Obesity is a major risk factor for the development of type 2 diabetes through the induction of insulin resistance. To understand the mechanisms driving obesity-associated insulin resistance, it is pertinent to characterise the cellular events preceding insulin resistance in adipocytes.

Hansson and colleagues describe the early changes associated with expansion of adipose cell volume and number following 14 days of high-fat feeding in mice. Their findings point towards autophagy as one of the earliest cellular processes that is perturbed in response to short term high-fat feeding. There was also progressive deterioration of insulin signalling, but interestingly this did not impact glucose uptake.

With respect to the longer term outcomes of their findings, the authors proposed two alternatives: either cellular insulin resistance will develop given enough time, or the observed increase in autophagic activity serves a compensatory protective function to maintain adipocyte function, thus preserving systemic glucose homeostasis. Longer term follow up studies will be key in answering these important questions.

Read the full article in Journal of Molecular Endocrinology doi:10.1530/JME-170195