1,721,194 research outputs found
Skeletal muscle mitochondrial protein metabolism and function in ageing and type 2 diabetes.
No full textPURPOSE OF REVIEW: Mitochondria are the site of oxidative substrate utilization to produce adenosine triphosphate for normal tissue function. Tissue substrate utilization is impaired in ageing and type 2 diabetes. Defects in mitochondrial gene expression, protein synthesis and function occur with ageing in various tissues including skeletal muscle, and are emerging in individuals with type 2 diabetes. The current review will discuss advances in the understanding of skeletal muscle mitochondrial alterations associated with age and type 2 diabetes.
RECENT FINDINGS: Insulin acutely stimulates skeletal muscle mitochondrial protein synthesis and adenosine triphosphate production. These insulin effects are impaired in insulin-resistant patients with type 2 diabetes who also exhibit defective basal muscle mitochondrial function. The age-related reduction in mitochondrial adenosine triphosphate production has been confirmed in vivo in skeletal muscle in humans and rodents.
SUMMARY: The emerging concept that insulin stimulates mitochondrial protein synthesis and function indicates potential novel molecular mechanisms of metabolic defects in type 2 diabetes, particularly in the post-prandial period characterized by acute increments of plasma insulin concentrations. The potential relationship between insulin resistance and basal post-absorptive muscle mitochondrial defects should be further investigated. As ageing is characterized by insulin resistance, the hypothesis that impaired insulin action could contribute to age-related muscle mitochondrial dysfunction, and metabolic alterations should be addressed
Clinical nutrition university: Muscle physiology and bioenergetics
No full textSkeletal muscle relies on a constant, adequate ATP supply to sustain contractile activity and preserve tissue mass and protein content. Skeletal muscle mitochondrial oxidative phosphorylation provides adequate amounts of ATP under physiological conditions, contributing to preserve muscle protein mass and playing a major role in glucose and lipid substrate utilization. Inflammation, oxidative stress and insulin resistance are emerging contributors to skeletal muscle mitochondrial dysfunction occurring under several disease conditions including insulin resistant states and obesity. Skeletal muscle mitochondrial dysfunction may lead to loss of muscle mass and strength as well as to altered glucose and fatty acid utilization, and these effects are associated with poor clinical outcome. Exercise training enhances skeletal muscle mitochondrial biogenesis and whole-body oxygen consumption (aerobic capacity), and these effects are likely to represent relevant mediators of the positive clinical impact of controlled exercise programs. © 2011 European Society for Clinical Nutrition and Metabolism
Teoria mitocondriale dell'invecchiamento- Conseguenza metaboliche, prevenzione e terapia
No full textGhrelin forms in the modulation of energy balance and metabolism
No full textGhrelin is a gastric hormone circulating in acylated (AG) and unacylated (UnAG) forms. This narrative review aims at presenting current emerging knowledge on the impact of ghrelin forms on energy balance and metabolism. AG represents ~ 10% of total plasma ghrelin, has an appetite-stimulating effect and is the only form for which a receptor has been identified. Moreover, other metabolic AG-induced effects have been reported, including the modulation of glucose homeostasis with stimulation of liver gluconeogenesis, the increase of fat mass and the improvement of skeletal muscle mitochondrial function. On the other hand, UnAG has no orexigenic effects, however recent reports have shown that it is directly involved in the modulation of skeletal muscle energy metabolism by improving a cluster of interlinked functions including mitochondrial redox activities, tissue inflammation and insulin signalling and action. These findings are in agreement with human studies which show that UnAG circulating levels are positively associated with insulin sensitivity both in metabolic syndrome patients and in a large cohort from the general population. Moreover, ghrelin acylation is regulated by a nutrient sensor mechanism, specifically set on fatty acids availability. These recent findings consistently point towards a novel independent role of UnAG as a regulator of muscle metabolic pathways maintaining energy status and tissue anabolism. While a specific receptor for UnAG still needs to be identified, recent evidence strongly supports the hypothesis that the modulation of ghrelin-related molecular pathways, including those involved in its acylation, may be a potential novel target in the treatment of metabolic derangements in disease states characterized by metabolic and nutritional complications.Level of evidence Level V, narrative review
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