14 research outputs found
Body mass index in mid-life women: relative influence of menopause, hormone use, and ethnicity
The Relationship between Endogenous Androgens and Body Fat Distribution in Early and Late Postmenopausal Women
Relationships of Resting Energy Expenditure with Body Fat Distribution and Abdominal Fatness in Japanese Population.
Changes in body fat distribution through menopause increase blood pressure independently of total body fat in middle-aged women: the Korean National Health and Nutrition Examination Survey 2007–2010
Composição corpórea, distribuição de gordura e metabolismo de repouso em mulheres histerectomizadas no climatério: há diferenças de acordo com a forma da administração do estrogênio?
Neuropeptide Y mediates the short-term hypometabolic effect of estrogen deficiency in mice
Estrogen deficiency causes central leptin insensitivity and increased hypothalamic neuropeptide Y
OBJECTIVE: Altered fat distribution is a consequence of menopause, but the mechanisms responsible are unknown. Estrogen insufficiency in humans can be modeled using ovariectomized rats. We have shown that increased adiposity in these rats is due to reduced physical activity and transient hyperphagia, and can be reversed with 17β-estradiol treatment. The aims of this study were to examine whether this altered energy balance is associated with circulating leptin insufficiency, central leptin insensitivity, decreased hypothalamic leptin receptor (Ob-Rb) expression, and/or increased hypothalamic neuropeptide Y (NPY). METHODS: Plasma leptin levels, adipose tissue ob gene expression, energy balance responses to i.c.v. leptin, hypothalamic Ob-Rb expression and NPY concentration in five separate hypothalamic regions were measured in adult female rats after either ovariectomy or sham operations. RESULTS: Obesity was not associated with hypoleptinemia or decreased ob gene expression in ovariectomized rats; however, it was associated with insensitivity to central leptin administration. Food intake was less suppressed and spontaneous physical activity was less stimulated by leptin. This was not due to decreased hypothalamic Ob-Rb expression. NPY concentration in the paraventricular nucleus of the hypothalamus was elevated in the ovariectomized rats, consistent with leptin insensitivity; however this effect was transient and disappeared as body fat and leptin levels increased further and hyperphagia normalized. CONCLUSION: Impaired central leptin sensitivity and overproduction of NPY may contribute to excess fat accumulation caused by estrogen deficiency.DA Ainslie, MJ Morris, G Wittert, H Turnbull, J Proietto and AW Thorbur