Objective: The pathogenesis of nonalcoholic fatty liver disease (NAFLD) is multifactorial, and the presence of insulin resistance is recognized as the pathophysiological hallmark of this condition. Arterial hypertension is referred as an insulin-resistant state, and insulin resistance may substantially contribute to the cardiovascular risk in this disorder. We examined the inter-relationship between insulin sensitivity, adiponectin levels, and NAFLD in hypertensive patients with different circadian blood pressure profiles.
Methods: Eighty never-treated patients with essential hypertension were selected for having a nocturnal decrement of blood pressure that was at least 10% (dippers, n = 47) or less than 10% (nondippers, n = 33) of daytime values. No patient had diabetes mellitus, obesity, hyperlipidemia, or other risk factors for hepatic disease. The two groups were similar as to sex, age, and BMI. Abdominal fat distribution and NAFLD were assessed by ultrasonography.
Results: Hepatic steatosis was detected in 57.5% of all patients. Nondippers showed a higher prevalence of NAFLD than dippers (81.8 vs. 40.4%, P < 0.005). Insulin and the homeostasis model of assessment index were higher (P < 0.001) and adiponectin was lower (P < 0.001) in nondippers than in dippers, whereas no difference was found in regional fat, liver enzymes, and other metabolic parameters. At multivariate analysis, factors independently associated with nondipping were insulin (P < 0.05) and adiponectin (P < 0.01) with the homeostasis model of assessment index being of borderline significance.
Conclusion: In the absence of major risk factors for the development of NAFLD, a high prevalence of liver steatosis was associated with insulin resistance and low adiponectin levels in essential hypertensive patients with a nondipping profile.
aDepartment of Medical and Surgical Sciences, Italy
bDepartment of Statistical Sciences, Italy
cDepartment of Neurosciences, Biostatistical Section, University of Padova, Padua, Italy
dClinica Medica, Department of Experimental and Clinical Pathology and Medicine, University of Udine, Udine, Italy
eDepartment of Clinical Medicine and Neurology, University of Trieste, Trieste, Italy
Received 16 January, 2008
Revised 16 May, 2008
Accepted 24 June, 2008
Correspondence to Francesco Fallo, MD, Department of Medical and Surgical Sciences, Clinica Medica 3, University of Padova, Via Ospedale 105, 35128 Padua, Italy Tel: +39 049 8218747; fax: +39 049 8213332; e-mail: email@example.com