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A new study has uncovered the role of ACC1 enzyme in the regulation of glucagon secretion for the first time. This raises the prospect of a potential new therapeutic target in the context of type 2 diabetes and metabolic disorders characterised by hyperglycaemia.

Side by side pancreatic islets demonstrating prevalence of glucagon in normal animals and heavily reduced glucagon when ACC1 is knocked out
Pancreatic islets stained for insulin (red) and glucagon (green) - glucagon is more prevalent in left hand islet (control animals) vs the right hand islet (KO animals) where ACC1 is knocked out

The study was carried out between Department of Physiology, Anatomy & Genetics (DPAG), Oxford Centre for Diabetes, Endocrinology and Metabolism (Radcliffe Department of Medicine), and the University of Dundee, performed as part of the Oxford Novo Nordisk Fellowship Programme, with experimental work also performed at the Novo Nordisk Research Centre Oxford.

Led by Dr Anna Veprik (Radcliffe Department of Medicine) and Novo Nordisk project leaders Associate Professor Heidi de Wet (DPAG) and Dr James Cantley (University of Dundee), the study uncovered the essential role of the enzyme Acetyl-CoA-Carboxylase 1 (ACC1) in the function of pancreatic alpha cells and glucagon secretion. After an influx of nutrients enters the body following feeding, ACC1 is the first step in pathway called ‘de-novo lipogenesis’, which converts the available glucose from the nutrients into lipids to be stored for future use. In contrast to the hepatocytes of the liver, alpha cells in the pancreas are not known for substantial lipid storage. The research shows that ACC1 is acting as a central ‘nutrient availability sensor’ for the alpha cells, which is used to calculate the right amount of glucagon that needs to be released.

Read the full story on the DPAG website

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