Disturbed adiponectin - AMPK system in skeletal muscle of patients with metabolic syndrome
Faculty of Medicine and Health Sciences
European journal of preventive cardiology. - -
, p. 203-205
University of Antwerp
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 AMPK1 and AMPK2 subunits, as well as downstream targets in lipid and glucose metabolism. Skeletal muscle mRNA expression of AMPK1 and AMPK2 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). AMPK1 and AdipoR1 correlated positively in both the control (r=0.964, p<0.001) and the metabolic syndrome group (r=0.600, p=0.023). However, this relation was shifted upwards in metabolic syndrome patients, indicating increased AdipoR1mRNA expression for a similar AMPK1 expression. Previously, a blunted stimulatory effect of adiponectin on AMPK activation has been shown in metabolic syndrome patients. The present data suggest that the disturbed interaction of adiponectin with AMPK is located downstream of the AdipoR1 receptor.