作者: Fredrik Lönnqvist , Peter Arner , Louise Nordfors , Martin Schalling
DOI: 10.1038/NM0995-950
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摘要: Obesity is accompanied by complications such as hypertension, non–insulin–dependent diabetes mellitus and atherosclerosis, which in turn cause ischaemic heart disease, stroke premature death1–3. The underlying mechanisms behind imbalance energy intake expenditure that lead to obesity are still controversial. In most populations, more common among women than men a multifactorial phenotype, may result from complex network of genetic nongenetic factors. relative importance factors for under debate4–7. Genome searches using polymorphic markers inbred mice with phenotypes extreme obesity8,9 studies human candidate genes being performed an attempt identify contribute obesity. There evidence body weight physiologically regulated4,10,11 it has been postulated the storage fat provide signals brain obese, make subject eat less burn fuel12,13. One molecules be involved signalling obese (ob) gene product. Mutations ob profound type II mice14,15. mouse its homologue have cloned sequenced8. expressed adipose tissue product features secreted protein. We investigated expression subcutaneous omental obtained non–obese massively subjects situ hybridization histochemistry report on overexpression people.