Effects of fasting and food restriction on brown adipose tissue composition in normal and dystrophic hamsters

1986 ◽  
Vol 64 (7) ◽  
pp. 970-975 ◽  
Author(s):  
M. Desautels ◽  
R. A. Dulos ◽  
H. M. Yuen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Food Deprivation ◽  
Food Restriction ◽  
Tissue Mass ◽  
Tissue Protein ◽  
Guanosine Diphosphate ◽  
Isolated Mitochondria ◽  
Daily Food ◽  
Brown Adipose

Fasting for 36–48 h or food restriction (30% reduction of daily food intake for 6 weeks) caused brown adipose tissue (BAT) atrophy in hamsters. Fasting-induced atrophy was characterized by reductions in tissue mass, DNA, protein, and thermogenin. By contrast, food restriction had no effect on tissue cellularity (DNA) but markedly reduced the tissue protein and thermogenin contents. The concentration of thermogenin in isolated mitochondria was unchanged by fasting or food restriction. Dystrophic hamsters had a reduced BAT mass when compared with weight-matched control hamsters. This resulted from a reduction in tissue cellularity since BAT DNA, protein and thermogenin contents were all reduced. The extent of binding of [3H]guanosine diphosphate to isolated mitochondria and their content of thermogenin were similar in normal and dystrophic hamsters. In response to cold exposure, as in normal hamsters, BAT of dystrophic hamsters grew and the tissue thermogenin increased, but the mitochondrial concentration of thermogenin did not change. In response to fasting, in contrast with normal hamsters, there was no significant reduction in BAT DNA in dystrophic animals and the loss of tissue protein was reduced. However, the relative changes in BAT composition during chronic food restriction were similar in normal and dystrophic animals. Thus, reduction in hamster BAT thermogenic capacity during food deprivation may occur by loss of cells and (or) reduction in the tissue protein and thermogenin contents. The extent of protein and (or) DNA loss may be dependent upon the original tissue mass and the severity of food deprivation.

Brown adipose tissue in cafeteria-fed hamsters

1985 ◽  
Vol 248 (2) ◽  
pp. E230-E235
Author(s):  
R. J. Schimmel ◽  
L. McCarthy
Keyword(s):  
Adipose Tissue ◽  
Weight Gain ◽  
Brown Adipose Tissue ◽  
Brown Fat ◽  
Cafeteria Diet ◽  
Tissue Protein ◽  
Dietary Regulation ◽  
Isolated Mitochondria ◽  
Brown Adipose ◽  
Thermogenic Capacity

Hamsters consuming a “cafeteria diet” had more brown adipose tissue than did chow-fed hamsters. The growth of the brown fat depots in cafeteria-fed hamsters was accompanied by increases in tissue protein and cytochrome oxidase. To assess the thermogenic capacity of brown fat mitochondria, the binding of GDP to isolated mitochondria was measured. Mitochondrial GDP binding was not affected by feeding the cafeteria diet for 4 wk, but more prolonged cafeteria feeding for 8 wk did, however, increase the binding of GDP to isolated mitochondria. The morphology of brown adipose tissue was altered during cafeteria feeding. The brown adipose tissue of cafeteria-fed hamsters had more large unilocular cells than did the brown adipose tissue of chow-fed hamsters. In addition, the average adipocyte diameter was greater in brown adipose tissue of cafeteria-fed hamsters. These data support the presence of a dietary regulation of brown adipose tissue growth in hamsters. The growth of brown adipose tissue in hamsters eating the cafeteria diet appears to result largely from proliferation of adipocytes, as evidenced by the increases in tissue protein and cytochrome oxidase during cafeteria feeding, but some hypertrophy of the adipocytes also occurs. A dietary regulation of brown fat thermogenic capacity is also apparent but this regulation is evident only after more prolonged periods of cafeteria feeding. Hamsters eating a cafeteria diet increase their caloric intake but have the same or greater body weight gain efficiency as do chow-fed animals. The absence of dietary stimulation of thermogenesis may underlie the similar efficiencies of weight gain in chow- and cafeteria-fed hamsters.

