OBJECTIVE:To study the effects of three weight-maintenance diets with different macronutrient composition on carbohydrate, lipid metabolism, insulin and incretin levels in insulin-resistant subjects.

METHODS:A prospective study was performed in eleven (7 W, 4 M) offspring of obese and type 2 diabetes patients. Subjects had a BMI>25 Kg/m2, waist circumference (men/women)>102/88, HBA1c<6.5% and were regarded as insulin-resistant after an OGTT (Matsuda ISIm<4). They were randomly divided into three groups and underwent three dietary periods each of 28 days in a crossover design: a) diet high in saturated fat (SAT), b) diet rich in monounsaturated fat (MUFA; Mediterranean diet) and c) diet rich in carbohydrate (CHO).

RESULTS:Body weight and resting energy expenditure did not changed during the three dietary periods. Fasting serum glucose concentrations fell during MUFA-rich and CHO-rich diets compared with high-SAT diets (5.02 +/- 0.1, 5.03 +/- 0.1, 5.50 +/- 0.2 mmol/L, respectively. Anova<0.05). The MUFA-rich diet improved insulin sensitivity, as indicated by lower homeostasis model analysis-insulin resistance (HOMA-ir), compared with CHO-rich and high-SAT diets (2.32 +/- 0.3, 2.52 +/- 0.4, 2.72 +/- 0.4, respectively, Anova<0.01). After a MUFA-rich and high-SAT breakfasts (443 kcal) the postprandial integrated area under curve (AUC) of glucose and insulin were lowered compared with isocaloric CHO-rich breakfast (7.8 +/- 1.3, 5.84 +/- 1.2, 11.9 +/- 2.7 mmol . 180 min/L, Anova<0.05; and 1004 +/- 147, 1253 +/- 140, 2667 +/- 329 pmol . 180 min/L, Anova<0.01, respectively); while the integrated glucagon-like peptide-1 response increased with MUFA and SAT breakfasts compared with isocaloric CHO-rich meals (4.22 +/- 0.7, 4.34 +/- 1.1, 1.85 +/- 1.1, respectively, Anova<0.05). Fasting and postprandial HDL cholesterol concentrations rose with MUFA-rich diets, and the AUCs of triacylglycerol fell with the CHO-rich diet. Similarly fasting proinsulin (PI) concentration fell, while stimulated ratio PI/I was not changed by MUFA-rich diet.

CONCLUSIONS:Weight maintenance with a MUFA-rich diet improves HOMA-ir and fasting proinsulin levels in insulin-resistant subjects. Ingestion of a virgin olive oil-based breakfast decreased postprandial glucose and insulin concentrations, and increased HDL-C and GLP-1 concentrations as compared with CHO-rich diet.

OBJECTIVES:This study evaluated the glycemic, insulinemic, and glucagon-like peptide-1 (GLP-1) responses of subjects with type 2 diabetes mellitus to consumption of two diabetes-specific tube-feeding formulas (slowly digested carbohydrate formula [SDC] and diabetes-specific formula [DSF]) and one formula intended for individuals without diabetes (standard formula [STND]).

METHODS:Forty-eight subjects controlled with diet and/or oral antihyperglycemic medications received the SDC, DSF, and STND. Postprandial glucose, insulin, and GLP-1 were measured on three occasions after an overnight fast in a double-blinded, randomized, three-treatment, crossover design.

RESULTS:The positive area under the curve for glucose and insulin with the STND was higher (P<0.001) compared with the SDC and DSF. The adjusted GLP-1 concentration at 60 min was higher for the SDC compared with the DSF and STND (P<0.05).

CONCLUSION:Both lower-carbohydrate diabetes-specific formulas resulted in a lower postprandial blood glucose response compared with the STND. The formula also rich in slowly digested carbohydrate and monounsaturated and omega-3 fatty acids (SDC) produced significantly lower blood glucose and insulin responses and higher levels of GLP-1 in the presence of significantly lower insulin concentrations. These results support the view that the quantity and quality of carbohydrate and fat may play important roles in the management of patients with type 2 diabetes mellitus and could result in improved beta-cell function over the long term.

Fermentable dietary fiber has been shown to cause fat loss and to increase peptide-YY (PYY) and glucagon-like peptide 1 (GLP-1) levels in rodents. In single meal tests, humans have an increase in PYY and GLP-1 to dietary fiber, but the response of these hormones to longer-term treatment is not known. Viscofiber (Cevena Bioproducts Inc., Edmonton, AB, Canada) is a high-viscosity fermentable dietary fiber made by a proprietary process from oats and barley. Seven healthy overweight and obese subjects were treated with a calorie-restricted diet, a lifestyle change program, and 4 g of Viscofiber/day for 16 weeks. Hunger, satiety, PYY, and GLP-1 were measured before and 1 hour after a standard meal test before and at week 14 of the study. Hunger and satiety were measured by Visual Analog Scales. PYY and GLP-1 were measured by radioimmunoassay and enzyme-linked immunosorbent assay, respectively. Weight was reduced 3.07 +/- 3.13 kg (P<.05) over the 16 weeks. Fasting PYY increased 8.67 +/- 6.62 pg/mL (P<.05) and fasting GLP-1 increased 2.67 +/- 0.84 pmol/L (P<.01) at 14 weeks compared to baseline. Satiety increased 1.78 +/- 1.43 cm (P<.01) at the 1-hour post-meal time point on week 14 compared to the study baseline. We conclude that 14 weeks of treatment with Viscofiber at 4 g/day along with a lifestyle change program and diet causes weight loss and increases fasting PYY, fasting GLP-1, and satiety at 1 hour following a standard meal, which extends the single meal test observations in humans.

