Insulin resistance is characterized by disturbances in lipid metabolism in skeletal muscle. Our aim was to investigate whether gene expression and fatty acid (FA) profile of skeletal muscle lipids are affected by diets differing in fat quantity and quality in subjects with the metabolic syndrome (MetS) and varying degrees of insulin sensitivity. 84 subjects (age 57.3±0.9 y, BMI 30.9±0.4kg/m(2), 42M/42F) were randomly assigned to one of four iso-energetic diets: high-SFA (HSFA); high-MUFA (HMUFA) or two low-fat, high-complex carbohydrate diets, supplemented with 1.24g/day of long-chain n-3 PUFA (LFHCCn-3) or control oil (LFHCC) for 12weeks. In a subgroup of men (n=26), muscle TAG, DAG, FFA and phospholipid contents were determined including their fractional synthetic rate (FSR) and FA composition at fasting and 4h after consumption of a high-fat mixed-meal, both pre- and post-intervention. Genes involved in lipogenesis were downregulated after HMUFA (mean fold change -1.3) and after LFHCCn-3 (fold change -1.7) in insulin resistant subjects (< median of (S(I))), whereas in insulin sensitive subjects (>median of insulin sensitivity) the opposite effect was shown (fold change +1.6 for both diets). HMUFA diet tended to decrease FSR in TAG (P=.055) and DAG (P=.066), whereas the LFHCCn-3 diet reduced TAG content (P=.032). In conclusion, HMUFA and LFHCCn-3 diets reduced the expression of the lipogenic genes in skeletal muscle of insulin resistant subjects, whilst HMUFA reduced the fractional synthesis rate of DAG and TAG and LFHCC n-3 the TAG content. Our data indicate that these diets may reduce muscle fat accumulation by affecting the balance between FA synthesis, storage and oxidation.
"In addition, increased omega-3 exposure has been implicated in increasing the oxidative potential of isolated muscle cells and rodent skeletal muscle through mitochondrial biogenesis in some (Totland et al. 2000; Vaughan et al. 2012), but not all (Smith et al. 2010) studies. Recently, it has been shown that omega-3s can also increase gene expression in human skeletal muscle (Jans et al. 2012), but we are unaware of any work demonstrating that these changes translate into protein changes. The first aim of this study was to re-examine the effects of omega-3 supplementation on whole body resting energy expenditure and substrate oxidation by utilizing a high dosage, long supplementation period, and large sample size. "
[Show abstract][Hide abstract] ABSTRACT: Omega-3 supplementation has been purported to improve the function of several organs in the body, including reports of increased resting metabolic rate (RMR) and reliance on fat oxidation. However, the potential for omega-3s to modulate human skeletal muscle metabolism has received little attention. This study examined the effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) supplementation on whole-body RMR and the content of proteins involved in fat metabolism in human skeletal muscle. Recreationally active males supplemented with 3.0 g/day of EPA and DHA (n = 21) or olive oil (n = 9) for 12 weeks. Resting muscle biopsies were sampled in a subset of 10 subjects before (pre) and after (post) omega-3 supplementation. RMR significantly increased (5.3%, p = 0.040) following omega-3 supplementation (Pre, 1.33 ±0.05; Post, 1.40 ±0.04 kcal/min) with variable individual responses. When normalizing for body mass, this effect was lost (5.2%, p = 0.058). Omega-3s did not affect whole-body fat oxidation, and olive oil did not alter any parameter assessed. Omega-3 supplementation did not affect whole muscle, sarcolemmal, or mitochondrial FAT/CD36, FABPpm, FATP1 or FATP4 contents or mitochondrial electron chain and PDH proteins, but did increase the long form of UCP3 by 11%. In conclusion, supplementation with a high dose of omega-3s for 12 weeks increased RMR in a small and variable manner in a group of healthy young men. Omega-3 supplementation also had no effect on several proteins involved in skeletal muscle fat metabolism and did not cause mitochondrial biogenesis.
"In both cases, evidence of MD effects on MetS has now refuted the traditional assumption that low fat and low carbohydrates diets are the best for improving blood lipids. Indeed, it has been clearly demonstrated that indication for fat and carbohydrates quality rather than quantity may exert better outcomes in terms of prevention of cardiovascular risk factors and pathological conditions associated with MetS. Diets rich of MUFAs improve the metabolic profile both in normal and obese individuals  and in diabetic patients , who are insulin resistant. In contrast, lowfat diets have been demonstrated to be largely ineffective in insulin resistant patient lipid profile response . "
[Show abstract][Hide abstract] ABSTRACT: The metabolic syndrome (MetS) represents a cluster of medical disorders, such as hyperglycemia, dyslipidemia, hypertension, and abdominal obesity that, when occurring together, increase the risk of developing cardiovascular disease. The role of food and nutrients in the aetiology of chronic diseases has become clearer over the last 15 years. In this review we collected evidence on the beneficial impact ofthe Mediterranean diet on MetS by analyzing epidemiological reports documenting its prevalence in subjects who have adopted this dietary pattern. We also explored the role of the individual components of the diet on the specific aspects characterizing the MetS (i.e. metabolic indices, body weight and blood pressure). There is ample evidence showing that subjects adherent to the Mediterranean diet have lower prevalence and incidence rates of MetS than non-adherent. Moreover, it has been widely documented that specific components of this dietary pattern play a role in the prevention of several morbid conditions related to the MetS.
Current pharmaceutical design 12/2013; 20(31). DOI:10.2174/1381612819666131206112144 · 3.45 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Metabolic syndrome (MetS) is a cluster of metabolic abnormalities characterized by central obesity, dyslipidemias, hypertension, high fasting glucose, chronic low-grade inflammation and oxidative stress. This condition has become an increasing problem in our society where about 34 % of adults are diagnosed with MetS. In parallel with the adult situation, a significant number of children present lipid abnormalities and insulin resistance, which can be used as markers of MetS in the pediatric population. Changes in lifestyle including healthy dietary regimens and increased physical activity should be the first lines of therapy to decrease MetS. In this article, we present the most recent information on successful dietary modifications that can reduce the parameters associated with MetS. Successful dietary strategies include energy restriction and weight loss, manipulation of dietary macronutrients-either through restriction of carbohydrates, fat, or enrichment in beneficial fatty acids, incorporation of functional foods and bioactive nutrients, and adherence to dietary and lifestyle patterns such the Mediterranean diet and diet/exercise regimens. Together, the recent findings presented in this review serve as evidence to support the therapeutic treatment of MetS through diet.
Reviews in Endocrine and Metabolic Disorders 08/2013; 14(3). DOI:10.1007/s11154-013-9251-y · 4.89 Impact Factor
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