Plasticity in food intake, thermogenesis and body mass in the tree shrew (Tupaia belangeri) is affected by food restriction and refeeding

2016 ◽  
Vol 66 (2) ◽  
pp. 201-217 ◽  
Author(s):  
Wen-rong Gao ◽  
Wan-long Zhu ◽  
Fang-yan Ye ◽  
Mu-lin Zuo ◽  
Zheng-kun Wang
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Body Mass ◽  
Food Restriction ◽  
Uncoupling Protein ◽  
Tissue Mass ◽  
Serum Leptin ◽  
Brown Adipose ◽  
Ad Libitum

Physiological adjustments are important strategies for small mammals in response to variation in food availability. To determine the physiological mechanisms affected by food restriction and refeeding, tree shrews were restricted to 85% of initial food intake for 4 weeks and refedad libitumfor another 4 weeks. Changes in food intake, body mass, thermogenesis, body composition, mitochondrial cytochromecoxidase activity, uncoupling protein-1 content in brown adipose tissue and serum leptin levels were measured. The results showed that body mass, body fat mass and serum leptin levels significantly decreased in food restricted tree shrews, and increased when the restriction ended, showing a short “compensatory growth” rather than over-weight or obesity compared withad libitumcontrols. Resting metabolic rate, non-shivering thermogenesis, brown adipose tissue mass (mg), and uncoupling protein-1 content decreased significantly in response to food restriction, and returned to the control levels after the animals were refedad libitum, while the brown adipose tissue mass (%) and cytochromecoxidase activity remained stable during food restriction and refeeding. Food intake increased shortly after refeeding, which perhaps contributed to the rapid regaining of body mass. These results suggest thatTupaia belangerican adjust the status of its physiology integratively to cope with the lack of food by means of decreasing body mass, thermogenesis and serum leptin levels. Leptin may act as a starvation signal to predominantly mediate the reduction in body mass and energy expenditure.

Caloric Restriction Paradoxically Increases Adiposity in Mice With Genetically Reduced Insulin

Endocrinology ◽  
2016 ◽  
Vol 157 (7) ◽  
pp. 2724-2734 ◽  
Author(s):  
Derek A. Dionne ◽  
Søs Skovsø ◽  
Nicole M. Templeman ◽  
Susanne M. Clee ◽  
James D. Johnson
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Caloric Restriction ◽  
Gene Dosage ◽  
Tissue Growth ◽  
Tissue Mass ◽  
Brown Adipose ◽  
Paradoxical Effects ◽  
Plasma Insulin Levels ◽  
Ad Libitum

Antiadiposity effects of caloric restriction (CR) are associated with reduced insulin/IGF-1 signaling, but it is unclear whether the effects of CR would be additive to genetically reducing circulating insulin. To address this question, we examined female Ins1+/−:Ins2−/− mice and Ins1+/+:Ins2−/− littermate controls on either an ad libitum or 60% CR diet. Although Igf1 levels declined as expected, CR was unable to reduce plasma insulin levels in either genotype below their ad libitum-fed littermate controls. In fact, 53-week-old Ins1+/−:Ins2−/− mice exhibited a paradoxical increase in circulating insulin in the CR group compared with the ad libitum-fed Ins1+/−:Ins2−/− mice. Regardless of insulin gene dosage, CR mice had lower fasting glucose and improved glucose tolerance. Although body mass and lean mass predictably fell after CR initiation, we observed a significant and unexpected increase in fat mass in the CR Ins1+/−:Ins2−/− mice. Specifically, inguinal fat was significantly increased by CR at 66 weeks and 106 weeks. By 106 weeks, brown adipose tissue mass was also significantly increased by CR in both Ins1+/−:Ins2−/− and Ins1+/+:Ins2−/− mice. Interestingly, we observed a clear whitening of brown adipose tissue in the CR groups. Mice in the CR group had altered daily energy expenditure and respiratory exchange ratio circadian rhythms in both genotypes. Multiplexed analysis of circulating hormones revealed that CR was associated with increased fasting and fed levels of the obesogenic hormone, glucose-dependent insulinotropic polypeptide. Collectively these data demonstrate CR has paradoxical effects on adipose tissue growth in the context of genetically reduced insulin.

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.

