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Obese adipose tissue is known to have higher basal rates of lipolysis than lean adipose tissue. This chronic outflow of lipids leads to the ectopic deposition of lipids into non-adipose, insulin-sensitive tissues such as the heart, liver, and skeletal muscle. This process, known as lipotoxicty, promotes the development of insulin resistance in these tissues. Therefor developing ways to control lipolysis in obese individuals is a useful intervention that would help curtail the development of type II diabetes. Adenosine, a nucleoside released from cells during metabolic stress or inflammation, may play an important role in this process. Our lab has discovered that adipocytes tightly regulate Adenosine receptor 2B (A2BR) expression during the transition from the postabsorptive (fasting) to postprandial (fed) state. QPCR data has confirmed that A2BR levels increase postprandially and decrease postabsorptively in adipose tissue, but not other insulin-sensitive organs. Administration of an A2BR agonist in mice yields a large lipolytic response in the postprandial, but not postabsorptive state. Genetic deletion of A2BR from adipose tissue confirms that this lipolytic response depends on A2BR signaling in the individual adipocytes. Importantly we have also shown that A2BR levels in obese mouse adipose tissue are constitutively high regardless of nutritional state, suggesting these cells are primed for lipolytic stimulation. Therefore, pharmacological antagonists of A2BR could reduce basal lipolysis in obese individuals and in turn improve whole body insulin sensitivity. 5T32GM139787-03 5R01GM136900-04. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Daniel Lank (Wed,) studied this question.