Brown adipose tissue in genetically obese (fa/fa) rats: response to cold and diet

1983 ◽  
Vol 244 (2) ◽  
pp. E145-E150 ◽  
Author(s):  
J. Triandafillou ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cafeteria Diet ◽  
Chow Diet ◽  
Purine Nucleotides ◽  
Noradrenaline Content ◽  
Bat Mitochondria ◽  
Brown Adipose ◽  
Consequent Reduction ◽  
Diet Induced Thermogenesis

Young genetically obese (fatty, fa/fa) rats (7-8 wk old) maintained on a chow diet at 28 degrees C have a relatively normal amount of brown adipose tissue (BAT) (normal protein content, normal noradrenaline content, normal or slightly reduced cytochrome oxidase content, 30% reduction in DNA content) with cells grossly hypertrophied by accumulation of lipid. The binding of purine nucleotides by BAT mitochondria is lower in fa/fa rats than in lean rats, suggesting a lesser thermogenic activation of this tissue. Acute exposure to cold (24 h at 4 degrees C) activates BAT thermogenesis (visible hyperemia, marked increase in mitochondrial binding of purine nucleotides, depletion of noradrenaline content) in fa/fa rats as in lean rats. In contrast, feeding a cafeteria diet to young fa/fa rats fails to activate BAT (no increase in mitochondrial binding of purine nucleotides) as it does in lean rats, and these rats accumulate more extra fat (increase in weight of gonadal white adipose tissue) than do cafeteria diet-fed lean rats. It is concluded that the young fa/fa rat has normal cold-induced nonshivering thermogenesis in BAT but defective diet-induced thermogenesis in BAT and that the consequent reduction in energy expenditure, coupled with hyperphagia, contributes to the development of its obesity. The most probable location for the defect is suggested to be associated with the hypothalamus.

Brown adipose tissue of cafeteria-fed rats

1981 ◽  
Vol 241 (2) ◽  
pp. E116-E120 ◽  
Author(s):  
J. Himms-Hagen ◽  
J. Triandafillou ◽  
C. Gwilliam
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Tissue Growth ◽  
Total Protein Content ◽  
Chow Diet ◽  
Control Mechanisms ◽  
Purine Nucleotides ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Wet Weight

Feeding a "cafeteria" diet for 2 wk to male Holtzman rats resulted in a weight gain that was, on average, only slightly more than that of control rats fed a regular chow diet. Wet weight, DNA, and total protein content of interscapular brown adipose tissue were more than doubled in the cafeteria-fed rats and proliferation of mitochondria paralleled tissue growth. After 2 wk of recovery from cafeteria feeding, the expanded size of the tissue had completely regressed to a normal level. Brown adipose tissue mitochondria of cafeteria-fed rats bound 3 times more purine nucleotides than mitochondria of chow-fed control rats, but no change in the proportion of polypeptides with molecular weight in the region of 32,000 could be detected. The changes in brown adipose tissue and its mitochondria in cafeteria-fed rats correspond to those seen previously in noradrenaline-treated rats, i.e., tissue growth accompanied by mitochondrial proliferation and an unmasking of proton conductance pathways. The increase in 32,000-mol-wt polypeptides seen in brown adipose tissue mitochondria of cold-acclimated rats does not occur in the cafeteria-fed rats. Control mechanisms are presumed to differ, either quantitatively or qualitatively, in the two situations, cold exposure and overeating, which both cause growth of brown adipose tissue.

scholarly journals Intact innervation is essential for diet-induced recruitment of brown adipose tissue

2019 ◽  
Vol 316 (3) ◽  
pp. E487-E503 ◽  
Author(s):  
Alexander W. Fischer ◽  
Christian Schlein ◽  
Barbara Cannon ◽  
Joerg Heeren ◽  
Jan Nedergaard
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Chow Diet ◽  
Metabolic Efficiency ◽  
Protein Levels ◽  
Brown Adipose ◽  
Ucp1 Expression ◽  
Diet Induced Thermogenesis

