Disturbed adiponectin - AMPK system in skeletal muscle of patients with metabolic syndrome

Abstract

Patients with metabolic syndrome are characterized by low circulating adiponectin levels and reduced adiponectin sensitivity in skeletal muscles. Through binding on its main skeletal muscle receptor AdipoR1, adiponectin activates AMP-activated protein kinase (AMPK), a key player in energy homeostasis. Fourteen metabolic syndrome patients and seven healthy control subjects were included. Blood samples were taken to determine insulin resistance, adiponectin, lipoproteins, and C-reactive protein. Muscle biopsies (m. vastus lateralis) were obtained to assess mRNA expression of AdipoR1 and both AMPKα1 and AMPKα2 subunits, as well as downstream targets in lipid and glucose metabolism. Skeletal muscle mRNA expression of AMPKα1 and AMPKα2 was lower in metabolic syndrome patients (100-±-6 vs. 122-±-8 AU, p-=-0.030 and 64-±-4 vs. 85-±-9 AU, p-=-0.044, respectively), whereas the expression of AdipoR1 was upregulated (138-±-9 vs. 105-±-7, p-=-0.012). AMPKα1 and AdipoR1 correlated positively in both the control (r-=-0.964, p-