Of fat mice and men: the rise of the adipokines

    1. Simon J Dunmore
    1. Diabetes and Metabolic Disease Research Group, Department of Biomedical Science and Physiology, School of Applied Sciences, Research Institute in Healthcare Science, University of Wolverhampton, Wolverhampton WV1 1LY, UK
    1. (Correspondence should be addressed to S J Dunmore; Email: s.dunmore{at}wlv.ac.uk)

    The inexorable rise in obesity around the planet, particularly in developed countries but increasingly in the developing world, is accompanied by a parallel rise in co-morbid metabolic diseases including type 2 diabetes and vascular disease. Obesity, defined by an excess of adipose tissue, has complex aetiological factors that vary considerably between individual cases and across ethnic groupings but primarily involve genetic (and indeed epigenetic – see Drong et al. (2012)), environmental and behavioural contributions. New obesity genes are being identified regularly and range from those causing monogenic obesity such as mutations in the Lep gene to those that make a small but significant contribution to polygenic obesity such as the TCF7L2 and FTO genes. The cloning by Zhang et al. (1994), of the ob or Lep gene in mice, which produces a single-gene obesity, led to the identification of leptin, the first hormone-like product of adipose tissue to be identified and arguably one of the first ‘adipokines’ to be identified. This discovery underlined the increasingly apparent fact that adipose tissue is not merely an inert store of triacylglycerols but a highly metabolically active …

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