The possibility that recruitment and activation of brown adipose tissue (BAT) thermogenesis could be beneficial for curtailing obesity development in humans prompts a need for a better understanding of the control of these processes [that are often referred to collectively as diet-induced thermogenesis (DIT)]. Dietary conditions are associated with large changes in blood-borne factors that could be responsible for BAT recruitment, but BAT is also innervated by the sympathetic nervous system. To examine the significance of the innervation for DIT recruitment, we surgically denervated the largest BAT depot, i.e., the interscapular BAT depot in mice and exposed the mice at thermoneutrality to a high-fat diet versus a chow diet. Denervation led to an alteration in feeding pattern but did not lead to enhanced obesity, but obesity was achieved with a lower food intake, as denervation increased metabolic efficiency. Conclusively, denervation totally abolished the diet-induced increase in total UCP1 protein levels observed in the intact mice, whereas basal UCP1 expression was not dependent on innervation. The denervation of interscapular BAT did not discernably hyper-recruit other BAT depots, and no UCP1 protein could be detected in the principally browning-competent inguinal white adipose tissue depot under any of the examined conditions. We conclude that intact innervation is essential for diet-induced thermogenesis and that circulating factors cannot by themselves initiate recruitment of brown adipose tissue under obesogenic conditions. Therefore, the processes that link food intake and energy storage to activation of the nervous system are those of significance for the further understanding of diet-induced thermogenesis.

Effects of diet and photoperiod on NE turnover and GDP binding in Siberian hamster brown adipose tissue

1986 ◽  
Vol 250 (3) ◽  
pp. R383-R388 ◽  
Author(s):  
J. F. McElroy ◽  
P. W. Mason ◽  
J. M. Hamilton ◽  
G. N. Wade
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Turnover Rate ◽  
Siberian Hamsters ◽  
Bat Mitochondria ◽  
Brown Adipose ◽  
Diet Induced Thermogenesis ◽  
Long Photoperiod

This experiment examined the effects of diet and photoperiod on food intake, body weight, and brown adipose tissue (BAT) activity in female Siberian hamsters (Phodopus sungorus sungorus). BAT function was assessed by measuring both the sympathetic nervous system activity of BAT [estimated by the rate of norepinephrine (NE) turnover] and BAT thermogenic activity (estimated by GDP binding to BAT mitochondria). Nineteen weeks of high-fat feeding in long photoperiod [16:8 light-dark cycle (LD)] caused a 20% increase in food intake but did not affect body weight. Both NE turnover rate and GDP binding in interscapular BAT (IBAT) were increased four- to eightfold relative to that from chow-fed controls. Thus it appears that in Siberian hamsters BAT can serve the same energy-dissipating function during diet-induced overeating previously established in rats and mice. Nineteen-week exposure to a short photoperiod (LD 8:16) produced a reduction in body weight but did not affect food intake. Both NE turnover rate and GDP binding in IBAT were increased two- to fourfold relative to that from long-photoperiod controls. Thus it appears that in Siberian hamsters the photoperiod-induced improvements in thermogenic capacity are mediated via the same mechanisms as are cold- or diet-induced thermogenesis.

scholarly journals Evidence for masking of brown adipose tissue mitochondrial GDP-binding sites in response to fasting in rats made obese by dietary manipulation. Effects of reversion to standard diet

1991 ◽  
Vol 279 (2) ◽  
pp. 575-579 ◽  
Author(s):  
P Puigserver ◽  
I Lladó ◽  
A Palou ◽  
M Gianotti
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Binding Sites ◽  
Uncoupling Protein ◽  
Cafeteria Diet ◽  
Standard Diet ◽  
Dietary Manipulation ◽  
Bat Mitochondria ◽  
Brown Adipose ◽  
Obese Rats

