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Hormonal regulation of malic enzyme and glucose-6-phosphate dehydrogenase in brown adipose tissue

Hormonal regulation of malic enzyme and glucose-6-phosphate dehydrogenase in brown adipose tissue BROWN ADIPOSE TISSUE (BAT) is a major site of facultative thermogenesis in small mammals. The abundant BAT mitochondria contain a unique uncoupling protein (UCP) that dissipates the proton gradient created by the respiratory chain, bypassing the less abundant ATP synthetase. This markedly accelerates mitochondrial respiration without the corresponding synthesis of ATP (25) The primary stimulus for BAT thermogenesis is norepinephrine (NE) reaching the brown adipocytes via sympathetic innervation. Several known physiological stimuli (e.g., cold exposure, cafeteria diet, arousal from hibernation) are integrated in the hypothalamus, travel via sympathetic nerves, and cause the release of NE from BAT nerve terminals, triggering various biochemical responses, including the stimulation of UCP gene expression and metabolic pathways, all leading to enhanced tissue thermogenesis (17). We have previously shown that, in addition to the sympathetic nervous system (SNS), thyroid hormones are critical for the BAT thermogenic response to adrenergic activation (3-5). UCP gene expression and enzyme activities key to BAT lipogenesis and mitochondrial function are stimulated by the SNS, and these responses are reduced or absent in hypothyroid rats. Replacement with thyroid hormones, particularly thyroxine (TJ, promptly restores these BAT responses to cold stimulation, indicating that thyroid hormones are necessary to the full http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Endocrinology and Metabolism The American Physiological Society

Hormonal regulation of malic enzyme and glucose-6-phosphate dehydrogenase in brown adipose tissue

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Publisher
The American Physiological Society
Copyright
Copyright © 1993 the American Physiological Society
ISSN
0193-1849
eISSN
1522-1555
Publisher site
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Abstract

BROWN ADIPOSE TISSUE (BAT) is a major site of facultative thermogenesis in small mammals. The abundant BAT mitochondria contain a unique uncoupling protein (UCP) that dissipates the proton gradient created by the respiratory chain, bypassing the less abundant ATP synthetase. This markedly accelerates mitochondrial respiration without the corresponding synthesis of ATP (25) The primary stimulus for BAT thermogenesis is norepinephrine (NE) reaching the brown adipocytes via sympathetic innervation. Several known physiological stimuli (e.g., cold exposure, cafeteria diet, arousal from hibernation) are integrated in the hypothalamus, travel via sympathetic nerves, and cause the release of NE from BAT nerve terminals, triggering various biochemical responses, including the stimulation of UCP gene expression and metabolic pathways, all leading to enhanced tissue thermogenesis (17). We have previously shown that, in addition to the sympathetic nervous system (SNS), thyroid hormones are critical for the BAT thermogenic response to adrenergic activation (3-5). UCP gene expression and enzyme activities key to BAT lipogenesis and mitochondrial function are stimulated by the SNS, and these responses are reduced or absent in hypothyroid rats. Replacement with thyroid hormones, particularly thyroxine (TJ, promptly restores these BAT responses to cold stimulation, indicating that thyroid hormones are necessary to the full

Journal

AJP - Endocrinology and Metabolism – The American Physiological Society

Published: Jun 1, 1993

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