Allometric scaling of metabolic rate from molecules and mitochondria to cells and mammals

被引:481
作者
West, GB
Woodruff, WH
Brown, JH
机构
[1] Los Alamos Natl Lab, Los Alamos, NM 87545 USA
[2] Santa Fe Inst, Santa Fe, NM 87501 USA
[3] Univ New Mexico, Dept Biol, Albuquerque, NM 87131 USA
关键词
D O I
10.1073/pnas.012579799
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
The fact that metabolic rate scales as the three-quarter power of body mass (M) in unicellular, as well as multicellular, organisms suggests that the same principles of biological design operate at multiple levels of organization. We use the framework of a general model of fractal-like distribution networks together with data on energy transformation in mammals to analyze and predict allometric scaling of aerobic metabolism over a remarkable 27 orders of magnitude in mass encompassing four levels of organization: individual organisms, single cells, intact mitochondria, and enzyme molecules. We show that, whereas rates of cellular metabolism in vivo scale as M-1/4, rates for cells in culture converge to a single predicted value for all mammals regardless of size. Furthermore, a single three-quarter power allometric scaling law characterizes the basal metabolic rates of isolated mammalian cells, mitochondria, and molecules of the respiratory complex; this overlaps with and is indistinguishable from the scaling relationship for unicellular organisms. This observation suggests that aerobic energy transformation at all levels of biological organization is limited by the transport of materials through hierarchical fractal-like networks with the properties specified by the model. We show how the mass of the smallest mammal can be calculated (approximate to1 g), and the observed numbers and densities of mitochondria and respiratory complexes in mammalian cells can be understood. Extending theoretical and empirical analyses of scaling to suborganismal levels potentially has important implications for cellular structure and function as well as for the metabolic basis of aging.
引用
收藏
页码:2473 / 2478
页数:6
相关论文
共 34 条
[1]   UNIVERSAL BIOLOGICAL SCALING AND MORTALITY [J].
AZBEL, MY .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (26) :12453-12457
[2]   OXYGEN ACTIVATION AND THE CONSERVATION OF ENERGY IN CELL RESPIRATION [J].
BABCOCK, GT ;
WIKSTROM, M .
NATURE, 1992, 356 (6367) :301-309
[3]   LOW MITOCHONDRIAL FREE-RADICAL PRODUCTION PER UNIT O-2 CONSUMPTION CAN EXPLAIN THE SIMULTANEOUS PRESENCE OF HIGH LONGEVITY AND HIGH AEROBIC METABOLIC-RATE IN BIRDS [J].
BARJA, G ;
CADENAS, S ;
ROJAS, C ;
PEREZCAMPO, R ;
LOPEZTORRES, M .
FREE RADICAL RESEARCH, 1994, 21 (05) :317-327
[4]   Dependence of energy metabolism on the density of cells in culture [J].
Bereiter-Hahn, J ;
Münnich, A ;
Woiteneck, P .
CELL STRUCTURE AND FUNCTION, 1998, 23 (02) :85-93
[5]  
BIAGLOW JE, 1984, ADV EXP MED BIOL, V180, P323
[6]   PROLIFERATION-ASSOCIATED OXYGEN-CONSUMPTION AND MORPHOLOGY OF TUMOR-CELLS IN MONOLAYER AND SPHEROID CULTURE [J].
BREDELGEISSLER, A ;
KARBACH, U ;
WALENTA, S ;
VOLLRATH, L ;
MUELLERKLIESER, W .
JOURNAL OF CELLULAR PHYSIOLOGY, 1992, 153 (01) :44-52
[7]   Complex I deficiency is associated with 3243G:C mitochondrial DNA in osteosarcoma cell cybrids [J].
Dunbar, DR ;
Moonie, PA ;
Zeviani, M ;
Holt, IJ .
HUMAN MOLECULAR GENETICS, 1996, 5 (01) :123-129
[8]  
ECONOMOS AC, 1979, GERONTOLOGY, V26, P90
[9]   RESPIRATION OF MITOCHONDRIA ISOLATED FROM DIFFERENTIATED AND UNDIFFERENTIATED HT29 COLON CANCER-CELLS IN THE PRESENCE OF VARIOUS SUBSTRATES AND ADP GENERATING SYSTEMS [J].
GAUTHIER, T ;
DENISPOUXVIEL, C ;
MURAT, JC .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY, 1990, 22 (04) :411-417
[10]   Biochemical evidence for nuclear gene involvement phenotype of non-syndromic deafness associated with mitochondrial 12S rRNA mutation [J].
Guan, MX ;
FischelGhodsian, N ;
Attardi, G .
HUMAN MOLECULAR GENETICS, 1996, 5 (07) :963-971