The long isoform uncoupling protein-3 (UCP3L) in human energy homeostasis

被引：0

作者：

WK Chung

A Luke

RS Cooper

C Rotini

A Vidal-Puig

M Rosenbaum

D Gordon

SM Leal

S Caprio

R Goldsmith

AL Andreu

C Bruno

S DiMauro

M Heo

WL Lowe

BB Lowell

DB Allison

RL Leibel

机构：

[1] Columbia University,Departments of Pediatrics and Medicine, Division of Molecular Genetics

[2] College of Physicians and Surgeons,Department of Preventive Medicine and Epidemiology

[3] Naomi Berrie Diabetes Center,Division of Endocrinology

[4] Russ Berrie Medical Science Pavilion,Division of Pediatric Endocrinology

[5] Loyola University Medical Center,Department of Medicine

[6] Beth Israel-Deaconess Medical Center,undefined

[7] The Rockefeller University,undefined

[8] Yale University School of Medicine,undefined

[9] St Luke’s / Roosevelt Hospital Center,undefined

[10] Obesity Research Center,undefined

[11] Columbia University College of Physicians and Surgeons,undefined

[12] Northwestern University School of Medicine,undefined

[13] Columbia University College of Physicians & Surgeons,undefined

[14] H. Houston Merritt Clinical Research Centre for Muscular Dystrophy and Related Diseases,undefined

来源：

International Journal of Obesity | 1999年 / 23卷

关键词：

obesity; diabetes; skeletal muscle; thermogenesis;

D O I：

暂无

中图分类号：

学科分类号：

摘要：

The biological role(s) proposed for UCP3 in energy homeostasis have been based primarily upon amino acid sequence homology to UCP1. Spontaneous mutations of UCP3 have been described in humans, but not in rodents. The functional consequences—or lack thereof—of these mutations in humans will be of great importance in elucidating the biology of this protein. The results of two such studies are summarized here.

引用

页码：S49 / S50

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