Effects of dietary fat modification on skeletal muscle fatty acid handling in the metabolic syndrome.

OBJECTIVE: In the metabolic syndrome (MetS), increased fat storage in 'nonadipose' tissues such as skeletal muscle may be related to insulin resistance ('lipid overflow' hypothesis). The objective of this study was to examine the effects of dietary fat modification on the capacity of skeletal muscle to handle dietary and endogenous fatty acids (FAs). SUBJECTS AND METHODS: In total, 29 men with the MetS were randomly assigned to one of four diets for 12 weeks: a high-fat saturated fat diet (HSFA, n=6), a high-fat monounsaturated fat diet (HMUFA, n=7) and two low-fat high-complex carbohydrate diets supplemented with (LFHCCn-3, n=8) or without (LFHCC, n=8) 1.24 g per day docosahexaenoic and eicosapentaenoic acid. Fasting and postprandial skeletal muscle FA handling was examined by measuring arteriovenous concentration differences across the forearm muscle. [(2)H(2)]-palmitate was infused intravenously to label endogenous triacylglycerol (TAG) and free fatty acids in the circulation and subjects received a high-fat mixed meal (2.6 MJ, 61 energy% fat) containing [U-(13)C]-palmitate to label chylomicron-TAG. RESULTS: Postprandial circulating TAG concentrations were significantly lower after dietary intervention in the LFHCCn-3 group compared to the HSFA group (DeltaiAUC -139+/-67 vs 167+/-70 micromol l(-1) min(-1), P=0.009), together with decreased concentrations of [U-(13)C]-labeled TAG, representing dietary FA. Fasting TAG clearance across forearm muscle was decreased on the HSFA diet, whereas no differences were observed in postprandial forearm muscle FA handling between diets. CONCLUSION: Chronic manipulation of dietary fat quantity and quality did not affect forearm muscle FA handling in men with the MetS. Postprandial TAG concentrations decreased on the LFHCCn-3 diet, which could be (partly) explained by lower concentration of dietary FA in the circulation.

Several obesity- and nutrient-related gene polymorphisms but not FTO and UCP variants modulate postabsorptive resting energy expenditure and fat-induced thermogenesis in obese individuals: the NUGENOB study.

BACKGROUND: Part of the heterogeneity of the obesity phenotype may originate from genetic differences between obese individuals that may influence energy expenditure (EE). OBJECTIVE: To examine if common single-nucleotide polymorphisms (SNPs) in genes related to obesity-associated phenotypes are associated with postabsorptive resting energy expenditure (REE) and postprandial REE in obese individuals. DESIGN AND METHODS: Postabsorptive REE and 3-h postprandial REE (liquid test meal containing 95% fat, energy content 50% of estimated REE) were measured in 743 obese individuals from eight clinical centres in seven European countries. The analysis assessed the association of genotypes of 44 SNPs in 28 obesity-related candidate genes with postabsorptive REE and postprandial REE taking into consideration the influence of body composition, habitual physical activity, insulin sensitivity, circulating thermogenic hormones and metabolites. RESULTS: After adjustment for fat-free mass (FFM), age, sex and research centre, SNPs in CART, GAD2, PCSK1, PPARG3, HSD11B1 and LIPC were significantly associated with postabsorptive REE. SNPs in GAD2, HSD11B1 and LIPC remained significantly associated with postabsorptive REE after further adjustment for fat mass (FM). SNPs in CART, PPARG2 and IGF2 were significantly associated with postprandial REE after similar adjustments. These associations with postprandial REE remained significant after further adjustment for FM. FTO, UCP2 and UCP3 variants were not associated with postabsorptive or postprandial REE. CONCLUSIONS: Several gene polymorphisms associated with obesity-related phenotypes but not FTO and UCP variants may be responsible for some of the inter-individual variability in postabsorptive REE and fat-induced thermogenesis unaccounted for by FFM, FM, age and sex. The association between FTO and obesity that has been reported earlier may not be mediated directly through modulation of EE in obese individuals.

An intervention study of the effects of calcium intake on faecal fat excretion, energy metabolism and adipose tissue mRNA expression of lipid-metabolism related proteins.

