High levels of serum dihomo-γ-linolenic acid are associated with non-alcoholic fatty liver disease in type 2 diabetic patients.

Abstract

An elevated level of saturated fatty acids (SFAs) can cause non-alcoholic fatty liver disease (NAFLD). While n-3 polyunsaturated fatty acids (PUFAs) were shown to improve NAFLD, the effects of n-6 PUFAs in the liver have not been fully elucidated. We examined the association between NAFLD and n-6 PUFAs, particularly dihomo-γ-linolenic acid (DGLA), in patients with type 2 diabetes. A total of 60 patients with type 2 diabetes were included in the study. Patients were categorized into the NAFLD group (n = 35) and non-NAFLD group (n = 25) based on the presence of fatty liver as determined by abdominal ultrasound. We demonstrated that the levels of serum SFAs, specifically palmitic acid and stearic acid, and the levels of n-6 PUFAs, specifically DGLA, and arachidonic acid (AA), were significantly higher in the NAFLD group. The serum palmitic acid, stearic acid, DGLA and AA levels were positively correlated with liver enzyme gamma-glutamyl transpeptidase (GGT). We further demonstrated by multivariate analysis that serum DGLA was a predictor of NAFLD. The serum DGLA level was negatively correlated with blood adiponectin and was positively correlated with blood leptin, high-sensitivity CRP, C-peptide index, and triglyceride-glucose index. Furthermore, delta-5-desaturase (D5D), the AA (product)/DGLA (precursor) ratio calculated from the product-to-precursor ratio of fatty acids, was significantly lower in the NAFLD group. These findings suggest that high serum DGLA levels in NAFLD group may be due to an excessive intake of n-6 PUFAs and changes in desaturase in the human body. High serum DGLA levels may also be associated with insulin resistance and inflammatory factors.