Metabolic programming of adipose tissue in female C57Bl 6 mice offspring by maternal high fat feeding and obesity results in greater adaptability to dietary fat content and resistance to high fat diet-induced glucose intolerance compared to male mice

Maternal lifestyle influence may be a factor in the worldwide prevalence of obesity and its complications, including diabetes. Studies investigating the effect of the perinatal maternal environment have produced a range of results, sometimes diametrically opposite. The present study was designed to investigate how obesity and weight gain in pregnant mice affects energy balance, body composition and glucose homeostasis in their offspring, both at a young age on standard diet and when older and fed a high-fat diet. At six weeks of age both male and female offspring from mothers fed a high fat diet had a shorter body length than those from mothers fed standard chow. In contrast to males, female offspring also contained a higher proportion of fat and had elevated circulating leptin and adiponectin. Their gonadal fat pads were heavier and contained larger adipocytes, whereas male offspring had proportionally more smaller adipocytes. Six-week-old female, but not male, offspring had increased gonadal fat gene expression of acetyl CoA carboxylase 1, the rate-limiting step in lipid biosynthesis, and decreased gene expression of carnitine palmitoyl transferase 1, the rate-limiting step in fatty acid oxidation. Maternal high fat diet had no effect on glucose tolerance in six-week-old mice, but this was achieved with higher insulin levels in females. Contrastingly, when the offspring were fed a high fat diet for three months, female, but not male, offspring were leaner than those from mothers fed standard chow. Their gonadal fat depots were lighter and the adipocytes were smaller. Female, but not male, offspring fed high fat diet had decreased gonadal fat gene expression of acetyl CoA carboxylase 1, and increased gene expression of carnitine palmitoyl transferase 1. High fat diet-induced glucose intolerance and elevated plasma insulin concentration were improved in female, but not male, offspring. Plasma leptin and adiponectin remained higher in female offspring on high fat diet with resistin levels being lower. These results suggest that the gonadal fat of female offspring is more adaptable to different levels of dietary fat exposure, increasing storage when levels are low and increasing oxidation when levels are high. This may help female offspring be more resistant to the detrimental effects of high fat diet than male mice.

Oral Glucose Tolerance Test with Insulin Assay and the evaluation of Insulin Resistance and Impaired Beta-cell function in primary prevention for Type 2 Diabetes

Background: Insulin resistance and impaired beta-cell function are associated with type 2 diabetes mellitus (T2DM). Many insulin resistance and beta-cell function indices have been developed using the data from an oral glucose tolerance test (OGTT) with insulin assay. However, insulin assays are not widely used along with the OGTT in primary prevention outpatient clinics. We aimed to evaluate the association of having impaired fasting glucose (IFG), impaired glucose tolerance (IGT), isolated or combined, with insulin resistance and impaired beta-cell function in subjects at risk for T2DM. Methods: This is a cross-sectional study that included 376 subjects who underwent an OGTT who had at least two risk factors for T2DM without any chronic disease. Results: Participants were 51.6±8.2 years old, 71.8% were women, had a mean body mass index (BMI) of 30.1±6.5 kg/m2, 42.4% had obesity and 26.7% hypertension. A HOMA-IR ≥2.5 was independently associated with male sex, BMI>25kg/m2, and with isolatedIFG, isolated-IGT, or combined (p<0.05 for all). On the other hand, only overweight, but not obesity, was independently associated with impaired beta-cell function (disposition index <1.24). Additionally, combined IFG and IGT had 29.7 higher odds to have impaired beta-cell function compared with those that had a normal OGTT. Conclusions: IFG alone, IGT alone, or the presence of both, are associated with higher odds to have insulin resistance and impaired beta-cell function in asymptomatic subjects at risk for T2DM without any chronic disease. Further studies are needed to evaluate this associations with the risk to develop T2DM, cardiovascular events and mortality.

Glycemic Index and Glycemic Load to the Biochemical Profile of Dyslipidemic Patients

Background: The positive and negative health effects of dietary carbohydrates are of interest to both researchers and consumers. Low glycemic index (GI) and glycemic load (GL) carbohydrates have been shown to have favourable effects on blood lipid parameters. Objective: This study aims to investigate whether the GI and GL diet in dyslipidemic individuals. Methods: The subjects, 15 men and 15 women, dyslipidemic patients followed up at Hospital de Coari, were invited to answer a self-administered questionnaire for 3 days about food intake. The fasting biochemical profile was analyzed, such as total cholesterol, triglycerides and blood glucose. Results: Low GI diet daily value were observed in women and men and GL diet daily value below the minimum low line for both. A correlation was found between GI and GL diet with triglycerides levels and woman and not in men. Lunch GL value were associated with blood triglycerides parameters. Biochemical profile showed an increase in fasting blood glucose only in men and in lipid levels for both. Conclusion: Dyslipidemic individuals might be potential influencing factors in the associations between GI and GL diet and dyslipidemia, suggesting such modifications could potentially be a useful public health recommendation.