British Journal of Nutrition

Horizons in Nutritional Science

Lactate and the GPR81 receptor in metabolic regulation: implications for adipose tissue function and fatty acid utilisation by muscle during exercise

Kieron Rooneya1a2 and Paul Trayhurna3a4 c1

a1 Exercise, Health and Performance, Faculty of Health Sciences, University of Sydney, East Street, Lidcombe NSW 2141, Australia

a2 Faculty of Medicine, Boden Institute, University of Sydney, NSW, Australia

a3 Clore Laboratory, University of Buckingham, Hunter Street, Buckingham MK18 1EG, UK

a4 Obesity Biology Research Unit, Institute of Ageing and Chronic Diseases, University of Liverpool, Liverpool L69 3GA, UK

Abstract

Lactate is increasingly recognised to be more than a simple end product of anaerobic glycolysis. Skeletal muscle and white adipose tissue are considered to be the main sites of lactate production and release. Recent studies have demonstrated that there is a specific G-protein coupled receptor for lactate, GPR81, which is expressed primarily in adipose tissue, and also in muscle. Lactate inhibits lipolysis in adipose tissue by mediating, through GPR81, the anti-lipolytic action of insulin. A high proportion (50 % or more) of the glucose utilised by white adipose tissue is converted to lactate and lactate production by the tissue increases markedly in obesity; this is likely to reflect a switch towards anaerobic metabolism with the development of hypoxia in the tissue. During exercise, there is a shift in fuel utilisation by muscle from lipid to carbohydrate, but this does not appear to be a result of the inhibition of lipolysis in the main adipose tissue depots by muscle-derived lactate. It is suggested instead that a putative autocrine lactate loop in myocytes may regulate fuel utilisation by muscle during exercise, operating via a muscle GPR81 receptor. In addition to being an important substrate, lactate is a key signal in metabolic regulation.

(Received July 21 2011)

(Accepted July 21 2011)

(Online publication September 09 2011)

Correspondence:

c1 Corresponding author: Professor P. Trayhurn, email paul.trayhurn@buckingham.ac.uk

Footnotes

Abbreviations: cAMP, cyclic AMP; PKA, protein kinase A

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