Insulin Resistance and Beta Cell Function in Hepatogenous Diabetes

The present study aimed to examine the change in beta cell function and insulin resistance (IR) over 6 months in patients with liver cirrhosis (LC) and hepatogenous diabetes (HD) and to assess their correlation with liver disease severity.

One hundred and seventy-three patients with LC without a prior history/risk factors of type 2 diabetes mellitus and with non-diabetic fasting blood glucose and glycated haemoglobin were subjected to a 75-g oral glucose tolerance test (OGTT). Those with 2-h plasma glucose ≥140 mg/dl were categorised as having HD. Plasma insulin and glucose were analysed during OGTT. Indices for IR and beta cell function, such as Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), oral glucose sensitivity index - 3 h (OGIS-3h) and insulinogenic index (IGI) were examined at baseline and repeated after a 6-month follow-up.

HD was detected in 65.8% (114/173) of the study cohort. Eighty-nine patients were recruited to the study, and 40 were available for follow-up. The majority (89.8%) were males with a mean body mass index of 23 ± 4.1 kg/m². Alcohol was the most common cause of LC (76.4%), and most (84.3%) belonged to Child-Turcot-Pugh (CTP) classes B and C. Plasma fasting insulin and HOMA-IR values were significantly higher in higher CTP classes and worsened at the 6-month follow-up. Peripheral insulin sensitivity measured by OGIS-3h was significantly worse in patients with a worse Model for End-Stage Liver Disease value at baseline but did not change during follow-up. Beta cell function measured by IGI was neither different across CTP classes at baseline nor changed during follow-up.

Peripheral hyperinsulinaemia and IR, rather than beta cell dysfunction, predominate in patients with LC and glucose abnormalities on OGTT and worsen with worsening liver dysfunction.