The study was designed to compare the effects of weight loss induced by a low-carbohydrate-high-fat diet or a normal diet, with and without exercise, on glucose tolerance measured as area under the curve (AUC), and android (A) and gynoid (G) fat distribution. The study was registered at clinicaltrials.gov; NCT04100356. In total, 57 women classified as overweight or obese (age 40 ± 3.5 years, body mass index 31.1 ± 2.6 kg/m2) were randomly assigned and completed a 10-week intervention using a low-carbohydrate high-fat diet or a normal diet, with or without aerobic interval exercise. An equal deficit of 700 kcal/day was prescribed, either restricting the diet only, or moderately restricting diet and including three 50-min high-intensity bicycle sessions per week. There were thus four groups: normal diet (NORM); low-carbohydrate-high-fat diet (LCHF); normal diet with exercise (NORM-EX); and low-carbohydrate-high-fat diet with exercise (LCHF-EX). Linear mixed models was used to assess differences between groups. With all groups pooled, the intervention resulted in a weight loss of 6.7 ± 2.5% (p < 0.001). The intervention did not result in differences between groups in AUC glucose, nor in fasting glucose or indicis for insulin resistance such as Homeostatic Model Assessment, Matsuda Insulin Sensitivity Index, insulinogenic index and disposition index. Post-intervention android fat was lower in LCHF than NORM (3,223 ± 727 vs. 2,533 ± 535 g, p = 0.041). LCHF reached a lower A/G ratio than NORM (0.94 ± 0.12 vs. 1.04 ± 0.09, p = 0.011) and LCHF-EX (0.94 ± 0.12 vs. 1.09 ± 0.09, p < 0.001) after the intervention. LCHF resulted in lower android fat mass compared to NORM and the lowest A/G ratio compared to the other matched groups, but with no accompanying improvement in AUC glucose. In conclusion, although all groups achieved improvements in glucose tolerance, no superior effect was observed with the LCHF diet, neither with nor without exercise.
The role of selective β2-adrenergic stimulation in regulation of leg glucose uptake and free fatty acid (FFA) balance is inadequately explored in humans. The objective of this study was to investigate β2-adrenergic effects on net leg glucose uptake and clearance, as well as FFA balance at rest and during exercise. The study was a randomized, placebo-controlled crossover trial where 10 healthy men received either infusion of β2-agonist terbutaline (0.2 to 0.4 mg) or placebo. Net leg glucose uptake and clearance and FFA balance were determined at rest and during 8 minutes of knee extensor exercise using Fick’s principle. Vastus lateralis muscle biopsies were collected at rest and at cessation of exercise. The primary outcome measure was net leg glucose uptake. At rest, net leg glucose uptake and clearance were 0.35 (±0.16) mmol/min and 41 (±17) mL/min (mean ± 95% CI) higher (P < 0.001) for terbutaline than placebo, corresponding to increases of 84% and 70%. During exercise, no treatment differences were observed in net leg glucose uptake, whereas clearance was 101 (±86) mL/min lower (P < 0.05) for terbutaline than placebo. At rest, terbutaline induced a net leg FFA release of 21 (±14) µmol/min, being different from placebo (P = 0.04). During exercise, net leg FFA uptake was not different between the treatments. These observations indicate that β2-agonist alters net leg glucose uptake and clearance, as well as FFA balance in humans, which is associated with myocellular β2-adrenergic and insulin-dependent signaling. Furthermore, the study shows that exercise confounds the β2-adrenergic effect on net leg glucose uptake and FFA balance.
In spite of amazing progress in food supply and nutritional science, and a striking increase in life expectancy of approximately 2.5 months per year in many countries during the previous 150 years, modern nutritional research has a great potential of still contributing to improved health for future generations, granted that the revolutions in molecular and systems technologies are applied to nutritional questions. Descriptive and mechanistic studies using state of the art epidemiology, food intake registration, genomics with single nucleotide polymorphisms (SNPs) and epigenomics, transcriptomics, proteomics, metabolomics, advanced biostatistics, imaging, calorimetry, cell biology, challenge tests (meals, exercise, etc.), and integration of all data by systems biology, will provide insight on a much higher level than today in a field we may name molecular nutrition research. To take advantage of all the new technologies scientists should develop international collaboration and gather data in large open access databases like the suggested Nutritional Phenotype database (dbNP). This collaboration will promote standardization of procedures (SOP), and provide a possibility to use collected data in future research projects. The ultimate goals of future nutritional research are to understand the detailed mechanisms of action for how nutrients/foods interact with the body and thereby enhance health and treat diet-related diseases.
Insulin resistance and dysglycemia are associated with physical inactivity and adiposity, and may be improved by exercise.Investigate the effect of exercise on insulin sensitivity, body composition and adipose depots in sedentary men with (n = 11) or without (n = 11) overweight and dysglycemia.Euglycemic-hyperinsulinemic clamp, ankle-to-neck MRI, MRS, muscle and adipose tissue biopsies before and after 12 weeks combined strength and endurance exercise.Insulin sensitivity, VO2max, strength, whole-body and muscle fat content, and abdominal adipose depots were improved without obvious differences between normo- and dysglycemic men. Hepatic fat, waist circumference and subcutaneous adipose tissue were reduced in the dysglycemic group. For both groups plasma adiponectin was reduced, whereas IL-6 was unchanged. Visceral fat was preferentially lost compared with other adipose depots.Body composition, fat distribution and insulin sensitivity improved following training in sedentary middle-aged men with and without dysglycemia.
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