1,721,112 research outputs found
Essential role of Ubc9, a SUMO-conjugating enzyme, in regulation of the glucose transport system in adipocytes.
No full textEssential role of the SUMO-conjugating enzyme Ubc9 for insulin-stimulated glucose transport in adipocytes.
No full textCross-Talk between PPARgamma and Insulin Signaling and Modulation of Insulin Sensitivity
No full textPPARgamma activation in type 2 diabetic patients results in a marked improvement in insulin and glucose parameters, resulting from an improvement of whole-body insulin sensitivity. Adipose tissue is the major mediator of PPARgamma action on insulin sensitivity. PPARgamma activation in mature adipocytes induces the expression of a number of genes involved in the insulin signaling cascade, thereby improving insulin sensitivity. PPARgamma is the master regulator of adipogenesis, thereby stimulating the production of small insulin-sensitive adipocytes. In addition to its importance in adipogenesis, PPARgamma plays an important role in regulating lipid, metabolism in mature adipocytes by increasing fatty acid trapping. Finally, adipose tissue produces several cytokines that regulate energy homeostasis, lipid and glucose metabolism. Disturbances in the production of these factors may contribute to metabolic abnormalities, and PPARgamma activation is also associated with beneficial effects on expression and secretion of a whole range of cytokines
Exercise-induced protein kinase C isoform-specific activation in human skeletal muscle
No full textWe determined whether protein kinase C (PKC) isoforms are redistributed and phosphorylated in response to acute exercise in skeletal muscle. Muscle biopsies were obtained from six healthy subjects (four women, two men; age 25 +/- 1 years) before, during, and after 60 min of one-leg cycle ergometry at approximately 70% VO(2peak). Exercise for 30 and 60 min was associated with a three- and fourfold increase in PKC-zeta/lambda abundance and a four- and threefold increase in phosphorylation, respectively, in total membranes (P < 0.05) and a decrease in PKC-zeta/lambda phosphorylation in cytosolic fractions. During exercise recovery, PKC-zeta/lambda abundance and phosphorylation remained elevated. PKC-zeta/lambda abundance and phosphorylation were increased in nonexercised muscle upon cessation of exercise, indicating a systemic response may contribute to changes in PKC abundance and phosphorylation. Exercise did not change PKC-delta or -epsilon abundance or phosphorylation in either the cytosolic or total membrane fraction. In conclusion, exercise is associated with an isoform-specific effect on PKC. PKC-zeta/lambda are candidate PKC isoforms that may play a role in the regulation of exercise-related changes in metabolic and gene-regulatory responses
Human adipose tissue precursor cells: a new factor linking regulation of fat mass to obesity and type 2 diabetes?
No full textThe current epidemic of obesity has caused a surge of interest in the study of the mechanisms regulating adipose tissue formation. It has been observed that adipose tissue contains a pool of adult stem cells with multipotent properties, which provide for the physiological cell turnover, and can be isolated and potentially utilized for tissue engineering and regenerative medical applications. These "stromal" cells exhibit pre-adipocyte characteristics, can be isolated from adipose tissue of adult subjects, propagated in vitro, and induced to differentiate into adipocytes. Different populations of multi-potent precursor cells can be isolated from human fat fragments. Thus, adipose precursors cells are a heterogeneous cells population, consisting of fibroblast-like multi-potential stem cells generally termed adipose-derived stem cells (ASCs). In this review, we discuss some aspects of ASCs basic biology, the methodology involved in ASCs isolation and culture, and some implications of ASCs availability for the understanding of metabolic diseases in humans
Biological specificity of visceral adipose tissue and therapeutic intervention
No full textWith excess energy storage, obesity develops, leading to increased risk for type 2 diabetes and cardiovascular diseases. The distribution of body fat appears to be even more important than the total amount of fat. Abdominal and, in particular, visceral adiposity is strongly linked to insulin resistance, type 2 diabetes, hypertension, dyslipidaemia, sleep apnea, and other complications of obesity. Visceral adiposity, manifested as a high waist circumference, is now accepted as a major component of the metabolic syndrome. However, the biological mechanisms underlying the adverse impact of visceral fat accumulation remain to be established. This review will focus on the analysis of the biological specificity of adipose tissue located in the abdominal region, and will explore intervention strategies targeting the impaired function of the visceral adipocyte as potential therapies for the cardio-metabolic outcomes of patients with the metabolic syndrome
mUbc9 enhances insulin action on glucose transport by augmenting GLUT4 via a post-transcriptional mechanism.
No full textp66Shc, a multifaceted protein linking Erk signalling, glucose metabolism, and oxidative stress
No full textp66Shc, a 66 kDa proto-oncogene Src collagen homologue (Shc) adaptor protein, is classically known as a signalling protein implicated in receptor tyrosine kinase signal transduction. The p66Shc isoform exerts a physiologically relevant, inhibitory signalling effect on the Erk pathway in skeletal muscle myoblasts, which is necessary for actin cytoskeleton polymerization and normal glucose transport responses. More recently, p66Shc has been also identified as a sensor of oxidative stress-induced apoptosis and as a longevity protein in mammals, actions which require Ser36 phosphorylation of the protein and consequent accumulation of intracellular reactive oxygen species. Oxidative stress plays a key role in dysfunction of several organs and tissues, and this is of interest in metabolic diseases such as type 2 diabetes. Thus changes in p66Shc expression and/or function may play an important role in the pathogenesis of type 2 diabetes and potentially serve as an effective target for its treatment
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