Diabetes, Vol 38, Issue 9 1117-1122, Copyright © 1989 by American Diabetes Association

ARTICLES

Skeletal muscle proteolysis in rats with acute streptozocin-induced diabetes

OL Smith, CY Wong and RA Gelfand
John B. Pierce Foundation Laboratory, Yale University School of Medicine, New Haven, Connecticut 06519.

Skeletal muscle proteolysis was studied in rats 1 day after induction of diabetes with 65 mg/kg streptozocin. An evisceration procedure, including functional hepatectomy-nephrectomy, was performed, and the rate of proteolysis in the remaining tissues, primarily skeletal muscles, was evaluated over 2 h. With cycloheximide to block protein synthesis, total protein breakdown was measured from the rate of rise in plasma tyrosine concentration. The rate of degradation of contractile (myofibrillar) protein was estimated from the rate of rise in plasma concentration of 3-methylhistidine released from the breakdown of actomyosin. Compared with nondiabetic control preparations, the total protein degradation rate was increased 30% by diabetes (P less than .001), and myofibrillar catabolism was accelerated by 60% (P less than .005). In diabetes, the increase in proteolysis was accompanied by reductions in circulating insulin to 25-50% of normal level, whereas food intake did not differ from control. Treatment of diabetic rats with exogenous insulin, including acute infusions postoperatively, completely reversed the proteolytic effects of diabetes. The findings demonstrate that the hypoinsulinemia of acute diabetes increases the catabolism of skeletal muscle protein and that the inhibitory effect of normal levels of insulin includes a specific action to restrain myofibrillar proteolysis.
CiteULike    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				A. P. W. Johnston, J. E. Campbell, J. G. Found, M. C. Riddell, and T. J. Hawke Streptozotocin induces G2 arrest in skeletal muscle myoblasts and impairs muscle growth in vivo Am J Physiol Cell Physiol, March 1, 2007; 292(3): C1033 - C1040. [Abstract] [Full Text] [PDF]

				L. I. Rachek, S. I. Musiyenko, S. P. LeDoux, and G. L. Wilson Palmitate Induced Mitochondrial Deoxyribonucleic Acid Damage and Apoptosis in L6 Rat Skeletal Muscle Cells Endocrinology, January 1, 2007; 148(1): 293 - 299. [Abstract] [Full Text] [PDF]

				O. A. Sanchez, L. M. Snow, D. A. Lowe, R. C. Serfass, and L. V. Thompson Effects of endurance exercise-training on single-fiber contractile properties of insulin-treated streptozotocin-induced diabetic rats J Appl Physiol, August 1, 2005; 99(2): 472 - 478. [Abstract] [Full Text] [PDF]

				M. Aragno, R. Mastrocola, M. G. Catalano, E. Brignardello, O. Danni, and G. Boccuzzi Oxidative Stress Impairs Skeletal Muscle Repair in Diabetic Rats Diabetes, April 1, 2004; 53(4): 1082 - 1088. [Abstract] [Full Text] [PDF]

				J. C. Kostyak, S. R. Kimball, L. S. Jefferson, and P. A. Farrell Severe diabetes inhibits resistance exercise-induced increase in eukaryotic initiation factor 2B activity J Appl Physiol, July 1, 2001; 91(1): 79 - 84. [Abstract] [Full Text] [PDF]

				P. A. Farrell, M. J. Fedele, J. Hernandez, J. D. Fluckey, J. L. Miller III, C. H. Lang, T. C. Vary, S. R. Kimball, and L. S. Jefferson Hypertrophy of skeletal muscle in diabetic rats in response to chronic resistance exercise J Appl Physiol, September 1, 1999; 87(3): 1075 - 1082. [Abstract] [Full Text] [PDF]

				W. E. Mitch, J. L. Bailey, X. Wang, C. Jurkovitz, D. Newby, and S. R. Price Evaluation of signals activating ubiquitin-proteasome proteolysis in a model of muscle wasting Am J Physiol Cell Physiol, May 1, 1999; 276(5): C1132 - C1138. [Abstract] [Full Text] [PDF]

				P. A. Farrell, M. J. Fedele, T. C. Vary, S. R. Kimball, C. H. Lang, and L. S. Jefferson Regulation of protein synthesis after acute resistance exercise in diabetic rats Am J Physiol Endocrinol Metab, April 1, 1999; 276(4): E721 - E727. [Abstract] [Full Text] [PDF]

				J. Kuusisto, L. Mykkanen, K. Pyorala, and M. Laakso Hyperinsulinemic Microalbuminuria : A New Risk Indicator for Coronary Heart Disease Circulation, February 1, 1995; 91(3): 831 - 837. [Abstract] [Full Text]