BACKGROUND:We have shown that individually, dietary fiber and protein increase secretion of the anorexigenic and insulinotropic hormone, glucagon-like peptide-1 (GLP-1).

OBJECTIVE:Our objective was to combine, in one diet, high levels of fiber and protein to maximize GLP-1 secretion, improve glucose tolerance, and reduce weight gain.

METHODS AND PROCEDURES:Lean (+/?) and obese (cp/cp) male James C Russell corpulent (JCR:LA-cp) rats lacking a functional leptin receptor were fed one of four experimental diets (control, high protein (HP), high fiber (HF, prebiotic fiber inulin), or combination (CB)) for 3 weeks. An oral glucose tolerance test (OGTT) was performed to evaluate plasma GLP-1, insulin and glucose. Plasma lipids and intestinal proglucagon mRNA expression were determined.

RESULTS:Energy intake was lower with the HF diet in lean and obese rats. Weight gain did not differ between diets. Higher colonic proglucagon mRNA in lean rats fed a CB diet was associated with higher GLP-1 secretion during OGTT. The HP diet significantly reduced plasma glucose area under the curve (AUC) during OGTT in obese rats, which reflected both an increased GLP-1 AUC and higher fasting insulin. Diets containing inulin resulted in the lowest plasma triglyceride and total cholesterol levels.

DISCUSSION:Overall, combining HP with HF in the diet increased GLP-1 secretion in response to oral glucose, but did not improve glucose tolerance or lipid profiles more than the HF diet alone did. We also suggest that glycemic and insulinemic response to prebiotics differ among rat models and future research work should examine their role in improving glucose tolerance in diet-induced vs. genetic obesity with overt hyperleptinemia.

BACKGROUND: As the first step in ingesting food, the effects of mastication on energy intake and gut hormones in both obese and lean subjects have not been extensively evaluated.

OBJECTIVE: The current study aimed to compare the differences in chewing activities between obese and lean subjects and to examine the effects of chewing on energy intake and gut hormone concentrations in both obese and lean subjects.

DESIGN: Sixteen lean and 14 obese young men participated in the current research. In study 1, we investigated whether the chewing factors of obese subjects were different from those of lean subjects. In study 2, we explored the effects of chewing on energy intake. A test meal consisting of 2200 kJ (68% of energy as carbohydrate, 21% of energy as fat, and 11% of energy as protein) was then consumed on 2 different sessions (15 chews and 40 chews per bite of a 10-g food) by each subject to assess the effects of chewing on plasma gut hormone concentrations.

RESULTS: Compared with lean participants, obese participants had a higher ingestion rate and a lower number of chews per 1 g of food. However, obese participants had a bite size similar to that of lean subjects. Regardless of status, the subjects ingested 11.9% less after 40 chews than after 15 chews. Compared with 15 chews, 40 chews resulted in a lower energy intake and postprandial ghrelin concentration and higher postprandial glucagon-like peptide 1 and cholecystokinin concentrations in both lean and obese subjects.

CONCLUSION: Interventions aimed at improving chewing activity could become a useful tool for combating obesity. This trial was registered at chictr.org as ChiCTR-OCC-10001181.

The clinical implications of non-alcoholic fatty liver diseases (NAFLD) derive from their potential to progress to fibrosis and cirrhosis. Inappropriate dietary fat intake, excessive intake of soft drinks, insulin resistance and increased oxidative stress results in increased free fatty acid delivery to the liver and increased hepatic triglyceride (TG) accumulation. An olive oil-rich diet decreases accumulation of TGs in the liver, improves postprandial TGs, glucose and glucagon-like peptide-1 responses in insulin-resistant subjects, and upregulates glucose transporter-2 expression in the liver. The principal mechanisms include: decreased nuclear factor-kappaB activation, decreased low-density lipoprotein oxidation, and improved insulin resistance by reduced production of inflammatory cytokines (tumor necrosis factor, interleukin-6) and improvement of jun N-terminal kinase-mediated phosphorylation of insulin receptor substrate-1. The beneficial effect of the Mediterranean diet is derived from monounsaturated fatty acids, mainly from olive oil. In this review, we describe the dietary sources of the monounsaturated fatty acids, the composition of olive oil, dietary fats and their relationship to insulin resistance and postprandial lipid and glucose responses in non-alcoholic steatohepatitis, clinical and experimental studies that assess the relationship between olive oil and NAFLD, and the mechanism by which olive oil ameliorates fatty liver, and we discuss future perspectives.