Role of neural input in photoperiod-induced changes in hamster brown adipose tissue

1990 ◽  
Vol 68 (6) ◽  
pp. 677-681 ◽  
Author(s):  
M. Desautels ◽  
R. A. Dulos
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cellular Proliferation ◽  
Uncoupling Protein ◽  
Isolated Mitochondria ◽  
Short Day ◽  
Protein Energy ◽  
Neural Input ◽  
Brown Adipose ◽  
6 Hydroxydopamine

Repeated injections of 6-hydroxydopamine in Syrian hamster neonates maintained under long-day (16L:8D) photoperiod for 30 days retarded body growth and cellular proliferation in brown adipose tissue but did not affect the cellular content of mitochondrial proteins. Sympathectomy reduced GDP binding to isolated mitochondria without affecting the organelle uncoupling protein (UCP) content. Unilateral surgical denervation of the brown fat pad of 30-day-old hamsters caused loss of tissue protein and succinate dehydrogenase as well as reductions in GDP binding and UCP content of isolated mitochondria but did not prevent an increase in GDP binding observed after 1 month exposure to a short-day photoperiod. The increased GDP binding was not due to increased UCP content. These results indicate that an adrenergic neural input may not be essential for UCP expression in Syrian hamsters and that changes in GDP binding observed in a short-day photoperiod environment can be observed in denervated tissue in the absence of changes in mitochondrial UCP content.Key words: mitochondria, nonshivering thermogenesis, uncoupling protein, energy balance.

scholarly journals Diminished response to food deprivation of the rat brown adipose tissue mitochondrial uncoupling system with age

IUBMB Life ◽  
1997 ◽  
Vol 42 (6) ◽  
pp. 1151-1161
Author(s):  
Francisco Garcia-Palmer ◽  
Jordi Pericas ◽  
Juan Matamala ◽  
Pere Puigserver ◽  
María Bonet ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Food Deprivation ◽  
Mitochondrial Uncoupling ◽  
Brown Adipose

Effect of adrenalectomy and glucocorticoid replacement on development of obesity

1986 ◽  
Vol 250 (4) ◽  
pp. R595-R607 ◽  
Author(s):  
M. R. Freedman ◽  
B. A. Horwitz ◽  
J. S. Stern
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Protein Content ◽  
Body Fat ◽  
Plasma Insulin ◽  
Tissue Protein ◽  
Steroid Dose ◽  
Brown Adipose ◽  
Obese Rats

Female obese and lean Zucker rats were adrenalectomized (ADX) or sham-operated at 4 wk of age. ADX animals were given daily injections of 0.01, 0.05, 0.50, 1.0, or 2.0 mg hydrocortisone/100 g body wt for 30 days. ADX rats gained less weight than sham-operated controls. Obese ADX rats at the lowest dose (0.01) had a net positive energy gain but lost body fat. As steroid dose increased, obese rats deposited more fat and less protein. Doses of 0.01 and 0.05 mg produced rats that were less fat than sham-operated controls, whereas doses of 0.50, 1.0, and 2.0 mg produced rats of comparable body fat composition. Obese rats were consistently fatter and had a significantly smaller percentage body protein than lean rats at each dose. Body fat elevation was reflected by heavier parametrial and retroperitoneal fat depots and larger fat cells at all doses except the lowest. Compared with sham-operated controls, lean and obese rats at the two lowest replacement doses (0.01, 0.05) exhibited significantly decreased plasma insulin and triglyceride levels and significantly elevated brown adipose tissue protein content and citrate synthase (CS) activity. Obese rats at these doses had significantly reduced adipose tissue lipoprotein lipase (LPL) activity in the retroperitoneal depot and lower food intake. Furthermore, these obese rats had adipose depot weights, cell sizes, LPL activity, and plasma insulin, glucose, and triglyceride comparable to that of lean sham-operated controls. As steroid dose increased (0.5, 1.0, 2.0), plasma insulin and triglyceride and food intake markedly increased only in obese rats. Adipose tissue LPL activity appeared unaffected by dose. Brown adipose tissue protein content and CS activity significantly decreased as dose increased in both lean and obese rats. At all doses of replacement obese rats were more responsive to steroid than were lean rats. Obese rats receiving 0.01 mg had comparable fat depot weights, cell sizes, and plasma insulin and triglyceride as lean rats receiving 50 times as much steroid per day (0.50 mg). These results suggest glucocorticoids play an important role in the early development of obesity in the Zucker rat and support the hypothesis that obese rats are more responsive to glucocorticoids than are lean rats.

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