Diabetic myopathy: impact of diabetes mellitus on skeletal muscle progenitor cells

Abstract

Diabetes mellitus is defined as a group of metabolic diseases that are associated with the presence of a hyperglycemic state due to impairments in insulin release and/or function. While the development of each form of diabetes (Type 1 or Type 2) drastically differs, resultant pathologies often overlap. In each diabetic condition, a failure to maintain healthy muscle is often observed, and is termed diabetic myopathy. This significant, but often overlooked, complication is believed to contribute to the progression of additional diabetic complications due to the vital importance of skeletal muscle for our physical and metabolic well-being. While studies have investigated the link between changes to skeletal muscle metabolic health following diabetes mellitus onset (particularly Type 2 diabetes mellitus), few have examined the negative impact of diabetes mellitus on the growth and reparative capacities of skeletal muscle that often coincides with disease development. Importantly, evidence is accumulating that the muscle progenitor cell population (particularly the muscle satellite cell population) is also negatively affected by the diabetic environment, and as such, likely contributes to the declining skeletal muscle health observed in diabetes mellitus. In this review, we summarize the current knowledge surrounding the influence of diabetes mellitus on skeletal muscle growth and repair, with a particular emphasis on the impact of diabetes mellitus on skeletal muscle progenitor cell populations.

Inorganic Nitrate Mimics Exercise-Stimulated Muscular Fiber-Type Switching and Myokine and γ-Aminobutyric Acid Release

“…We have shown that nitrate increases muscle -oxidation and mitochondrial biogenesis (23), and therefore may have utility in treating the intramuscular lipid deposition-induced lipotoxicity and insulin resistance associated with diabetes. However, diabetic myopathy is a major complication of diabetes and is characterized by muscle atrophy and reduced physical performance and muscle capacity (20). Skeletal muscle from diabetic patients exhibits a higher concentration of glycolytic fibers (38), and evidence of a switch towards a glycolytic phenotype (39).…”

“…5 Exercise is an effective intervention for both the prevention and treatment of type 2 diabetes mellitus (T2DM) (19). Diabetic myopathy, characterized by reduced muscle functional capacity, atrophy and a glycolytic fiber-type, is a major diabetic complication (20). Furthermore, the proportion of type I fibers in muscle is positively correlated with systemic insulin sensitivity (21); and decreased levels of type I fibers are associated with insulin resistant states including T2DM (22).…”

Activation of the Pro-Oxidant PKCβII-p66Shc Signaling Pathway Contributes to Pericyte Dysfunction in Skeletal Muscles of Patients With Diabetes With Critical Limb Ischemia

“…Satellite cells are well acknowledged targets of diabetes-induced damage and contributors of diabetic vascular myopathy (7)(8)(9)(10). Recent evidence indicates pericytes play key role in vascular and muscular regeneration (11)(12)(13) and have potential to become favorite candidates for cell therapy of PAD and myocardial ischemia (14)(15)(16)(17).…”

Insulin receptor binding motif tagged with IgG4 Fc (Yiminsu) works as an insulin sensitizer to activate Akt signaling in hepatocytes

“…In skeletal muscles, insulin promotes glucose uptake by stimulating a cascade of signaling processes initiated by the binding of insulin to the extracellular α-subunit of the IR on the cellular membrane (D'Souza et al, 2013). After binding, the intracellular tyrosine kinase domain of the IR becomes activated by IR autophosphorylation of its intracellular β-subunit.…”