The current study aimed to examine lipid abnormalities and liver steatosis in patients with HbA1c-defined prediabetes and type 2 diabetes in contrast to individuals with HbA1c-defined normoglycaemia.

The study included 91 participants with prediabetes according to HbA1c, ranging from 5.7 to 6.4% (39-46 mmol/mol), 50 newly diagnosed patients with HbA1c-defined type 2 diabetes (HbA1c ≥6.5% [≥48 mmol/mol]), and 67 controls with HbA1c lower than 5.7% (<39 mmol/mol). All participants underwent fasting blood samples for lipid profiles, fatty liver index (FLI), bioimpedance analysis, ultrasound scan of the liver, and BARD (body mass index, aspartate aminotransferase /alanine aminotransferase ratio, diabetes) score for evaluation of liver fibrosis.

Participants with prediabetes were typified by lower apolipoprotein AI and HDL cholesterol levels, higher blood pressure, triglycerides levels and apolipoprotein B/apolipoprotein AI ratio, higher FLI, increased prevalence of and more severe hepatic steatosis, similar BARD score, and higher total body fat mass, as compared to controls. Moreover, participants with prediabetes had similar blood pressure and apolipoprotein B/apolipoprotein AI ratio, similar FLI, decreased prevalence of and less severe hepatic steatosis, lower BARD score, increased percent fat and lower total body muscle mass, in contrast to participants with diabetes., Participants with diabetes exhibited lower apolipoprotein AI and HDL cholesterol levels, higher blood pressure and triglycerides levels, higher FLI, increased prevalence of and more severe hepatic steatosis, higher BARD score, and higher total body muscle mass when compared with controls.  HbA1c was found to be associated with various parameters such as BMI, HOMA-IR, triglycerides, HDL cholesterol, AST, and ALT.

Thus, the study concluded that abnormalities in lipid profile and liver steatosis are one of the main characteristics of HbA1c-defined prediabetes and type 2 diabetes, suggestive of a severe risk profile for cardiovascular and liver diseases.

Source: Nutr Metab Cardiovasc Dis. 2014 Jun;24(6):670-6.