Decrease in irisin in patients with chronic kidney disease

PLoS One. 2013 May 7;8(5):e64025. doi: 10.1371/journal.pone.0064025. Print 2013.

Abstract

Patients with chronic kidney disease have abnormal energy expenditure and metabolism. The mechanisms underlying altered energy expenditure in uremia are unknown and remain to be elucidated. Irisin is a peroxisome proliferator-activated receptor γ coactivator 1-α-dependent myokine, and it increases energy expenditure in the absence of changes in food intake or activity. We hypothesize that chronic kidney disease patients have altered irisin levels. We measured resting irisin levels in 38 patients with stage 5 chronic kidney disease and in 19 age- and sex-matched normal subjects. Plasma irisin levels were significantly decreased in chronic kidney disease patients (58.59%; 95% CI 47.9%-69.2%, p<0.0001). The decrease in irisin levels was inversely correlated with the levels of blood urea nitrogen and creatinine. Further association analysis revealed that irisin level is independently associated with high-density lipoprotein cholesterol level. Our results suggest that chronic kidney disease patients have lower than normal irisin levels at rest. Furthermore, irisin may play a major role in affecting high-density lipoprotein cholesterol levels and abnormal energy expenditure in chronic kidney disease patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Case-Control Studies
  • Creatinine / blood
  • Demography
  • Female
  • Fibronectins / blood*
  • Humans
  • Indican / pharmacology
  • Male
  • Middle Aged
  • Muscle Cells / drug effects
  • Muscle Cells / metabolism
  • Muscle, Skeletal / pathology
  • Renal Insufficiency, Chronic / blood*

Substances

  • FNDC5 protein, human
  • Fibronectins
  • Creatinine
  • Indican

Grant support

CYW received support from National Health Research Institute (NHRI-EX100-9925SC), National Science Council (101-2314-B-182A-009, 101-2314-B-182A-098-MY3), and Chang Gung Memorial Hospital (CMRPG3B1641). KCH received support from Chang Gung Memorial Hospital (CMRPG 371953). LSL received support from the National Science Council (101-2321-B-002-060) and Mrs. Hsiu-Chin Lee Kidney Research Foundation. MSW received support from National Research Program for Biopharmaceuticals (PMRPG3B0091) and Chang Gung Memorial Hospital (CMRPG3A1072). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.