Differential control of muscle mass in type 1 and type 2 diabetes mellitus

• Published in: Cellular and molecular life sciences : CMLS Vol. 72; no. 20; pp. 3803 - 3817
• Main Authors: Sala, David, Zorzano, Antonio
• Format: Journal Article
• Language: English
• Published: Basel Springer Basel 01.10.2015; Springer Nature B.V
• Subjects: Amino acids; Animal models; Animals; Atrophy; Autophagy; Biochemistry; Biomedical and Life Sciences; Biomedicine; Cell Biology; Diabetes; Diabetes Complications - metabolism; Diabetes Complications - pathology; Diabetes mellitus; Diabetes mellitus (insulin dependent); Diabetes mellitus (non-insulin dependent); Diabetes Mellitus - metabolism; Diabetes Mellitus - pathology; Disease Models, Animal; glucose; Glucose metabolism; Humans; Insulin; Insulin - metabolism; Insulin resistance; insulin-dependent diabetes mellitus; Life Sciences; Lipid metabolism; Lipids; metabolism; Mice; Models, Biological; Muscles; muscular atrophy; Muscular Atrophy - complications; Muscular Atrophy - metabolism; Muscular system; noninsulin-dependent diabetes mellitus; Proteases; Proteins - metabolism; Rats; Regulatory mechanisms (biology); Review; Muscle atrophy; Proteostasis; Autophagy; TP53INP2; Proteasome
• ISSN: 1420-682X; 1420-9071; 1420-9071
• DOI: 10.1007/s00018-015-1954-7

Diabetes mellitus—whether driven by insulin deficiency or insulin resistance—causes major alterations in muscle metabolism. These alterations have an impact on nutrient handling, including the metabolism of glucose, lipids, and amino acids, and also on muscle mass and strength. However, the ways in which the distinct forms of diabetes affect muscle mass differ greatly. The most common forms of diabetes mellitus are type 1 and type 2. Thus, whereas type 1 diabetic subjects without insulin treatment display a dramatic loss of muscle, most type 2 diabetic subjects show no changes or even an increase in muscle mass. However, the most commonly used rodent models of type 2 diabetes are characterized by muscle atrophy and do not mimic the features of the disease in humans in terms of muscle mass. In this review, we analyze the processes that are differentially regulated under these forms of diabetes and propose regulatory mechanisms to explain them.