4.7 Review

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

Journal

CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 72, Issue 20, Pages 3803-3817

Publisher

SPRINGER BASEL AG
DOI: 10.1007/s00018-015-1954-7

Keywords

Muscle atrophy; Autophagy; TP53INP2; Proteasome; Proteostasis

Funding

  1. FPU fellowship from Ministerio de Educacion y Cultura, Spain
  2. California Institute for Regenerative Medicine (CIRM) Training grant [TG2-01162]
  3. MINECO [SAF2008-03803, SAF2013-40987R]
  4. Generalitat de Catalunya, CIBERDEM (Instituto de Salud Carlos III) [2009SGR915, 2014SGR48]
  5. INTERREG IV-B-SUDOE-FEDER (DIOMED) [SOE1/P1/E178]
  6. DEXLIFE [279228]
  7. ICREA Academia (Generalitat de Catalunya)

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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.

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