Obesity is a major risk factor for type 2 diabetes (T2D). Weight loss by low calorie diet can induce remission of T2D. However, this is challenging to achieve and maintain in the long-term due to weight regain.  Our research is centred on elucidating the mechanisms by which weight loss bring about remission of diabetes in order to develop novel therapies. Obesity also alters hepatic lipid export, leading to dyslipidaemia, a key pathophysiological feature associated with the metabolic syndrome.  One reason for this is increased de novo lipogenesis (DNL), a pathway whose flux is increased in fatty liver disease and T2D. We have previously demonstrated that hepatic DNL-derived fatty acids decrease after weight loss and remission of diabetes in humans and have more recently confirmed that we can replicate this in a polygenic mouse model of T2D. The lab’s primary focus is on the DNL pathway as a potential mechanism leading to elevated lipoprotein export, intrapancreatic fat deposition, loss of acinar cell mass, and beta cell dysfunction (collectively termed “pancreas lipotoxicity”).