Type 2 diabetes mellitus per se, is typically characterised by altered lipoprotein metabolism but it is not usually associated with severe hypertriglyceridaemia. We describe a case of a 41 year old obese woman who presented with severe and non-specific abdominal pain. Based on a HbA1c of 10.8%, minimal ketones and negative anti-GAD antibodies, she was diagnosed with type 2 diabetes mellitus. She was also found to have hepatomegaly (liver span 20 cm) with fatty infiltration, a splenic infarct and severe hypertriglyceridaemia (cholesterol 32 mmol/L and triglyceride 206 mmol/L). Her severe hypertrigylceridaemia promptly resolved over a week with fasting, insulin and dextrose infusion and she was subsequently established on maintenance therapy with low fat diet, basal bolus subcutaneous insulin, fish oil and atorvastatin. On day 10 she was discharged with cholesterol and triglyceride levels of 19 and 20 mmol/L respectively. Two months after diagnosis her cholesterol was 3.2 mmol/L, triglycerides 0.9 mmol/L and her HDL was 1.2 mmol/L. At three months, her HbA1c was 6.6%. On re-imaging, her liver span had normalised to 13 cm and there was resolution of hepatic fatty infiltration.

Insulin resistance is known to be associated with elevated intracellular fatty acid levels and fatty acid metabolites which in turn, has an inhibitory effect on pancreatic beta cell function which leads to a state of lipotoxicity and glucotoxicity. Superimposed on this, it is likely that this woman has an underlying predisposition to decreased lipoprotein lipase activity leading to reduced lipolytic activity and enhanced triglyceride levels fuelled by a high fat diet. This case demonstrates probable compound pathology in aspects of lipoprotein metabolism interlinked with insulin resistance and glucotoxicity.