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

• Published in: Kidney international Vol. 68; no. 4; pp. 1857 - 1865
• Main Authors: Pupim, Lara B., Flakoll, Paul J., Majchrzak, Karen M., Aftab Guy, Deanna L., Stenvinkel, Peter, Alp Ikizler, T.
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01-10-2005; Nature Publishing; Elsevier Limited
• Subjects: Adult; Amino Acids - blood; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Biological and medical sciences; Body Composition; diabetes; Diabetes Mellitus, Type 2 - complications; Diabetes Mellitus, Type 2 - metabolism; dialysis; Emergency and intensive care: renal failure. Dialysis management; Energy Metabolism; Female; Forearm; Humans; Intensive care medicine; Kidney Failure, Chronic - complications; Kidney Failure, Chronic - metabolism; Kidney Failure, Chronic - therapy; Male; Medical sciences; Medicin och hälsovetenskap; metabolism; Middle Aged; Muscle Proteins - metabolism; Muscle, Skeletal - metabolism; Muscular Atrophy - etiology; Muscular Atrophy - metabolism; Nephrology. Urinary tract diseases; nutrition; Oxidation-Reduction; Renal Dialysis; dialysis; nutrition; metabolism; diabetes; Endocrinopathy; Type 2 diabetes; Human; Nephrology; Nutrition; Hemodialysis; Metabolic diseases; Protein; Urology; Feeding; Extrarenal dialysis; Chronic; Diet; Dialysis; Muscle
• ISSN: 0085-2538; 1523-1755
• DOI: 10.1111/j.1523-1755.2005.00605.x

Increased muscle protein breakdown in chronic hemodialysis patients with type 2 diabetes mellitus.
The presence of diabetes mellitus (DM) in chronic hemodialysis (CHD) patients has potential to increase body protein losses and muscle wasting.
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 HbA1C = 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-(1-13C) leucine and L-(ring-2H5) phenylalanine.
CHD patients with T2DM had significantly increased (83%) skeletal muscle protein breakdown (137 ± 27 vs. 75 ± 25 μg/100 mL/min). There was no significant difference in muscle protein synthesis between groups (78 ± 27 vs. 66 ± 21 μg/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 μg/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.
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.