Food restriction attenuates oxidative stress in brown adipose tissue of striped hamsters acclimated to a warm temperature

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.

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Effects of fasting and food restriction on sympathetic activity in brown adipose tissue in mice

Journal of Comparative Physiology B ◽

10.1007/bf00296640 ◽

1992 ◽

Vol 162 (7) ◽

pp. 602-606 ◽

Cited By ~ 7

Author(s):

M. A. Griggio ◽

D. Richard ◽

J. Leblanc

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Sympathetic Activity ◽

Food Restriction ◽

Brown Adipose

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Food restriction increases torpor and improves brown adipose tissue thermogenesis in ob/ob mice

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1985.248.5.e531 ◽

1985 ◽

Vol 248 (5) ◽

pp. E531-E539 ◽

Cited By ~ 19

Author(s):

J. Himms-Hagen

Keyword(s):

Adipose Tissue ◽

Body Temperature ◽

Brown Adipose Tissue ◽

Rectal Temperature ◽

Food Restriction ◽

Normal Body Temperature ◽

Cold Intolerance ◽

Brown Adipose ◽

Brown Adipose Tissue Thermogenesis ◽

Ad Libitum

Restricting the food intake of the genetically obese (ob/ob) mouse is known to ameliorate its cold intolerance. Cold intolerance of the ob/ob mouse is associated with defective thermogenesis in its brown adipose tissue. The objective of the experiments was to find out whether food restriction could increase the thermogenic function of brown adipose tissue of the ob/ob mouse. Obese and lean mice were fed a restricted amount of chow in one meal per day for 3-7 mo. Both lean and ob/ob mice were torpid (rectal temperature of approximately 32 degrees C) in the early morning and aroused spontaneously to a normal body temperature before the anticipated meal time. Obese mice were also torpid during the dark phase, whereas lean mice were active and had a normal body temperature at this time. Brown adipose tissue was in a thermogenically inactive state (low level of mitochondrial GDP binding) in torpid lean and ob/ob mice but became thermogenically active (increase in mitochondrial GDP binding) during stimulated arousal when body temperature increased by 6-7 degrees C in 15-30 min. Ad libitum-fed ob/ob mice had a normal diurnal rhythm in a rectal temperature that was at a lower level than in lean ad libitum-fed mice. They did not raise their rectal temperatures when stimulated and no activation of brown adipose tissue thermogenesis occurred under these conditions. Food restriction increased the capacity of both lean and ob/ob mice to raise their metabolic rate in response to injection of noradrenaline, indicating an increased capacity for thermogenesis in their brown adipose tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

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

Animal Biology ◽

10.1163/15707563-00002498 ◽

2016 ◽

Vol 66 (2) ◽

pp. 201-217 ◽

Cited By ~ 3

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.

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Effect of chronic food restriction on energy balance, thermogenic capacity, and brown-adipose-tissue activity in the rat

Bioscience Reports ◽

10.1007/bf01314214 ◽

1982 ◽

Vol 2 (8) ◽

pp. 543-549 ◽

Cited By ~ 78

Author(s):

Nancy J. Rothwell ◽

Michael J. Stock

Keyword(s):

Adipose Tissue ◽

Energy Balance ◽

Brown Adipose Tissue ◽

Food Restriction ◽

Brown Adipose ◽

Brown Adipose Tissue Activity ◽

Chronic Food Restriction ◽

Thermogenic Capacity

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Ellagic Acid Affects Metabolic and Transcriptomic Profiles and Attenuates Features of Metabolic Syndrome in Adult Male Rats

Nutrients ◽

10.3390/nu13030804 ◽

2021 ◽

Vol 13 (3) ◽

pp. 804

Author(s):

Adéla Kábelová ◽

Hana Malínská ◽

Irena Marková ◽

Olena Oliyarnyk ◽

Blanka Chylíková ◽

...

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Body Weight ◽

Adipose Tissue ◽

Brown Adipose Tissue ◽

Ellagic Acid ◽

High Fat Diet ◽

Male Rats ◽

High Fat ◽

Brown Adipose

Ellagic acid, a natural substance found in various fruits and nuts, was previously shown to exhibit beneficial effects towards metabolic syndrome. In this study, using a genetic rat model of metabolic syndrome, we aimed to further specify metabolic and transcriptomic responses to ellagic acid treatment. Adult male rats of the SHR-Zbtb16Lx/k.o. strain were fed a high-fat diet accompanied by daily intragastric gavage of ellagic acid (50 mg/kg body weight; high-fat diet–ellagic acid (HFD-EA) rats) or vehicle only (high-fat diet–control (HFD-CTL) rats). Morphometric and metabolic parameters, along with transcriptomic profile of liver and brown and epididymal adipose tissues, were assessed. HFD-EA rats showed higher relative weight of brown adipose tissue (BAT) and decreased weight of epididymal adipose tissue, although no change in total body weight was observed. Glucose area under the curve, serum insulin, and cholesterol levels, as well as the level of oxidative stress, were significantly lower in HFD-EA rats. The most differentially expressed transcripts reflecting the shift induced by ellagic acid were detected in BAT, showing downregulation of BAT activation markers Dio2 and Nr4a1 and upregulation of insulin-sensitizing gene Pla2g2a. Ellagic acid may provide a useful nutritional supplement to ameliorate features of metabolic syndrome, possibly by suppressing oxidative stress and its effects on brown adipose tissue.

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