Abstract
We summarize the existing literature data concerning the involvement of skeletal muscle (SM) in whole body glucose homeostasis and the contribution of SM insulin resistance (IR) to the metabolic derangements observed in several endocrine disorders, including polycystic ovary syndrome (PCOS), adrenal disorders and thyroid function abnormalities. IR in PCOS is associated with a unique postbinding defect in insulin receptor signaling in general and in SM in particular, due to a complex interaction between genetic and environmental factors. Adrenal hormone excess is also associated with disrupted insulin action in peripheral tissues, such as SM. Furthermore, both hyper- and hypothyroidism are thought to be insulin resistant states, due to insulin receptor and postreceptor defects. Further studies are definitely needed in order to unravel the underlying pathogenetic mechanisms. In summary, the principal mechanisms involved in muscle IR in the endocrine diseases reviewed herein include abnormal phosphorylation of insulin signaling proteins, altered muscle fiber composition, reduced transcapillary insulin delivery, decreased glycogen synthesis, and impaired mitochondrial oxidative metabolism.
Highlights
Insulin resistance (IR) constitutes a common and broadly prevalent metabolic disorder, which seems to govern the pathophysiology of diabetes mellitus, metabolic syndrome, and obesity [1]
It has been generally suggested that Thyroid hormones (THs) are not the only factors involved in the initiation of the IR cascade, but they most commonly interact with various tissues and molecules, in order to regulate glucose metabolism and insulin action
Specific alterations at the insulin receptor level or the signal transduction pathway have been suggested as the main underlying pathogenetic mechanisms which lead to impaired insulin-mediated glucose uptake (IMGU) and defective glycogen synthesis
Summary
Insulin resistance (IR) constitutes a common and broadly prevalent metabolic disorder, which seems to govern the pathophysiology of diabetes mellitus, metabolic syndrome, and obesity [1]. From a pathophysiological point of view, IR appears to be the end result of a complex interaction between genetic predisposition and environmental factors. IR indicates the presence of an impaired peripheral tissue response to endogenously secreted insulin. It is typically manifested as both decreased insulin-mediated glucose uptake (IMGU) at the level of adipose and skeletal muscle (SM) tissue, and as an impaired suppression of hepatic glucose output. A significant body of evidence supports the critical role of SM for the development of IR, most commonly through an interactive cross-talk with adipose and liver tissue [6,7,8]
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