Journal Article10.1038/286274A0
Increased proton conductance pathway in brown adipose tissue mitochondria of rats exhibiting diet-induced thermogenesis
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TL;DR: Results are reported which indicate that the proton conductance pathway is augmented in cafeteria-fed rats, and suggest that it operates to dissipate their excess energy intake through diet-induced thermogenesis.
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Abstract: It has recently been demonstrated1 that in rats induced to overeat by being fed a varied and palatable diet (the ‘cafeteria diet’) there is a marked increase in heat production which serves to reduce, or prevent, the development of obesity. This diet-induced thermogenesis is associated with increases in sympathetic activity, and with changes in brown adipose tissue. Following cafeteria feeding, brown adipose tissue hypertrophies and exhibits increased lipolysis and an apparently greater thermogenesis in response to noradrenaline. These metabolic changes resemble those seen during non-shivering thermogenesis in cold-adapted rats, and it was proposed1 that non-shivering thermogenesis and diet-induced thermogenesis have a similar metabolic origin which depends on the unique capacity of brown adipose tissue for thermogenesis. During non-shivering thermogenesis heat is produced in brown adipose tissue through a proton conductance pathway across the inner mitochondrial membrane that dissipates the proton gradient generated by respiration2. The activity of the proton conductance pathway can be modulated by purine nucleotides, and changes in the pathway seem to be related to the level of purine nucleotide binding to brown adipose tissue mitochondria. We now report results which indicate that the proton conductance pathway is augmented in cafeteria-fed rats, and suggest that it operates to dissipate their excess energy intake through diet-induced thermogenesis.
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Citations
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α- and β-adrenergic control of thermogenin mRNA expression in brown adipose tissue
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Factors affecting brown adipose tissue activity in animals and man
Daniel Ricquier,G. Mory +1 more
TL;DR: Brown adipose tissue (BAT) is the only known tissue whose main function is heat production, and is an important site of non-shivering thermogenesis and perhaps of diet-induced thermogenesis.
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Effects of diet and acute noradrenaline treatment on brown adipose tissue development and mitochondrial purine‐nucleotide binding
TL;DR: Feeding rats a highly palatable 'cafeteria' diet resulted in a two-fold increase in interscapular brown adipose tissue (b.a.t.) mass and GDP binding diminished but after 10 d brown fat mass and noradrenaline-stimulated GDP binding were still significantly higher than control levels, providing further evidence for the involvement of b. a.t. and its mitochondrial proton conductance pathway in diet-induced changes in thermogenic capacity.
57
References
A role for brown adipose tissue in diet-induced thermogenesis
TL;DR: Measurement of energy balance during voluntary over-eating in rats unequivocally establishes the quantitative importance of diet-induced thermogenesis in energy balance and suggests that this tissue may determine metabolic efficiency and resistance to obesity.
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Thermoregulation and non-shivering thermogenesis in the genetically obese (ob/ob) mouse
Paul Trayhurn,W. P. T. James +1 more
TL;DR: One cause of the obesity of the ob/ob mouse is its high metabolic efficiency, which is suggested to be due, at least in part, to less energy being expended on thermoregulatory thermogenesis.
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Hamster Brown-Adipose-Tissue Mitochondria
TL;DR: The rate of controlled respiration of hamster brown-adipose-tissue mitochondria is dependent on the pH of the incubation medium, and on the presence of albumin and exogenous purine nucleotide, and the steady-state protonmotive force across the inner membrane isdependent on the same parameters.
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Increased purine nucleotide binding, altered polypeptide composition, and thermogenesis in brown adipose tissue mitochondria of cold-acclimated rats
TL;DR: Results are interpreted in terms of the appearance of an increased amount of the purine nucleotide-sensitive proton conductance pathway in association with the development of an enhanced thermogenic capacity of brown adipose tissue mitochondria during acclimation of the rat to cold.
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