CONTEXT: In various observational studies, an inverse relation between calcium intake and body weight has been observed. A possible explanation could be an increased calcium excretion through the faeces caused by an increased dietary calcium intake. OBJECTIVE: To examine whether an increased calcium intake could lead to changes in faecal fat and energy excretion. DESIGN: Four different isocaloric diets with various calcium contents (400, 1200 and 2500 mg from dairy and 1200 mg from calcium carbonate (1200S)) were administered in a crossover design for 7 days each. SUBJECTS: Five healthy men and five healthy women (age=28+/-2, body mass index=24.1+/-0.4, body fat%=25.6+/-2.4) were recruited by local announcement. MEASUREMENTS: At the end of every intervention period, faecal samples were collected for determination of fat, energy and calcium content, blood samples were obtained for determination of relevant blood parameters; and fat samples were obtained for measurement of the mRNA expression. Furthermore, resting energy expenditure and fat oxidation were measured with the ventilated-hood technique. RESULTS: We observed a non-significant 56% increase in fat excretion (P=0.159) on the 2500 mg diet, compared to the 400 mg diet. The 2500 mg diet significantly reduced the expression of fatty acid synthase (FAS) mRNA (P<0.05) and the calcium content of the diets significantly affected calcium excretion. Furthermore, we saw a significant decrease of serum triglycerides on the 1200S diet (P<0.05). CONCLUSION: In this study, we observed a trend towards a higher fat excretion on the high-calcium diet, but this difference failed to reach statistical significance. It is possible that the relatively high protein content of the experimental diets increased calcium absorption from the intestine, thus decreasing the amount of calcium available for binding to fat and eliminating possible effects of dietary calcium on fat excretion. Furthermore, we observed decreases in FAS mRNA expression and serum triglycerides as a result of a high calcium intake.

The effect of low-intensity exercise training on fat metabolism of obese women.

OBJECTIVE: Previous studies have shown that fat metabolism is different in upper body (UB) and lower body (LB) obese women. The present study investigated whether the effect of low-intensity exercise training on fat metabolism is different in UB and LB obese premenopausal women. RESEARCH METHODS AND PROCEDURES: Twenty-one healthy, premenopausal women with either LB obesity (waist-to-hip ratio of < or =0.79; n = 8) or UB obesity (waist-to-hip ratio of > or =0.85; n = 13) participated in the present study. The UB obese women were matched and randomly divided in an exercise training group (UB) and a nonexercising control group (UB-C). Subjects in the UB and LB groups participated in a low-intensity exercise training program (40% VO2max) three times per week for 12 weeks. Before and after the intervention, measurements of fat metabolism at rest and during exercise, body composition, and maximal aerobic capacity were performed. RESULTS: Exercise training did not change the respiratory exchange ratio at rest in the UB and LB groups. During exercise, relative fat oxidation increased in the UB group by 19% (p < 0.05), whereas no change in the LB and UB-C groups was found. Plasma free fatty acid oxidation did not change by exercise training, and nonplasma fatty acid oxidation tended to increase in the UB group compared with the UB-C group (p = 0.08). DISCUSSION: Low-intensity exercise training increased the contribution of fat oxidation to total energy expenditure during exercise but not at rest in UB obese women. Exercise training had no significant effect on fat metabolism in the LB obese women.

Short-term effects of weight loss with or without low-intensity exercise training on fat metabolism in obese men.

BACKGROUND: Energy restriction is known to induce a decline in fat oxidation during the postdiet period. Reduced fat oxidation may contribute to weight regain. OBJECTIVE: The present study investigated the effect of the addition of low-intensity exercise training to energy restriction on postdiet fat oxidation and on the contribution of the sympathetic nervous system to fat oxidation. DESIGN: Forty obese men were divided randomly into 2 groups: diet (D) and diet plus exercise (DE). Both groups followed an energy restriction program for 10 wk. Subjects in the DE group also participated in a low-intensity exercise training program [40% maximal oxygen uptake (VO2max)] for 12 wk. Before the intervention and after 12 wk, with subjects at stable body weights, we measured body composition, VO2max, and substrate oxidation at rest, during exercise at 50% VO2max, and during recovery. Measurements were made with and without administration of the beta-adrenergic antagonist propranolol. RESULTS: Both interventions led to significant decreases in body weight, fat mass, and fat-free mass (P < 0.001); these decreases did not differ significantly between the D and DE groups. Neither intervention significantly affected VO2max. The effect of the intervention on the respiratory exchange ratio differed significantly between the D and DE groups [two-way analysis of variance (ANOVA), P < 0.05]. The effect on the beta-adrenergic-mediated respiratory exchange ratio tended to be different between the 2 groups (two-way ANOVA, P = 0.09). CONCLUSION: Addition of low-intensity exercise training to energy restriction counteracts the decline in fat oxidation during the postdiet period.