An increased circulating angiotensin II concentration is associated with hypoadiponectinemia and postprandial hyperglycemia in men with nonalcoholic fatty liver disease

Abstract

Objective: Nonalcoholic fatty liver disease (NAFLD) is a condition associated with type 2 diabetes (T2D). Insulin resistance, a common pathogenesis of NAFLD and T2D, is partially caused by alterations in angiotensin II (Ang II) and is accompanied by hypoadiponectinemia. We aimed to investigate whether the circulating Ang II and adiponectin concentrations are related to hyperglycemia in male NAFLD patients.

Methods: Thirty-five controls and 85 NAFLD patients without prior known T2D were enrolled. All participants were non-smoking men who performed 75-g oral glucose tolerance tests. According to the American Diabetes Association (ADA) criteria, the NAFLD patients were divided into the euglycemia and hyperglycemia groups. The NAFLD patients with hyperglycemia were further divided into the isolated impaired fasting glucose (I-IFG) and postprandial hyperglycemia subgroups. The fasting serum Ang II and adiponectin concentrations were measured.

Results: Among the 85 NAFLD patients, 40 (47%) had hyperglycemia, including I-IFG (18%) and postprandial hyperglycemia (29%). The serum Ang II concentrations in the euglycemia and hyperglycemia groups were significantly higher than those observed in the control and euglycemia groups, respectively; whereas the serum adiponectin concentrations were significantly lower. The serum Ang II concentrations were significantly higher in the postprandial hyperglycemia subgroup than in the I-IFG subgroup. The serum Ang II and adiponectin concentrations were found to be independent predictors of hyperglycemia in the NAFLD patients. The serum Ang II concentration was significantly associated with the serum adiponectin and 2-hour postprandial glucose concentrations in the NAFLD patients.

Conclusion: An increased circulating Ang II concentration is associated with hypoadiponectinemia and postprandial hyperglycemia in male NAFLD patients and may be involved in the pathogenesis of T2D in NAFLD patients.