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논문 기본 정보
- 자료유형
- 학술대회자료
- 저자정보
- 저널정보
- 한국응용약물학회 한국응용약물학회 추계학술발표논문집 한국응용약물학회 2003년도 Annual Meeting of KSAP : International Symposium on Pharmaceutical and Biomedical Sciences on Obesity
- 발행연도
- 2003.1
- 수록면
- 15 - 23 (9page)
이용수
초록· 키워드
Interest in the regulation of body weight and the pathological physiology of obesity has been rekindled by the cloning of the obese(ob) gene and identification of its product, leptin, in 1994. The first publication appeared in Nature and is a milestone of obesity research. The remarkable metabolic effects of leptin in rodents are: a) inhibition of food intake, b) stimulation of energy expenditure, and c) reversal of obesity. These effects, though mostly desirable, have not been fully demonstrated in humans. The central action of leptin in the regulation of body weight includes two pathways in rodents: a) When the body weight increasing, more leptin is secreted from adipose tissue, which acts on hypothalamus, probably through a POMC or MSH pathway via M4 receptor, initiates a series of response to obesity, i.e. sympathetic tone increased, energy expenditure enhanced and food intake reduced. b) When body weight reduced, leptin concentration decreased with the shrinkage of fat mass, which may also act on the hypothalamus, probably through a NPY-Y5 receptor pathway. Then a cascade of response to hungry was induced, i.e. increase of parasympathetic tone and food intake, decrease of energy expenditure and body temperature, as well as shut-down of the reproductive function.
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