Editorials

Leptin in obesity

BMJ 1996; 313 doi: http://dx.doi.org/10.1136/bmj.313.7063.953 (Published 19 October 1996) Cite this as: BMJ 1996;313:953
  1. Thorkild Ia Sorensen, Professor of clinical epidemiology,
  2. Soren M Echwald, Research fellow,
  3. Jens-Christian Holm, Research fellow
  1. Danish Epidemiology Science Center, Institute of Preventive Medicine, Copenhagen University Hospital, Denmark
  2. Hagedorn Research Institute, Gentofte, Denmark
  3. Department of Pediatrics Glostrup University Hospital Glostrup, Denmark

    Tells the brain how much fat there is, but in obese people the message may not get through

    Obesity runs in families, mainly due to genetic factors.1 Several different mendelian inherited, monogenic forms of obesity exist in rodents, but they are rare in humans.1 Analysis of the distribution of fatness in families suggests that a few major genes may act on a polygenic and environmental background, but it remains unclear which genes are involved.1

    The identification and sequencing of the mouse obese (ob) gene by Friedman's group in 19942 opened important new avenues in obesity research and have already led to overwhelming research activity.3 In homozygous ob/ob mice, the mutation of the ob gene results in increased food intake, reduced energy expenditure, elevated insulin and cortisol levels, and subsequently, in massive obesity and non-insulin dependent diabetes mellitus.2 The ob gene encodes a protein, leptin, which is produced only in fat cells and secreted into the blood. There are two different strains of ob/ob mice: one with a mutation that establishes a stop codon within the ob gene, resulting in the production of a truncated, inactive protein; the other with a mutation that produces no protein at all.2 Administration of leptin corrects the multiple metabolic disturbances.4

    The finding of a human homologue of …

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