A specific immunoassay of uncoupling protein (UCP) and measurement of GDP binding were used to study the chronic responses of brown adipose tissue (BAT) mitochondria from rats made obese by dietary means (cafeteria rats) and from obese rats subsequently fed a standard diet (post-cafeteria rats). We studied the response to fasting in order to assess the masking/unmasking responses in these groups. These studies have shown the following. (1) In the obese rats (cafeteria and post-cafeteria) the chronic increase in mitochondrial UCP concentration compared with controls parallels the increase in GDP binding. (2) In 24 h-fasted control rats the decrease in GDP binding is associated with a change in UCP concentration, but in fasting cafeteria and post-cafeteria obese rats the decrease in GDP binding is not associated with any change in UCP concentration. (3) Post-cafeteria obese rats showed increased GDP binding and higher UCP concentrations than the controls, but these values were less than in cafeteria obese rats. (4) Control rats at 8 months old showed greater GDP binding and had a higher UCP concentration than 11-month-old control rats. (5) The responses of GDP binding and UCP concentration to fasting in post-cafeteria obese rats were similar to those in cafeteria obese rats, suggesting that such abbreviations are related to the obese status itself rather than to the composition of the cafeteria diet. The evidence supports the hypothesis that the response of the cafeteria and post-cafeteria obese rats to fasting is associated with a masking of UCP, whereas with chronic manipulation of diet changes in UCP concentration predominate.

Brown adipose tissue of mice with gold thioglucose-induced obesity: effect of cold and diet

1983 ◽  
Vol 244 (6) ◽  
pp. E581-E588 ◽  
Author(s):  
S. Hogan ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Acclimation ◽  
Obese Mouse ◽  
Metabolic Efficiency ◽  
Obese Mice ◽  
Gold Thioglucose ◽  
Bat Mitochondria ◽  
Brown Adipose ◽  
Diet Induced Thermogenesis

Gold thioglucose (GTG)-obese mice have a larger than normal amount of brown adipose tissue (BAT) with ultrastructurally normal mitochondria. The tissue grows normally when the mice adapt to cafeteria feeding or to cold (8 degrees C). Acute exposure to cold causes a fairly normal thermogenic activation of BAT mitochondria of GTG-obese mice, both in dynamic and static phases of their obesity. However, chow-fed GTG-obese mice have BAT mitochondria that are in a low state of thermogenic activation, and these mice fail to respond to eating a cafeteria diet for 3 wk by a normal thermogenic activation of their BAT mitochondria. More prolonged cafeteria feeding for 11-13 wk, into the static phase of obesity, is associated with thermogenic activation of BAT mitochondria of GTG-obese mice. The capacity of GTG-obese mice to respond to noradrenaline (norepinephrine) by an increase in metabolic rate is greater than that of lean mice and is further enhanced by cold acclimation. It is concluded that BAT of the GTG-obese mouse is inherently functional, as is control of its thermogenic function and growth during cold exposure and cold acclimation. Dietary influences on BAT thermogenic function are, however, defective in the GTG-obese mouse at least during the dynamic phase of its obesity. The resulting failure of diet-induced thermogenesis would be expected to contribute to the known high metabolic efficiency of the GTG-obese mouse and, together with the hyperphagia, to the obesity induced by GTG.

Brown adipose tissue metabolism in ob/ob mice: effects of a high-fat diet and adrenalectomy

1987 ◽  
Vol 253 (2) ◽  
pp. E149-E157
Author(s):  
H. K. Kim ◽  
D. R. Romsos
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
High Fat ◽  
Adipose Tissue Metabolism ◽  
High Carbohydrate ◽  
Bat Mitochondria ◽  
Norepinephrine Turnover ◽  
Brown Adipose ◽  
Thermogenic Capacity

