Expression and regulation by insulin of low-density lipoprotein receptor-related protein mRNA in human skeletal muscle

Biochim Biophys Acta. 2002 Dec 12;1588(3):226-31. doi: 10.1016/s0925-4439(02)00169-2.

Abstract

Evidence suggests that increased hydrolysis and/or uptake of triglyceride-rich lipoprotein particles in skeletal muscle can be involved in insulin resistance. We determined the steady state mRNA levels of the low-density lipoprotein-related receptor (LRP) and lipoprotein lipase (LPL) in skeletal muscle of eight healthy lean control subjects, eight type 2 diabetic patients and eight nondiabetic obese individuals. The regulation by insulin of LRP and LPL mRNA expression was also investigated in biopsies taken before and at the end of a 3 h euglycemic hyperinsulinemic clamp (insulinemia of about 1 nM). LRP mRNA was expressed in human skeletal muscle (1.3+/-0.1 amol/microg total RNA in control subjects). Type 2 diabetic patients, but not nondiabetic obese subjects, were characterized by a reduced expression of LRP (0.8+/-0.2 and 1.3+/-0.3 amol/microg total RNA in diabetic and obese patients, respectively; P<0.05 in diabetic vs. control subjects). Insulin infusion decreased LRP mRNA levels in muscle of the control subjects but not in muscle of type 2 diabetic and nondiabetic obese patients. Similar results were found when investigating the regulation of the expression of LPL. Taken together, these results did not support the hypothesis that a higher capacity for clearance or hydrolysis of circulating triglycerides in skeletal muscle is present during obesity- or type 2 diabetes-associated insulin resistance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Diabetes Mellitus / metabolism
  • Diabetes Mellitus, Type 2 / metabolism
  • Female
  • Humans
  • Insulin / physiology*
  • Insulin Resistance*
  • Lipoproteins, LDL / genetics
  • Lipoproteins, LDL / metabolism
  • Male
  • Middle Aged
  • Muscle, Skeletal / metabolism*
  • Obesity
  • RNA, Messenger / analysis
  • Receptors, LDL / genetics
  • Receptors, LDL / metabolism*

Substances

  • Insulin
  • Lipoproteins, LDL
  • RNA, Messenger
  • Receptors, LDL