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Role of mitochondrial uncoupling pro...

Sun, Xiaocun.

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Role of mitochondrial uncoupling protein 2 (UCP2) in modulation of adiposity.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Role of mitochondrial uncoupling protein 2 (UCP2) in modulation of adiposity./
Author:	Sun, Xiaocun.
Description:	331 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-07, Section: B, page: 3390.
Contained By:	Dissertation Abstracts International65-07B.
Subject:	Health Sciences, Nutrition. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3141826
ISBN:	0496889060

Role of mitochondrial uncoupling protein 2 (UCP2) in modulation of adiposity.
Sun, Xiaocun.

Role of mitochondrial uncoupling protein 2 (UCP2) in modulation of adiposity. - 331 p.

Source: Dissertation Abstracts International, Volume: 65-07, Section: B, page: 3390.

Thesis (Ph.D.)--The University of Tennessee, 2004.

Obesity is a disorder of energy balance in which energy intake exceeds energy expenditure. Methods to control obesity through limiting energy intake have had limited success, and it is widely recognized that energy expenditure must also be increased if long-term weight loss is to be achieved. Uncoupling proteins (UCPs) are a family of integral membrane proteins of mitochondrial inner membrane, where they uncouple the process of mitochondrial respiration and decrease the metabolic efficiency of the organism. Unlike the other UCP family members, UCP2 is ubiquitously expressed, with the highest level in white adipose tissue. Stimulation of mitochondrial uncoupling in adipocytes in vitro demonstrates a direct inhibitory effect on lipogenesis and suppression on lipolysis, indicating a potential role of UCP2 in regulation of adiposity.

ISBN: 0496889060Subjects--Topical Terms:

1017801
Health Sciences, Nutrition.

Role of mitochondrial uncoupling protein 2 (UCP2) in modulation of adiposity.
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020 $a 0496889060
035 $a (UnM)AAI3141826
035 $a AAI3141826
040 $a UnM $c UnM
100 1 $a Sun, Xiaocun. $3 1901892
245 1 0 $a Role of mitochondrial uncoupling protein 2 (UCP2) in modulation of adiposity.
300 $a 331 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-07, Section: B, page: 3390.
500 $a Major Professor: Michael B. Zemel.
502 $a Thesis (Ph.D.)--The University of Tennessee, 2004.
520 $a Obesity is a disorder of energy balance in which energy intake exceeds energy expenditure. Methods to control obesity through limiting energy intake have had limited success, and it is widely recognized that energy expenditure must also be increased if long-term weight loss is to be achieved. Uncoupling proteins (UCPs) are a family of integral membrane proteins of mitochondrial inner membrane, where they uncouple the process of mitochondrial respiration and decrease the metabolic efficiency of the organism. Unlike the other UCP family members, UCP2 is ubiquitously expressed, with the highest level in white adipose tissue. Stimulation of mitochondrial uncoupling in adipocytes in vitro demonstrates a direct inhibitory effect on lipogenesis and suppression on lipolysis, indicating a potential role of UCP2 in regulation of adiposity.
520 $a Previous studies demonstrate that 1alpha, 25-dihydroxyvitamin D 3 (1alpha, 25-(OH)2-D3) plays a genomic role in regulating adipocyte UCP2 expression levels, indicating that the regulation of UCP2 and the resulting increased core temperature may contribute to increased rates of energy dissipation. Accordingly, the suppression of 1alpha, 25-(OH) 2-D3 by increasing dietary calcium attenuates adiposity by decreasing triglyceride accumulation in the adipocytes: increasing dietary calcium results in a net reduction in fat mass in the absence of caloric restriction, a marked augmentation of body weight and fat loss during energy restriction, and an inhibition of weight and fat regain during energy repletion.
520 $a Increasing dietary calcium also results in a deficit cells for lipid esterification. Physiological doses of 1alpha, 25-(OH)2-D 3 inhibit apoptosis in differentiated 3T3-L1 adipocytes, and the suppression of 1alpha, 25-(OH)2-D3 in vivo by increasing dietary calcium stimulates adipocyte apoptosis in refeeding following energy restriction in aP2 transgenic mice, indicating that the stimulation of adipocyte apoptosis contributes to adiposity reduction after high calcium diet administration. UCP2 plays a direct role in modulating adipocyte apoptosis by inducing mitochondrial potential collapse and inhibiting ATP production.
520 $a In summary, dietary calcium exerts anti-obesity effects in aP2 transgenic mice under conditions of varying nutrient status. These anti-obesity effects of dietary calcium are attributable to the up-regulation of UCP2, which stimulates energy expenditure, fat utilization and adipocyte apoptosis in white adipose tissue.
590 $a School code: 0226.
650 4 $a Health Sciences, Nutrition. $3 1017801
650 4 $a Health Sciences, Pathology. $3 1017854
650 4 $a Biology, Microbiology. $3 1017734
690 $a 0570
690 $a 0571
690 $a 0410
710 2 0 $a The University of Tennessee. $3 1022026
773 0 $t Dissertation Abstracts International $g 65-07B.
790 1 0 $a Zemel, Michael B., $e advisor
790 $a 0226
791 $a Ph.D.
792 $a 2004
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3141826