Towards a molecular understanding of adaptive thermogenesis

被引:1293
作者
Lowell, BB
Spiegelman, BM
机构
[1] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA
[2] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA
关键词
D O I
10.1038/35007527
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Obesity results when energy In lake exceeds energy expenditure. Naturally occurring genetic mutations, as well as ablative lesions, have shown that the brain regulates both aspects of energy balance and that abnormalities in energy expenditure contribute to the development of obesity. Energy can be expended by performing work or producing heat (thermogenesis). Adaptive thermogenesis, or the regulated production of heat, is influenced by environmental temperature and diet. Mitochondria, the organelles that convert food to carbon dioxide, water and ATP are fundamental in mediating effects on energy dissipation. Recently there have been significant advances in understanding the molecular regulation of energy expenditure in mitochondria and the mechanisms of transcriptional control of mitochondrial genes. Here we explore these developments in relation to classical physiological views of adaptive thermogenesis.
引用
收藏
页码:652 / 660
页数:9
相关论文
共 93 条
  • [1] Role of leptin in the neuroendocrine response to fasting
    Ahima, RS
    Prabakaran, D
    Mantzoros, C
    Qu, DQ
    Lowell, B
    MaratosFlier, E
    Flier, JS
    [J]. NATURE, 1996, 382 (6588) : 250 - 252
  • [2] Resting energy expenditure is sensitive to small dose changes in patients on chronic thyroid hormone replacement
    AlAdsani, H
    Hoffer, LJ
    Silva, JE
    [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1997, 82 (04) : 1118 - 1125
  • [3] Enhanced thermogenesis during recovery from diet-induced weight gain in the rat
    Almeida, NG
    Levitsky, DA
    Strupp, B
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 1996, 271 (05) : R1380 - R1387
  • [4] ATYPICAL BETA-ADRENOCEPTOR ON BROWN ADIPOCYTES AS TARGET FOR ANTI-OBESITY DRUGS
    ARCH, JRS
    AINSWORTH, AT
    CAWTHORNE, MA
    PIERCY, V
    SENNITT, MV
    THODY, VE
    WILSON, C
    WILSON, S
    [J]. NATURE, 1984, 309 (5964) : 163 - 165
  • [5] Up-regulation of UCP-2 gene expression by PPAR agonists in preadipose and adipose cells
    Aubert, J
    Champigny, O
    SaintMarc, P
    Negrel, R
    Collins, S
    Ricquier, D
    Ailhaud, G
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1997, 238 (02) : 606 - 611
  • [6] REGULATION OF OXIDATIVE-PHOSPHORYLATION IN THE MAMMALIAN-CELL
    BALABAN, RS
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 258 (03): : C377 - C389
  • [7] Characterization of the 5′-flanking and 5′-untranslated regions of the cyclic adenosine 3′,5′-monophosphate-responsive human type 2 iodothyronine deiodinase gene
    Bartha, T
    Kim, SW
    Salvatore, D
    Gereben, B
    Tu, HM
    Harney, JW
    Rudas, P
    Larsen, PR
    [J]. ENDOCRINOLOGY, 2000, 141 (01) : 229 - 237
  • [8] Blaxter K.L., 1989, Energy Metabolism in Animals and Man
  • [9] BLOCK BA, 1994, ANNU REV PHYSIOL, V56, P535
  • [10] Role of the β3-adrenergic receptor and/or a putative β4-adrenergic receptor on the expression of uncoupling proteins and peroxisome proliferator-activated receptor-γ coactivator-1
    Boss, O
    Bachman, E
    Vidal-Puig, A
    Zhang, CY
    Peroni, O
    Lowell, BB
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1999, 261 (03) : 870 - 876