Adrenalectomy prevents development of obesity in ob/ob mice fed high-carbohydrate stock diets partly by stimulating the low thermogenic capacity of their brown adipose tissue (BAT). Adrenalectomy, however, fails to prevent development of obesity in ob/ob mice fed a high-fat diet. Effects of adrenalectomy on BAT metabolism in ob/ob mice fed a high-fat diet were thus examined. ob/ob mice fed the high-fat diet developed gross obesity despite normal BAT metabolism, as assessed by rates of norepinephrine turnover in BAT, GDP binding to BAT mitochondria, and GDP-inhibitable, chloride-induced mitochondrial swelling. Adrenalectomy failed to arrest the development of obesity or to influence BAT metabolism in ob/ob mice fed the high-fat diet. Development of obesity in ob/ob mice fed a high-fat diet is not associated with low thermogenic capacity of BAT or with adrenal secretions, as it is in ob/ob mice fed high-carbohydrate stock diets.

CNS origins of the sympathetic nervous system outflow to brown adipose tissue

1999 ◽  
Vol 276 (6) ◽  
pp. R1569-R1578 ◽  
Author(s):  
Maryam Bamshad ◽  
C. Kay Song ◽  
Timothy J. Bartness
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Sympathetic Nervous System ◽  
Brown Adipose Tissue ◽  
Pseudorabies Virus ◽  
Critical Role ◽  
Hypothalamic Nucleus ◽  
Brown Adipose ◽  
Sympathetic Nervous ◽  
Diet Induced Thermogenesis

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.

Hypothalamic obesity, brown adipose tissue, and sympathoadrenal activity in rats

1985 ◽  
Vol 248 (5) ◽  
pp. E607-E617 ◽  
Author(s):  
J. G. Vander Tuig ◽  
J. Kerner ◽  
D. R. Romsos
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Heat Production ◽  
Adult Rats ◽  
Guanosine Diphosphate ◽  
Bat Mitochondria ◽  
Sympathoadrenal Activity ◽  
Brown Adipose ◽  
Energy Retention ◽  
Ad Libitum

Obesity-producing, hypothalamic knife cuts and ventromedial hypothalamic (VMH) lesions in ad libitum-fed adult rats increased intake of a high-fat diet (123 and 130%) and energy retention (880 and 1,099%) during the 4-wk period postsurgery; even when pair fed to control rats, energy retention of the knife-cut and lesioned rats was still elevated (105 and 155%). Thermogenic capacity of brown adipose tissue (BAT), estimated from guanosine diphosphate (GDP) binding to BAT mitochondria, was unchanged in hyperphagic knife-cut and VMH-lesioned rats and was reduced approximately 50% when these rats were pair fed to controls. Urinary excretion of norepinephrine (NE) was approximately twofold higher in ad libitum-fed, knife-cut, and lesioned rats than in control rats; restriction of energy intake decreased NE excretion to control values. Rates of NE turnover in heart paralleled urinary NE excretion, whereas NE turnover in BAT was generally not increased in the hyperphagic rats. Urinary epinephrine excretion, an index of adrenal medullary activity, was depressed in all knife-cut and VMH-lesioned rats. Hyperphagia coupled with a lack of increased heat production in BAT causes gross obesity in ad libitum-fed, knife-cut, and VMH-lesioned rats, whereas obesity in pair-fed rats develops in part at least as a result of reduced heat production by BAT.

Effect of glucose and other hexoses on efferent discharges of brown adipose tissue nerves

1986 ◽  
Vol 251 (2) ◽  
pp. R240-R242 ◽  
Author(s):  
A. Niijima
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Sympathetic Nerves ◽  
Nerve Activity ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Diet Induced Thermogenesis ◽  
Effect Of Glucose

The activity of sympathetic nerves innervating interscapular brown adipose tissue of the rat was recorded. Intravenous administrations of glucose (100-300 mg/kg) enhanced the nerve activity. However, mannose, fructose, or galactose (300 mg/kg) showed no effect, suggesting the response is related to diet-induced thermogenesis in the brown adipose tissue.

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