ich blick bei dem artikel nicht durch,nur scheints mir so als hättest du mir eine möglichkeit zur verschwendung unterschlagen,lol!und würg mich nicht,wenn ich das falsch aufgefasst hab(aber die gefahr is gering,das du mich erwürgen kannst mein ich,lol..)
kannst du den artikel in für einen laien verständliche worte fassen??
J Nutr 2000 Apr;130(4):711-4
Uncoupling protein homologs: emerging views of physiological function.
Adams SH
Department of Endocrinology, Genentech, Incorporated, South San Francisco, CA 94080, USA.
The widespread occurrence of excess weight and related diseases demands that efforts be made to understand energy expenditure from the gene to the whole animal. For some time, it has been understood that mitochondrial oxidation of fuels generates an electrochemical gradient via outward pumping of protons by the electron transport chain. ATP production via F(1)F(0) ATP synthase is then facilitated by the inward flux of protons down the gradient. There is a growing appreciation that a significant portion of the metabolic rate of endotherms is attributable to counteracting "proton leak" (uncoupling), wherein a flux of protons down the electrochemical gradient generates heat independently of ATP production. Proton leak is especially apparent in thermogenic brown adipose tissue, which expresses a tissue-specific uncoupling protein (UCP1). The recent discovery of widely expressed putative UCP1 homologs [UCP2, UCP3, UCP4, UCP5/brain mitochondrial carrier protein-1 (BMCP1)] raised the possibility that innate proton leak and metabolic rate are regulated by UCP1-like proteins. On the basis of current published data, one may not exclude the possibility that UCP homologs influence metabolic rate.
grüsse,klaus
kannst du den artikel in für einen laien verständliche worte fassen??
J Nutr 2000 Apr;130(4):711-4
Uncoupling protein homologs: emerging views of physiological function.
Adams SH
Department of Endocrinology, Genentech, Incorporated, South San Francisco, CA 94080, USA.
The widespread occurrence of excess weight and related diseases demands that efforts be made to understand energy expenditure from the gene to the whole animal. For some time, it has been understood that mitochondrial oxidation of fuels generates an electrochemical gradient via outward pumping of protons by the electron transport chain. ATP production via F(1)F(0) ATP synthase is then facilitated by the inward flux of protons down the gradient. There is a growing appreciation that a significant portion of the metabolic rate of endotherms is attributable to counteracting "proton leak" (uncoupling), wherein a flux of protons down the electrochemical gradient generates heat independently of ATP production. Proton leak is especially apparent in thermogenic brown adipose tissue, which expresses a tissue-specific uncoupling protein (UCP1). The recent discovery of widely expressed putative UCP1 homologs [UCP2, UCP3, UCP4, UCP5/brain mitochondrial carrier protein-1 (BMCP1)] raised the possibility that innate proton leak and metabolic rate are regulated by UCP1-like proteins. On the basis of current published data, one may not exclude the possibility that UCP homologs influence metabolic rate.
grüsse,klaus
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