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Centre for Diabetes and Metabolic Medicine, Institute of Cellular and Molecular Medicine, Queen Mary, University of London, 4 Newark Street, Whitechapel, London E1 2AT, UK
¹ Metabolic Research Laboratory, Oxford Centre for Diabetes, Endocrinology and Metabolism, Nuffield Department of Clinical Medicine, University of Oxford Churchill Hospital, Oxford, UK

(Requests for offprints should be addressed to M J Holness; Email: m.j.holness{at}qmul.ac.uk)

Peroxisome proliferator-activated receptor (PPAR) is a transcription factor that regulates enzymes involved in fatty acid (FA) utilisation. PPAR null mice have recently been demonstrated to have increased whole-body glucose turnover in vivo. This has been attributed to increased glucose uptake by adipose tissue, but the impact of PPAR deficiency on the characteristics of glucose handling by isolated adipocytes ex vivo is unknown. To determine directly the impact of PPAR deficiency on adipocyte glucose handling, thereby excluding any influence of humoral/neuronal factors, we examined total glucose metabolism as well as glucose disposition towards alternative fates in epididymal adipocytes isolated from wild-type and PPARnull mice. Total glucose metabolism (oxidation, incorporation into FA and glycerol moieties of triglyceride (TAG) and conversion to lactate) was measured under basal conditions (low glucose) and ‘stimulated lipogenic’ conditions (high glucose + insulin). Adipocytes from PPAR null mice had higher rates of glucose metabolism under both basal and stimulated lipogenic conditions, with increased glucose utilisation both for oxidation and entry into the synthesis of the FA and glycerol components of lipid. In particular, the capacity of adipocytes from PPAR-deficient mice to utilise glucose for synthesis of the glycerol backbone of TAG was greatly enhanced under stimulated (high glucose + insulin) conditions. The increased use of glucose for the glycerol moiety of adipocyte TAG may therefore contribute to, and provide explanation for, enhanced glucose turnover in PPAR null mice.