Regulation of brown adipose tissue lipogenesis by thyroid hormone and the sympathetic nervous system

1993 ◽  
Vol 265 (2) ◽  
pp. E252-E258 ◽  
Author(s):  
W. J. Yeh ◽  
P. Leahy ◽  
H. C. Freake

Thyroid hormone regulates lipogenesis differently in rat liver and brown adipose tissue (BAT). In the hypothyroid state, lipogenesis is suppressed in liver but enhanced in BAT. Here we investigated the mechanisms underlying increased lipogenesis in hypothyroid BAT. Housing the animals at 28 degrees C decreased lipogenesis in hypothyroid BAT to euthyroid levels. Denervation resulted in a 90% reduction in lipogenesis in hypothyroid BAT such that levels were lower than in euthyroid tissue. Thyroid hormone treatment of hypothyroid rats stimulated fatty acid synthesis in denervated BAT, as in liver, but decreased it in intact BAT. Steady-state levels of mRNA encoding acetyl-CoA carboxylase, fatty-acid synthase, and spor 14 were measured in similar animals by Northern analysis. The expression of these mRNAs mirrored the lipogenic data, showing that both thyroid hormone and the sympathetic nervous system work at a pretranslational level in this tissue. These data suggest that the increased BAT lipogenesis found with hypothyroidism is mediated by the sympathetic nervous system to counter the reduction in metabolic rate in these animals.

1999 ◽  
Vol 276 (6) ◽  
pp. R1569-R1578 ◽  
Author(s):  
Maryam Bamshad ◽  
C. Kay Song ◽  
Timothy J. Bartness

Brown adipose tissue (BAT) plays a critical role in cold- and diet-induced thermogenesis. Although BAT is densely innervated by the sympathetic nervous system (SNS), little is known about the central nervous system (CNS) origins of this innervation. The purpose of the present experiment was to determine the neuroanatomic chain of functionally connected neurons from the CNS to BAT. A transneuronal viral tract tracer, Bartha’s K strain of the pseudorabies virus (PRV), was injected into the interscapular BAT of Siberian hamsters. The animals were killed 4 and 6 days postinjection, and the infected neurons were visualized by immunocytochemistry. PRV-infected neurons were found in the spinal cord, brain stem, midbrain, and forebrain. The intensity of labeled neurons in the forebrain varied from heavy infections in the medial preoptic area and paraventricular hypothalamic nucleus to few infections in the ventromedial hypothalamic nucleus, with moderate infections in the suprachiasmatic and lateral hypothalamic nuclei. These results define the SNS outflow from the brain to BAT for the first time in any species.


1989 ◽  
Vol 67 (2) ◽  
pp. 116-121 ◽  
Author(s):  
Judy Eley ◽  
Jean Himms-Hagen

In a first study, mice made obese with gold thioglucose became hypothermic when exposed to 4 °C. In a second study, lean mice and mice made obese with gold thioglucose (dynamic phase) were acclimated to 14 °C for up to 2 weeks and their brown adipose tissue was studied. The cold-induced increase in thyroxine 5′-deiodinase activity was initially slightly smaller in obese mice, but by 24 h and 2 weeks in the cold the activity of thyroxine 5′-deiodinase was the same in lean and obese mice. Unexpectedly, the elevated activity of 5′-deiodinase returned to the low level seen in warm-acclimated mice in both lean and obese mice after 2 weeks of cold acclimation. In gold thioglucose obese mice, a progressive cold-induced increase in the binding of guanosine diphosphate to isolated mitochondria, an index of both acute thermogenic activation and a long-term increase in uncoupling protein concentration, paralleled that seen in normal lean mice and remained at a high level after 2 weeks in the cold, although still remaining slightly lower than normal. It is not clear how a high level of mitochondrial GDP binding is maintained in cold-acclimated mice at the same time as a low level of thyroxine 5′-deiodinase activity when both are believed to be controlled by the sympathetic nervous system. We conclude that the gold thioglucose obese mouse can activate its brown adipose tissue fairly normally when it is exposed to cold, but that some attenuation of this process may contribute to the impaired survival of this mouse at low temperatures.Key words: hypothalamus, thyroxine 5′-deiodinase, guanosine diphosphate binding, sympathetic nervous system, thermoregulation.


1983 ◽  
Vol 244 (3) ◽  
pp. C142-C149 ◽  
Author(s):  
U. Sundin ◽  
M. Nechad

Brown adipose tissue has earlier been suggested as an important site of the diet-induced thermogenesis that results from cafeteria feeding in rats. The aim of the present communication has been to see if any defined component of this diet can mimic the effects of the diet on the trophic response of brown fat and if these effects are mediated by the sympathetic nervous system. Rats fed a lipid emulsion did not show hypertrophy of brown adipose tissue. Rats fed a glucose solution, whether voluntarily or by force feeding, showed a clear trophic response of brown fat, as seen by the morphology of the tissue and its increased wet weight, increased protein content, increased total and specific cytochrome c oxidase activity, and increased mitochondrial guanosine diphosphate binding. Chemical sympathectomy of young rats by guanethidine prior to glucose feeding impaired the glucose-induced effects on brown fat. beta-Adrenergic blockade in adult rats also tended to depress the glucose effect. Consequently we conclude that chronic glucose ingestion can mimic cafeteria feeding with respect to the trophic response of brown fat and that an intact sympathetic nervous system is required for the mediation of the glucose effect to the brown adipose tissue.


1982 ◽  
Vol 242 (4) ◽  
pp. E253-E261 ◽  
Author(s):  
A. W. Knehans ◽  
D. R. Romsos

Obese (ob/ob) mice have a lower thermogenic capacity than lean mice. The possible role of brown adipose tissue (BAT) in this defect was investigated. Lean and obese mice were exposed to 33 (thermoneutral), 25, or 14 degrees C for up to 3 wk. BAT cytochrome oxidase activity and numbers of Na+-K+-ATPase enzyme units, enzymes involved in thermogenesis, were similar at 33 or 25 degrees C. Chronic exposure to 14 degrees C increased these enzymes 34 and 62%, respectively, in lean mice and nearly 150% in obese mice. Sympathetic nervous system activity, which stimulates thermogenesis in BAT, was evaluated by measuring norepinephrine (NE) turnover. At 25 degrees C, NE turnover rate in BAT of obese mice was only 40% as rapid as in BAT of lean mice. Chronic exposure to 33 degrees C depressed NE turnover in BAT of lean mice, but not in obese mice, whereas exposure to 14 degrees C accelerated NE turnover in both lean and obese mice. Lower sympathetic nervous system activity in BAT of obese mice at 25 degrees C is likely a major factor in their reduced nonshivering thermogenesis and resultant high efficiency of energy storage.


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