Over the past 20 y, higher-protein diets have been touted as a successful strategy to prevent or treat obesity through improvements in body weight man

Mitochondrial dysfunction has been implicated in the pathogenesis of insulin resistance, the hallmark of type 2 diabetes mellitus (T2DM). However, the cause-effect relationship remains to be fully elucidated. Compelling evidence suggest that boosting mitochondrial function may represent a valuable therapeutic tool to improve insulin sensitivity. Mitochondria are highly dynamic organelles which adapt to short- and long-term metabolic perturbations by undergoing fusion and fission cycles, spatial rearrangement of the electron transport chain complexes into supercomplexes as well as biogenesis governed by peroxisome proliferator-activated receptor γ co-activator 1 α (PGC 1α). However, these processes appear to be dysregulated in type 2 diabetic individuals. Herein we describe the mechanistic link between mitochondrial dysfunction and insulin resistance in skeletal muscle alongside the intracellular pathways orchestrating mitochondrial bioenergetics. We then review current evidence on nutritional tools, including fatty acids, amino acids, caloric restriction and food bioactive derivatives which may enhance insulin sensitivity by therapeutically targeting mitochondrial function and biogenesis

Background: Few well-controlled studies have comprehensively examined the effects of very-low-carbohydrate diets on type 2 diabetes (T2D).Objective: W

Background: The mechanism of protein-induced satiety remains unclear. Objective: The objective was to investigate 24-h satiety and related hormones and energy and substrate metabolism during a high-protein (HP) diet in a respiration chamber. Design: Twelve healthy women aged 18–40 y were fed in energy balance an adequate-protein (AP: 10%, 60%, and 30% of energy from protein, carbohydrate, and fat, respectively) or an HP (30%, 40%, and 30% of energy from protein, carbohydrate, and fat, respectively) diet in a randomized crossover design. Substrate oxidation, 24-h energy expenditure (EE), appetite profile, and ghrelin and glucagon-like peptide 1 (GLP-1) concentrations were measured. Results: Sleeping metabolic rate (6.40 ± 0.47 compared with 6.12 ± 0.40 MJ/d; P < 0.05), diet-induced thermogenesis (0.91 ± 0.25 compared with 0.69 ± 0.24 MJ/d; P < 0.05), and satiety were significantly higher, and activity-induced EE (1.68 ± 0.32 compared with 1.86 ± 0.41; P < 0.05), respiratory quotient (0.84 ± 0.02 compared with 0.88 ± 0.03; P < 0.0005), and hunger were significantly lower during the HP diet. There was a tendency for a greater 24-h EE during the HP diet (P = 0.05). Although energy intake was not significantly different between the diet groups, the subjects were in energy balance during the HP diet and in positive energy balance during the AP diet. Satiety was related to 24-h protein intake (r² = 0.49, P < 0.05) only during the HP diet. Ghrelin concentrations were not significantly different between diets. GLP-1 concentrations after dinner were higher during the HP than during the AP diet (P < 0.05). Conclusion: An HP diet, compared with an AP diet, fed at energy balance for 4 d increased 24-h satiety, thermogenesis, sleeping metabolic rate, protein balance, and fat oxidation. Satiety was related to protein intake, and incidentally to ghrelin and GLP-1 concentrations, only during the HP diet.

OBJECTIVE—To determine the effect of a high-protein (HP) weight loss diet compared with a lower-protein (LP) diet on fat and lean tissue and fasting and postprandial glucose and insulin concentrations. RESEARCH DESIGN AND METHODS—Replacing dietary protein for carbohydrate (CHO) during energy restriction and weight loss has been effective in sparing lean mass and improving insulin sensitivity in obese subjects but has not been tested in subjects with type 2 diabetes. We compared an HP diet (28% protein, 42% CHO, 28% fat [8% saturated fatty acids, 12% monounsaturated fatty acids, 5% polyunsaturated fatty acids]) with an LP diet (16% protein, 55% CHO, 26% fat [8% saturated fatty acids, 11% monounsaturated fatty acids, 5% polyunsaturated fatty acids]) in 54 obese men and women with type 2 diabetes during 8 weeks of energy restriction (1,600 kcal) and 4 weeks of energy balance. Body composition was determined by dual-energy X-ray absorptiometry at weeks 0 and 12. RESULTS—Overall, weight loss of 5.2 ±1.8 kg was achieved independently of diet composition. However, women on the HP diet lost significantly more total (5.3 vs. 2.8 kg, P=0.009) and abdominal (1.3 vs. 0.7 kg, P=0.006) fat compared with the women on the LP diet, whereas, in men, there was no difference in fat loss between diets (3.9 vs. 5.1 kg). Total lean mass decreased in all subjects independently of diet composition. LDL cholesterol reduction was significantly greater on the HP diet (5.7%) than on the LP diet (2.7%) (P < 0.01). CONCLUSIONS—Both dietary patterns resulted in improvements in the cardiovascular disease (CVD) risk profile as a consequence of weight loss. However, the greater reductions in total and abdominal fat mass in women and greater LDL cholesterol reduction observed in both sexes on the HP diet suggest that it is a valid diet choice for reducing CVD risk in type 2 diabetes.