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Effects of sex steroids and diet on ...

Shultz, Jennifer Marie.

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Effects of sex steroids and diet on adipose distribution and cardiovascular disease risk factors.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Effects of sex steroids and diet on adipose distribution and cardiovascular disease risk factors./
作者:	Shultz, Jennifer Marie.
面頁冊數:	141 p.
附註:	Chair: Michael E. Rosenfeld.
Contained By:	Dissertation Abstracts International63-01B.
標題:	Health Sciences, Medicine and Surgery. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3041057
ISBN:	0493544887

Effects of sex steroids and diet on adipose distribution and cardiovascular disease risk factors.
Shultz, Jennifer Marie.

Effects of sex steroids and diet on adipose distribution and cardiovascular disease risk factors. - 141 p.

Chair: Michael E. Rosenfeld.

Thesis (Ph.D.)--University of Washington, 2002.

Cardiovascular disease risk increases in women after menopause, coincident with increases in low-density lipoprotein cholesterol levels (1). While loss of estrogen results in lower LDL and higher HDL levels, estrogen loss also favors visceral adipose deposition (2). My aim was to investigate the potential of hormone replacement therapy in ameliorating many of these cardiovascular disease risk factors, and to determine how diet may influence these interactions.

ISBN: 0493544887Subjects--Topical Terms:

1017756
Health Sciences, Medicine and Surgery.

Effects of sex steroids and diet on adipose distribution and cardiovascular disease risk factors.
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245 1 0 $a Effects of sex steroids and diet on adipose distribution and cardiovascular disease risk factors.
300 $a 141 p.
500 $a Chair: Michael E. Rosenfeld.
500 $a Source: Dissertation Abstracts International, Volume: 63-01, Section: B, page: 0187.
502 $a Thesis (Ph.D.)--University of Washington, 2002.
520 $a Cardiovascular disease risk increases in women after menopause, coincident with increases in low-density lipoprotein cholesterol levels (1). While loss of estrogen results in lower LDL and higher HDL levels, estrogen loss also favors visceral adipose deposition (2). My aim was to investigate the potential of hormone replacement therapy in ameliorating many of these cardiovascular disease risk factors, and to determine how diet may influence these interactions.
520 $a To investigate the effects of estrogen and estrogen/progestin combinations on the development of atherosclerosis, apolipoprotein E knockout (apoE KO) mice received either a sham operation + placebo pellet or a bilateral ovariectomy + 1 of 9 combination estrogen/progestin hormone pellets. After 8 weeks of treatment, all hormone treatment groups had significantly smaller lesion sizes than untreated groups. Hormone treatment also suppressed ovariectomy-induced gain in adipose depot mass.
520 $a Next, I investigated whether ovariectomy-induced obesity, in conjunction with a high fat, high sucrose (HFHS) diet, could be ameliorated by HRT. First, I determined that the C57BL/6J mouse was an appropriate model for diet-induced, visceral obesity. C57BL/6J mice were then sham-operated or ovariectomized and administered placebo, estrogen alone, or combined hormone replacement therapy. Chow-fed animals administered estrogen had a greater percentage of subcutaneous adipose versus visceral adipose than untreated animals. HFHS-fed animals administered combined hormone therapy had significantly greater body weight gain and greater adipose depot weights than sham-operated and estrogen-treated animals, and had less percentage of subcutaneous adipose than estrogen-treated animals.
520 $a Finally, I determined whether obesity could be ameliorated by the estrogen-like soy isoflavone genistein. An additional group of sham-operated and ovariectomized animals received dietary genistein in lieu of the hormone pellets. Significant differences were only seen in animals fed the HFHS diet: genistein treatment resulted in less body weight change and less adipose depot mass compared to groups that did not receive genistein. In summary, genetic and dietary differences influenced the cardioprotective effects of sex hormones in this study. Future research needs to address the mechanisms by which genistein suppresses adipose gain, and needs to examine whether genistein inhibits lesion development in these mice.
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