Both thermogenin and 2,4-dinitrophenol (DNP) uncouple oxidation from ATP synthesis. Thermogenin is expressed in the mitochondria of brown fat cells in newborn animals and adult mammals that hibernate
DNP was marketed in the 1930s as a diet pill, but in addition to causing weight loss it sometimes caused death.
a. Compare the mechanisms by which these uncouplers affect ATP synthesis.
b. What function does thermogenin serve for brown fat cells?
c. Why is the rationale for DNP as a diet drug?
d. Considering locations of the effects in an animal and the possibility for allosteric regulation, suggest why thermogenin is advantageous and DNP dangerous for humans?
Answer:
a. Thermogenin is an inner mitochondrial membrane H+ channel and DNP is a H+ carrier. Both decrease pmf by equilibrating H+ across the inner mitochondrial membrane, releasing the energy as heat instead of driving ATP synthesis.
b. The purpose of thermogenin in brown fat is to generate heat for newborns and hibernating animals.
c. By dissipating the pmf, DNP requires the breakdown of more glucose/fat to supply sufficient amounts of ATP.
d. Thermogenin is expressed only in brown fat cells to keep newborns warm and has no effect on ATP generation in any other cell. As a protein, thermogenin channel activity is likely to be regulated by other cells activities or feedback processes. DNP likely effects ATP generation in all cells. It is difficult to correctly dose to have the desired effect and not cause overheating or ATP deficiency.
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