OBJECTIVE -To evaluate whether a 5-week low-glycemic index (LGI) diet versus a highglycemic index (HGI) diet can modify glucose and lipid metabolism as well as total fat mass in nondiabetic men.RESEARCH DESIGN AND METHODS -In this study, 11 healthy men were randomly allocated to 5 weeks of an LGI or HGI diet separated by a 5-week washout interval in a crossover design. RESULTS -TheLGI diet resulted in lower postprandial plasma glucose and insulin profiles and areas under the curve (AUCs) than the HGI diet. A 5-week period of the LGI diet lowered plasma triacylglycerol excursion after lunch (AUC, P Ͻ 0.05 LGI vs. HGI). These modifications were associated with a decrease in the total fat mass by ϳ700 g (P Ͻ 0.05) and a tendency to increase lean body mass (P Ͻ 0.07) without any change in body weight. This decrease in fat mass was accompanied by a decrease in leptin, lipoprotein lipase, and hormone-sensitive lipase RNAm quantities in the subcutaneous abdominal adipose tissue (P Ͻ 0.05).CONCLUSIONS -We concluded that 5 weeks of an LGI diet ameliorates some plasma lipid parameters, decreases total fat mass, and tends to increase lean body mass without changing body weight. These changes were accompanied by a decrease in the expression of some genes implicated in lipid metabolism. Such a diet could be of benefit to healthy, slightly overweight subjects and might play a role in the prevention of metabolic diseases and their cardiovascular complications. Diabetes Care 25:822-828, 2002T he insulin-resistance syndrome is a major risk factor for abnormal carbohydrate metabolism and atherosclerotic and coronary heart diseases (1). Recent prospective studies have incriminated the high-glycemic index (HGI) diet in the genesis of insulin resistance and type 2 diabetes (2). High postprandial plasma glucose and insulin excursions are assumed by some authors (3) to be independent predictors of risk for atherosclerotic diseases. Epidemiological evidence shows that the relationship between plasma glucose concentrations and cardiovascular diseases extends well below the glucose level defined for diabetes and even for impaired glucose tolerance. Therefore, interventions to reduce postprandial glycemia in the normal population could reduce the risk of developing atherosclerotic heart disease and/or diabetes. Dietary intervention might be one of the major approaches in diabetic patients' care, but it might even be useful in normal nondiabetic individuals.In diabetic subjects, the chronic consumption of a low-glycemic index (LGI) diet is generally found to improve plasma glucose and lipid profiles (4). In clinical practice, however, the chronic use of LGI foods is still questioned (5).In nondiabetic subjects, few data exist on the effects of short-and long-term consumption of LGI foods (6 -8). Behall et al. (6) demonstrated that an LGI diet resulted in a decrease in both glycemic area under the curve (AUC) and plasma cholesterol and triacylglycerol levels. Most of these studies, with one exception (8), have demonstrated beneficial effe...

We aimed to study the effects of chronic ingestion of short-chain fructooligosaccharides (FOS), an indigestible carbohydrate, on hepatic glucose production, insulin-mediated glucose metabolism, erythrocyte insulin binding, and blood lipids in healthy subjects. Twelve healthy volunteers received either 20 g FOS/d or sucrose for 4 wk in a double-blind crossover design. FOS did not modify fasting plasma glucose and insulin concentrations. Mean (+/- SEM) basal hepatic glucose production was lower after FOS than after sucrose consumption (2.18 +/- 0.10 compared with 2.32 +/- 0.09 mg.kg-1, min-1, respectively; P < 0.02, paired Student's t test). However, neither insulin suppression of hepatic glucose production nor insulin stimulation of glucose uptake measured by hyperinsulinemic clamp was significantly different between the two dietary periods. Erythrocyte insulin binding was also comparable. Serum triacylglycerols, total and high-density- lipoprotein cholesterol, apolipoproteins A-I and B, and lipoprotein(a) were not modified by FOS. To try to understand why FOS did not increase serum lipids, the in vitro production of short-chain fatty acids from FOS was evaluated by using human fecal inoculum and compared with that from lactulose, which was found to increase serum lipids. FOS produced an acetate-propionate ratio two times lower than that of lactulose. We conclude that 4 wk of 20 g FOS/d decreased basal hepatic glucose production but had no detectable effect on insulin-stimulated glucose metabolism in healthy subjects. The colonic fermentation pattern of undigestible carbohydrates may be relevant to predicting their metabolic effects.

