Consumption of resistant starch decreases postprandial lipogenesis in white adipose tissue of the rat

Chronic consumption of diets high in resistant starch (RS) leads to reduced fat cell size compared to diets high in digestible starch (DS) in rats and increases total and meal fat oxidation in humans. The aim of the present study was to examine the rate of lipogenesis in key lipogenic organs following a high RS or DS meal. Following an overnight fast, male Wistar rats ingested a meal with an RS content of 2% or 30% of total carbohydrate and were then administered an i.p bolus of 50 μCi 3H2O either immediately or 1 hour post-meal. One hour following tracer administration, rats were sacrificed, a blood sample collected, and the liver, white adipose tissue (WAT), and gastrocnemius muscle excised and frozen until assayed for total 3H-lipid and 3H-glycogen content. Plasma triglyceride and NEFA concentrations and 3H-glycogen content did not differ between groups. In all tissues, except the liver, there was a trend for the rate of lipogenesis to be higher in the DS group than the RS group which reached significance only in WAT at 1 h (p \u3c 0.01). On a whole body level, this attenuation of fat deposition in WAT in response to a RS diet could be significant for the prevention of weight gain in the long-term

Chronic glucokinase activation reduces glycaemia and improves glucose tolerance in high-fat diet fed mice.

Glucokinase (GK) plays a key role in maintaining glucose homeostasis by promoting insulin secretion from pancreatic beta cells and increasing hepatic glucose uptake. Here we investigate the effects of acute and chronic GK activation on glucose tolerance and insulin secretion in mice with diet-induced insulin resistance. In the acute study, a small molecule GK activator (GKA71) was administered to mice fed a high-fat diet for 8weeks. In the long-term study, GKA71 was provided in the diet for 4weeks to high-fat diet-fed mice. Glucose tolerance was measured after intravenous glucose administration, and insulin secretion was measured both in vivo and in vitro. Acute GK activation efficiently improved glucose tolerance in association with increased insulin secretion after intravenous glucose both in control and high-fat fed mice. Chronic GK activation significantly reduced basal plasma glucose and insulin, and improved glucose tolerance despite reduced insulin secretion after intravenous glucose, suggesting improved insulin sensitivity. Isolated islets from chronically GKA71-treated mice displayed augmented insulin secretion at 8.3mmol/l glucose, without affecting glucose oxidation. High-fat diet fed mice had reduced glycogen and increased triglyceride in liver compared to control mice, and these parameters were not altered by long-term GK activation. We conclude that GK activation in high-fat diet-fed mice potently reduces glycaemia and improves glucose tolerance, with combined effect both to stimulate insulin secretion from islets and improve insulin sensitivity

Consumption of resistant starch decreases postprandial lipogenesis in white adipose tissue of the rat

Chronic consumption of diets high in resistant starch (RS) leads to reduced fat cell size compared to diets high in digestible starch (DS) in rats and increases total and meal fat oxidation in humans. The aim of the present study was to examine the rate of lipogenesis in key lipogenic organs following a high RS or DS meal. Following an overnight fast, male Wistar rats ingested a meal with an RS content of 2% or 30% of total carbohydrate and were then administered an i.p bolus of 50 μCi (3)H(2)O either immediately or 1 hour post-meal. One hour following tracer administration, rats were sacrificed, a blood sample collected, and the liver, white adipose tissue (WAT), and gastrocnemius muscle excised and frozen until assayed for total (3)H-lipid and (3)H-glycogen content. Plasma triglyceride and NEFA concentrations and (3)H-glycogen content did not differ between groups. In all tissues, except the liver, there was a trend for the rate of lipogenesis to be higher in the DS group than the RS group which reached significance only in WAT at 1 h (p < 0.01). On a whole body level, this attenuation of fat deposition in WAT in response to a RS diet could be significant for the prevention of weight gain in the long-term

Dietary n-3 and n-6 fatty acids alter avian metabolism: metabolism and abdominal fat deposition

The effects of dietary saturated fatty acids and polyunsaturated fatty acids (PUFA) of the n-3 and n-6 series on weight gain, body composition and substrate oxidation were investigated in broiler chickens. At 3 weeks of age three groups of chickens (n 30; ten birds per group) were fed the fat-enriched experimental diets for 5 weeks. These diets were isonitrogenous, isoenergetic and contained 208 g protein/kg and 80 g edible tallow, fish oil or sunflower oil/kg; the dietary fatty acid profiles were thus dominated by saturated fatty acids, n-3 PUFA or n-6 PUFA respectively. Resting RQ was measured in five birds from each treatment group during weeks 4 and 5 of the experiment. There were no significant differences between treatments in total feed intake or final body mass. Birds fed the PUFA diets had lower RQ and significantly reduced abdominal fat pad weights (

Role of Dietary Factors: Macronutrients

Insulin resistance is an important early marker of the metabolic syndrome disease cluster. Our understanding of the role of dietary macronutrients in the etiology of insulin resistance is currently limited by a paucity of credible intervention studies in humans. In contemplating such studies there are many issues that need consideration from actual study design (e.g., duration of intervention, study population, cross-over or not, nutrient formulation) to practical issues such as palatability and compliance (i.e., that terribly important issue of achievability because realistically individuals must be free range in order to complete studies of sufficient duration). Initiatives to support well-designed multicenter studies on diet and insulin resistance would have a major impact on our ability to treat, but more importantly to prevent, the metabolic syndrome diseases