Non-alcoholic fatty liver disease (NAFLD) has a high prevalence in type 2 diabetes mellitus (T2DM) patients, being one of the disorders with a relevant global burden. Cross-sectional studies have shown that patients with T2DM and NAFLD have a higher prevalence of liver fibrosis, compared with the general population. Patients with non-alcoholic steatohepatitis (NASH) and T2DM have an increased mortality and morbidity, therefore they generate substantial health care costs. NASH worsens chronic diabetes complications, and T2DM aggravate the NASH progression to fibrosis, cirrhosis, and even hepatocellular carcinoma (HCC). The objectives in NAFLD and NASH therapy are to reduce disease activity, to slow down progression of fibrosis, and to lower the risk factors. Unfortunately, there are no specific validated pharmacological therapies. Several trials have demonstrated that anti-diabetic agents such as thiazolidindiones, sodium-glucose co-transporter inhibitors, glucagon like peptide-1 receptor analogs, or dipeptidyl peptidase-4 inhibitors might have complimentary benefits for patients with NAFLD. Some of the effect on reducing steatosis and fibrosis is explained by the weight loss these treatments produce. A goal in standard care is developing screening tools, early and non-invasive diagnosis methods, studying the pleiotropic effects of drugs, together with newer therapeutic agents, which can target mutual pathogenic mechanisms for diabetes and liver disease.
Keywords: non-alcoholic fatty liver disease; non-alcoholic steatohepatitis; nutrition; therapeutic agents; type 2 diabetes mellitus.
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