title: Myostatin expression is not altered by insulin deficiency and replacement in streptozotocin-diabetic rat skeletal muscles.
abstract: OBJECTIVE
  Insulin is a major post-prandial muscle-anabolic hormone. A substantial loss of skeletal muscle mass occurs in insulin-deprived diabetes and is reversed by insulin treatment. Myostatin is a negative regulator of muscle mass upregulated in several chronic catabolic conditions. Whether myostatin expression is altered in insulin-deprived diabetes is unknown. In spite of opposite effects on muscle mass the potential role of basal circulating insulin in the regulation of myostatin expression is also undetermined.
  
  
  METHODS
  We measured (Northern Blot) myostatin transcript levels in muscle groups with different fiber composition in streptozotocin-diabetic male rats receiving one of the following treatments for eight weeks: (1) control (C); (2) diabetes without treatment (DM); (3) diabetes with once-daily slow-acting insulin treatment (INS).
  
  
  RESULTS
  INS normalized plasma insulin and prevented weight reduction observed in DM. In fast-twitch gastrocnemius muscle myostatin transcript levels were unchanged (P>0.4) in both DM and INS compared to C. Myostatin transcripts were not measurable in any group in slow-twitch soleus muscle.
  
  
  CONCLUSIONS
  Muscle-specific myostatin expression is not increased under catabolic conditions in insulin-deprived diabetes. Insulin treatment also does not change myostatin transcript levels. The data provide the first assessment of potential interplay between insulin and myostatin and they do not support a major role of circulating insulin in the in vivo regulation of myostatin gene expression. A role of myostatin in muscle catabolism in chronic insulin-deprived diabetes is also not indicated by the current results.
authors.affiliation: Clinica Medica-DSCMT, University of Trieste, Ospedale Cattinara, Strada di Fiume 447, Trieste, Italy. barazzon@units.it
authors.forename: Rocco
authors.initials: R
authors.lastname: Barazzoni
authors.forename: Michela
authors.initials: M
authors.lastname: Zanetti
authors.forename: Alessandra
authors.initials: A
authors.lastname: Bosutti
authors.forename: Marco
authors.initials: M
authors.lastname: Stebel
authors.forename: Luigi
authors.initials: L
authors.lastname: Cattin
authors.forename: Gianni
authors.initials: G
authors.lastname: Biolo
authors.forename: Gianfranco
authors.initials: G
authors.lastname: Guarnieri
mesh_terms: D000818:Animals; D015152:Blotting, Northern; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy*; D005786:Gene Expression Regulation; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000172:deficiency* / Q000627:therapeutic use*; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism*; D055435:Myostatin; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013311:Streptozocin; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism*; D015431:Weight Loss / Q000502:physiology
chemical_list: D007004:Hypoglycemic Agents; D007328:Insulin; C525913:Mstn protein, rat; D055435:Myostatin; D016212:Transforming Growth Factor beta; D013311:Streptozocin