing body of evidence supports that avoidance overweight and the use of tobacco and alcohol is recommended to prevent colorectal cancer. CONCLUSION: Current data suggest that lifestyle modification including proper diet such as the ones rich in vegetable and poor in red meat and fat, regular physical activity and maintaining an appropriate body weight and avoiding the use of tobacco and alcohol may lead to reduce colorectal cancer risk.

Correlation of serum leptin and insulin levels of pregnant protein-restricted rats with predictive obesity variables.

During pregnancy and protein restriction, changes in serum insulin and leptin levels, food intake and several metabolic parameters normally result in enhanced adiposity. We evaluated serum leptin and insulin levels and their correlations with some predictive obesity variables in Wistar rats (90 days), up to the 14th day of pregnancy: control non-pregnant (N = 5) and pregnant (N = 7) groups (control diet: 17% protein), and low-protein non-pregnant (N = 5) and pregnant (N = 6) groups (low-protein diet: 6%). Independent of the protein content of the diet, pregnancy increased total (F1,19 = 22.28, P < 0.001) and relative (F1,19 = 5.57, P < 0.03) food intake, the variation of weight (F1,19 = 49.79, P < 0.000) and final body weight (F1,19 = 19.52, P < 0.001), but glycemia (F1,19 = 9.02, P = 0.01) and the relative weight of gonadal adipose tissue (F1,19 = 17.11, P < 0.001) were decreased. Pregnancy (F1,19 = 18.13, P < 0.001) and low-protein diet (F1,19 = 20.35, P < 0.001) increased the absolute weight of brown adipose tissue. However, the relative weight of this tissue was increased only by protein restriction (F1,19 = 15.20, P < 0.001) and the relative lipid in carcass was decreased in low-protein groups (F1,19 = 4.34, P = 0.05). Serum insulin and leptin levels were similar among groups and did not correlate with food intake. However, there was a positive relationship between serum insulin levels and carcass fat depots in low-protein groups (r = 0.37, P < 0.05), while in pregnancy serum leptin correlated with weight of gonadal (r = 0.39, P < 0.02) and retroperitoneal (r = 0.41, P < 0.01) adipose tissues. Unexpectedly, protein restriction during 14 days of pregnancy did not alter the serum profile of adiposity signals and their effects on food intake and adiposity, probably due to the short term of exposure to low-protein diet.

Correlation of serum leptin and insulin levels of pregnant protein-restricted rats with predictive obesity variables

During pregnancy and protein restriction, changes in serum insulin and leptin levels, food intake and several metabolic parameters normally result in enhanced adiposity. We evaluated serum leptin and insulin levels and their correlations with some predictive obesity variables in Wistar rats (90 days), up to the 14th day of pregnancy: control non-pregnant (N = 5) and pregnant (N = 7) groups (control diet: 17 percent protein), and low-protein non-pregnant (N = 5) and pregnant (N = 6) groups (low-protein diet: 6 percent). Independent of the protein content of the diet, pregnancy increased total (F1,19 = 22.28, P < 0.001) and relative (F1,19 = 5.57, P < 0.03) food intake, the variation of weight (F1,19 = 49.79, P < 0.000) and final body weight (F1,19 = 19.52, P < 0.001), but glycemia (F1,19 = 9.02, P = 0.01) and the relative weight of gonadal adipose tissue (F1,19 = 17.11, P < 0.001) were decreased. Pregnancy (F1,19 = 18.13, P < 0.001) and low-protein diet (F1,19 = 20.35, P < 0.001) increased the absolute weight of brown adipose tissue. However, the relative weight of this tissue was increased only by protein restriction (F1,19 = 15.20, P < 0.001) and the relative lipid in carcass was decreased in low-protein groups (F1,19 = 4.34, P = 0.05). Serum insulin and leptin levels were similar among groups and did not correlate with food intake. However, there was a positive relationship between serum insulin levels and carcass fat depots in low-protein groups (r = 0.37, P < 0.05), while in pregnancy serum leptin correlated with weight of gonadal (r = 0.39, P < 0.02) and retroperitoneal (r = 0.41, P < 0.01) adipose tissues. Unexpectedly, protein restriction during 14 days of pregnancy did not alter the serum profile of adiposity signals and their effects on food intake and adiposity, probably due to the short term of exposure to low-protein diet.