Author: ["Fredrik Lönnqvist","Peter Arner","Louise Nordfors","Martin Schalling"]
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Abstract
Obesity is accompanied by complications such as hypertension, non–insulin–dependent diabetes mellitus and atherosclerosis, which in turn cause ischaemic heart disease, stroke and premature death1–3. The underlying mechanisms behind imbalance in energy intake and energy expenditure that lead to obesity are still controversial. In most populations, obesity is more common among women than men and is a multifactorial phenotype, which may result from a complex network of genetic and nongenetic factors. The relative importance of genetic factors for obesity is under debate4–7. Genome searches using polymorphic markers in inbred mice with phenotypes that result in extreme obesity8,9 and studies of human candidate genes are being performed in an attempt to identify genes that contribute to obesity. There is evidence that body weight is physiologically regulated4,10,11 and it has been postulated that the storage of fat may provide signals to the brain that the body is obese, which in turn may make the subject eat less and burn more fuel12,13. One of the molecules that may be involved in such signalling is the obese (ob) gene product. Mutations in ob result in profound obesity and type II diabetes in mice14,15. The mouse ob gene and its human homologue have been cloned and sequenced8. The gene is expressed in adipose tissue and the product has features of a secreted protein. We have investigated human ob expression in subcutaneous and omental adipose tissue obtained from non–obese and massively obese subjects using in situ hybridization histochemistry and report on overexpression in obese people.Cite this article
Lönnqvist, F., Arner, P., Nordfors, L. et al. Overexpression of the obese (ob) gene in adipose tissue of human obese subjects. Nat Med 1, 950–953 (1995). https://doi.org/10.1038/nm0995-950 