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Short-chain fructooligosaccharides (FOS) are prebiotics, which escape digestion in the small intestine and are fermented by the colonic microflora into short-chain fatty acids. Recently, we found that the daily consumption of 20 g FOS decreased basal hepatic glucose production in healthy subjects without any effect on insulin-stimulated glucose metabolism. In this study, we evaluated the effects of the chronic ingestion of FOS on plasma lipid and glucose concentrations, hepatic glucose production and insulin resistance in type 2 diabetics. Type 2 diabetic volunteers (n = 10; 6 men, 4 women) received either 20 g/d FOS or sucrose for 4 wk in a double-blind crossover design. FOS did not modify fasting plasma glucose and insulin concentrations or basal hepatic glucose production. The plasma glucose response to a fixed exogenous insulin bolus did not differ at the end of the two periods. Erythrocyte insulin binding also did not differ. Serum triacylglycerol, total and HDL cholesterol, free fatty acid, apolipoproteins A1 and B and lipoprotein (a) concentrations were not modified by the chronic ingestion of FOS. We conclude that 4 wk of 20 g/d of FOS had no effect on glucose and lipid metabolism in type 2 diabetics.

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The aim of this study was to evaluate the effects of the chronic consumption of two starches, characterized by different glycemic indices and amylose-amylopectin content, on glucose metabolism in rat epididymal adipocytes. The two chosen starches were from mung bean (32% amylose) and cornstarch (0.5% amylose). The alpha-amylase digestibility was higher for the waxy cornstarch than that of the mung bean starch (60 +/- 4 vs. 45 +/- 3%, mean +/- SEM, respectively). The glycemic index of the waxy cornstarch diet (575 g starch /kg diet) was higher than that of the mung bean starch diet (107 +/- 7 vs. 67 +/- 5%, P < 0.01) when measured in vivo in two groups of normal rats (n = 9). In a subsequent study, normal and diabetic (streptozotocin-injected on d 2 of life) male Sprague-Dawley rats (18 per group) consumed a diet containing 575 g starch/kg diet as either waxy cornstarch or mung bean starch. After 3 wk, food intake, epididymal fat pad weights, and plasma glucose, insulin and triglyceride concentrations did not differ between diet groups. Adipocyte diameter was smaller in rats that consumed mung bean starch compared with those that consumed the waxy cornstarch diet (P < 0.01). The mung bean diet increased maximal insulin-stimulated 14C-glucose oxidation (% of basal values, P < 0. 05). In contrast, incorporation of 14C-glucose into total lipids was significantly lower in rats that consumed the mung bean diet (P < 0. 05). We conclude that in both normal and diabetic rats, the chronic replacement of a high glycemic index starch by a low glycemic index one in a mixed diet increases insulin-stimulated glucose oxidation, decreases glucose incorporation into total lipids and decreases epididymal adipocyte diameter. Thus, the type of starch mixed into the diet has important metabolic consequences at the cellular level in both normal and diabetic rats.

The present study aimed to assess the metabolic consequences of the chronic ingestion of two starches giving different postprandial glycaemic responses in normal and diabetic rats. The two starches chosen were mung-bean (Phaseolus aureus) starch (97% pure starch) and wheat starch presented as ground French toast. First, we studied the characteristics of these two starches. In vitro the a-amylase (EC 3.2.1.1) digestibilities of these starches were 40 (SE 3) and 62 (SE 4) % respectively at 30 min, whereas the contents of resistant starch were 77 (SE 4) and 22 (SE 4) g/kg respectively. In vivo the mungbean starch produced lower postprandial glycaemic responses than the wheat starch (areas under the curve were: 91 (SE 28) and 208 (SE 33) mmol.min/l, P < 0.05) in normal rats (n 8). We then submitted twenty-eight normal and twenty-eight diabetic (neonatal streptozotocin on second day of birth) male Sprague-Dawley rats (6 weeks old) to a diet containing 570 g starch/kg as either mung-bean starch or wheat starch (n 14 ratslgroup). After 5 weeks on the diets food intakes and body weights were identical in each group. Liver and kidney weights were comparable when expressed as relative weight. The mungbean-starch diet slightly decreased epididymal fat-pad weight (P < 0.14, ANOVA) and led to a marked decrease in adipocyte volume (P < 0.05). Plasma triacylglycerol and phospholipid concentrations were lower after the mung-bean-starch diet than after the wheat-starch diet in both normal and diabetic rats, whereas free fatty acid concentrations were lower only in normal rats. Similarly, non-fasting plasma glucose concentrations decreased (P < 0.05) in normal rats fed on mung-bean starch but not in diabetic ones (P < 0.14). Insulin levels tended to be lower, but not significantly, after mung-bean-starch feeding than after wheat starch. We conclude that the replacement of 570 g wheat starch/kg diet with mung-bean starch for 5 weeks resulted in (1) lowered non-fasting plasma glucose and free fatty acid levels in normal but not in diabetic rats, (2) a reduction in plasma triacylglycerol concentration and adipocyte volume in both normal and diabetic rats. Thus, the type of starch mixed into the diet may have important metabolic consequences in normal and diabetic rats.

The aim of this study was to improve the water resistance of a soybean meal-based adhesive with a low-cost lignin-based resin (LR).