Postprandial insulin response and mitochondrial oxidation in obese men nutritionally treated to lose weight

Abstract

Obesity, hyperglycemia, and insulin resistance have been associated to an oxidative mitochondrial dysfunction. The aim of this research was to evaluate the relation between carbohydrate metabolism and mitochondrial oxidation, as affected by the weight status and the weight loss induced by a calorie-restricted diet. Lean control men (BMIo25 kg/m 2 , n ¼ 6) and obese men (BMI430 kg/m 2 , n ¼ 14), who were characterized as insulin resistant (n ¼ 6) or insulin sensitive (n ¼ 8) based on HOMA index values, participated in the trial. Plasma insulin levels and mitochondrial oxidation estimated by the 2-keto(1-13 C)isocaproate breath test, were measured after ingestion of a test meal during 3 h. Obese subjects repeated the breath test protocol after a 10-week caloric restriction diet to lose weight. Postprandial insulin secretion tended to be marginally higher (P ¼ 0.059) in both obese groups than in controls, while the rate of postprandial mitochondrial oxidation was markedly decreased (P ¼ 0.019) in the obese subjects as compared with lean individuals. The nutritionally induced weight loss produced a rise in the postprandial oxidative process in volunteers initially considered as insulin resistant (P ¼ 0.036), while no statistical differences in the insulin-sensitive obese (P ¼ 0.241) were found. Interestingly, the percentage of oxidized tracer was inversely related to postprandial insulin secretion (r ¼ À0.56; P ¼ 0.001). In conclusion, these results support the hypothetized relation between carbohydrate metabolism and mitochondrial oxidation at a postprandial state in obese subjects, raising interest about mitochondria stimulation as a target in the therapy of obesity.

Energy restriction in obese subjects impact differently two mitochondrial function markers

“…Previous reports have shown a decrease in the tracer oxidation after an energy restriction treatment (1,23,24). The reason for the disparity with other studies may relate not only to the different nutritional treatment conditions, but also because the mitochondrial oxidation of KICA could be modulated by the type of nutritional intervention (1).…”

“…Before and after the nutritional treatment, selected anthropometric measurements were carried out and the obese volunteers were given a test drink (200 mL) in form of commercial orange juice (Kasfruit, Spain) containing 1mg/kg of 2-keto[1-13 C]isocaproate (Eriso-top, Fance) and 20 mg/kg of leucin (Sigma-Aldrich, USA) to perform the breath test that evaluates the mitochondrial oxidation (24). Moreover, in the fasting state the endogenous oxidation of proteins, carbohydrates and lipids was estimated by indirect calorimetric according conventional equations described elsewhere (13).…”

A Nutrigenomic Inflammation-Related PBMC-Based Approach to Predict the Weight-Loss Regain in Obese Subjects

“…Insulin resistance was indirectly determined by the ho-meostatic model assessment index (HOMA-IR), which was calculated as follows: [fasting plasma glucose (m M ) ! fasting plasma insulin ( U/ml)/22.5], as described elsewhere [28] .…”

Effectiveness of Dichrostachys glomerata Spice Phenolics in Reduction of Oxidative Stress Associated with Obesity and Type 2 Diabetes; a Randomized, Double-Blind Placebo-Controlled Clinical Trial

“…Antioxidant compounds in human foods or supplementary diets have been found to be beneficial against diabetes (Arulmozhi, Veeranjaneyulu, & Bodhankar, 2004). Further, nutritional intervention by means of antioxidant-enriched weight loss dietary supplements could produce protective effects against the redox unbalance thus increasing the health benefits related to weight loss (Parra, Martinez de Morentin, & Martinez, 2005;Crujeiras, Parra, Rodríguez, Martínez de Morenti, & Alfredo, 2006). Significant and possibly relevant effects on total plasma/serum antioxidant capacity have been reported for phenolic-rich foods and beverages, such as wine, tea, different fruits and their derivatives, both in short-and long-term human studies (Crujeiras et al, 2006;Tulipani et al, 2009;Hunter et al, 2012).…”