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Kidney Int. 2005 Oct;68(4):1857-65.

Increased muscle protein breakdown in chronic hemodialysis patients with type 2 diabetes mellitus.

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1
Division of Nephrology and Division of Pediatric Endocrinology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Abstract

BACKGROUND:

The presence of diabetes mellitus (DM) in chronic hemodialysis (CHD) patients has potential to increase body protein losses and muscle wasting.

METHODS:

In this study, we examined whole-body and skeletal muscle protein metabolism in 6 CHD patients with type 2 (T2) DM (2 male, 44.4 +/- 6.1 years old, 2 white/4 African American HbA(1)C = 9.5 +/- 1.1%), and 6 non-DM CHD patients (2 male, 43.3 +/- 6.7 years old, 2 white/4 African American) in a fasting state, using a primed-constant infusion of L-(1-(13)C) leucine and L-(ring-(2)H(5)) phenylalanine.

RESULTS:

CHD patients with T2DM had significantly increased (83%) skeletal muscle protein breakdown (137 +/- 27 vs. 75 +/- 25 microg/100 mL/min). There was no significant difference in muscle protein synthesis between groups (78 +/- 27 vs. 66 +/- 21 microg/100 mL/min, for DM and non-DM respectively), resulting in significantly more negative net protein balance in the muscle compartment in the DM group (-59 +/- 4 vs. -9 +/- 6 microg/100 mL/min, P < 0.05). A similar trend was observed in whole-body protein synthesis and breakdown. Plasma glucose levels were 113 +/- 16 and 71 +/- 2 mg/dL, P < 0.05, and insulin levels were 25.3 +/- 9.6 and 7.3 +/- 1.0 uU/mL, for DM versus non-DM, respectively, P < 0.05. No significant differences between DM and non-DM were found in other metabolic hormones.

CONCLUSION:

The results of this study demonstrate that CHD patients with T2DM under a suboptimal metabolic control display accelerated muscle protein loss compared with a matched group of non-DM CHD patients.

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