The people who carried the adiponectin gene promoter -11377C/G (GG)/GPx-1 gene C594T (TT) had a high risk of NAFLD (ORNAFL = 7.2800; ORNASH = 41.2941; ORNAFHC = 363.9724), and statistical analysis suggested a positive association between -11377C/G (GG) and C594T (TT) in increasing the risk of NAFLD (γ2NAFL = 2.2071, γ4 NAFL = 2.0773; γ2 NASH = 2.1084; γ4NASH = 2.0543; γ2 NAFHC = 2.1387; γ4NAFHC = 2.0004).
MMP-9 activity is increased by adiponectin in primary human hepatocytes but even negatively correlates with serum adiponectin in a rodent model of non-alcoholic steatohepatitis.
Variations in adiponectin levels could be an indicator of disease progression since inflammatory infiltrates are commonly associated with nonalcoholic steatohepatitis (NASH) in morbidly obese patients.
Nitrotyrosine and adiponectin concentrations and vitamin A intakes independently predicted alanine aminotransferase concentrations in NAFLD patients and liver histology in a subgroup of 29 subjects with biopsy-proven nonalcoholic steatohepatitis.
These studies 1) definitively demonstrate the presence of severe peripheral and hepatic insulin resistance in the affected subjects; 2) describe a stereotyped pattern of partial lipodystrophy associated with all the features of the metabolic syndrome and nonalcoholic steatohepatitis; 3) document abnormalities in the in vivo function of remaining adipose tissue, including the inability of subcutaneous abdominal adipose tissue to trap and store free fatty acids postprandially and the presence of very low circulating levels of adiponectin; 4) document the presence of severe hyperinsulinemia in prepubertal carriers of the proline-467-leucine (P467L) PPAR-gamma mutation; 5) provide the first direct evidence of cellular resistance to PPAR-gamma agonists in mononuclear cells derived from the patients; and 6) report on the metabolic response to thiazolidinedione therapy in two affected subjects.