White adipose tissue plays a critical role in whole body energy homeostasis, by storing energy in the form of triglycerides and producing circulating factors that regulate appetite and systemic insulin sensitivity. The role of AMPK remains far less studied in adipocytes than in other metabolic tissues such as muscle and liver. However, the former view of AMPK as being anti-lipolytic and an inhibitor of insulin-induced glucose uptake, has become more diverse as a consequence of recent studies employing novel AMPK activators, which bind to the Allosteric Drug and Metabolite (ADaM) site on AMPKβ. These studies demonstrate that AMPK activation is not always anti-lipolytic and that effects of AMPK activation on glucose uptake can be AMPK-independent. Given the established role of AMPK in the regulation of acetyl-CoA carboxylase (ACC), surprisingly few studies have addressed the effect of AMPK activation on fatty acid (FA) synthesis in adipocytes. Although FA synthesis is quantitatively a relatively minor pathway in these cells, it has been shown to correlate positively with the degree of insulin sensitivity in obese individuals and is important for the production of FA-derived signalling molecules. This talk will describe ongoing work and future directions related to the role of AMPK in the control of FA synthesis , with a focus on effects of ADaMs activators in different adipocyte models. I will also report on our work regarding relative levels of AMPKβ1 and -2 isoforms in adipocytes, since this is relevant for the interpretation and prediction of effects generated by ADaMs activators with different AMPKβ preference.
Olga Göransson, Lund University Diabetes Centre, Department of Experimental Medical Science, Medical faculty, Lund University, Sweden