Brown adipose tissue growth and development: significance and nutritional regulation

10.2741/3807 ◽  
2011 ◽  
Vol 16 (1) ◽  
pp. 1589 ◽  
Author(s):  
Michael Carey Satterfield
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Growth And Development ◽  
Tissue Growth ◽  
Nutritional Regulation ◽  
Brown Adipose

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.

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.

Relationship of brown adipose tissue with growth and obesity differences in genetically selected mouse lines

1984 ◽  
Vol 26 (3) ◽  
pp. 339-347 ◽  
Author(s):  
A. M. Saxton ◽  
E. J. Eisen ◽  
J. M. Leatherwood
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Single Gene ◽  
Tissue Growth ◽  
Growth Patterns ◽  
High Fat ◽  
Polygenic Control ◽  
Brown Adipose ◽  
Diet Induced Thermogenesis

A recent hypothesis considers brown adipose tissue (BAT) to be an important source of diet-induced thermogenesis (DIT). In turn, DIT and thermogenesis in general are believed to be key factors in the control of obesity of laboratory rodents. This hypothesis was developed from the study of single gene mutant obese rodents. The present research tested this hypothesis in mice with polygenic control of growth and obesity, which is more characteristic of the type of genetic variation expected in human and other mammalian populations. Control and high fat diets were used to test responses of five genetically selected lines of mice showing different patterns of growth and obesity. All lines deposited more fat on the high fat diet, but the most obese line showed the largest increase in BAT and the lipid-free dry (LFD) component of BAT. Use of LFD per unit body weight gave results which supported the hypothesis being tested, but it was argued that this measure is misleading. When brown and white adipose tissue growth relative to body weight were examined, 2 of the 10 line – diet groups showed alterations in BAT growth patterns. However, it was concluded that BAT, if involved at all, was not a major factor in growth and obesity differences.Key words: obesity, polygenes, adipose tissue, quantitative inheritance, mouse.

Glucagon stimulation of brown adipose tissue growth and thermogenesis

1987 ◽  
Vol 252 (1) ◽  
pp. R160-R165 ◽  
Author(s):  
C. J. Billington ◽  
T. J. Bartness ◽  
J. Briggs ◽  
A. S. Levine ◽  
J. E. Morley
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cytochrome Oxidase ◽  
Lipoprotein Lipase ◽  
Mitochondrial Protein ◽  
Tissue Growth ◽  
Whole Body ◽  
Control Group ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose

Despite long-standing observations of a whole-body thermogenic effect of glucagon, the role of glucagon in activating thermogenesis in brown adipose tissue has not often been studied. We investigated the ability of administered glucagon to produce alterations in brown adipose tissue similar to changes produced by accepted stimuli of brown fat activity: cold, norepinephrine, and overfeeding. Eighteen days of glucagon injections (1 mg/kg) to male Sprague-Dawley rats produced, relative to saline-injected controls, decreases in feed efficiency and increases in brown adipose tissue weight, protein content, DNA content, and mitochondrial mass as reflected in cytochrome oxidase activity. The observed changes were similar, though of lesser magnitude, to changes produced in these same parameters induced by administration of norepinephrine (250 micrograms/kg) for a positive control group. Four days of glucagon administration (1 mg/kg) produced increases in specific activity of cytochrome oxidase and lipoprotein lipase. After 8 days of glucagon administration, changes in whole-pad activity similar to those seen with 18 days of administration were present. Glucagon also increased whole-pad lipoprotein lipase activity after 4 and 8 days. Surgically denervated interscapular brown adipose tissue retained its ability to respond to exogenous glucagon, though the magnitude of the response was diminished. Guanosine 5'-diphosphate (GDP) binding to brown adipose tissue mitochondria was measured as an assessment of functional state after 5 days of glucagon (1 mg/kg). There was an increase in GDP binding relative to controls whether expressed as picomoles per milligram mitochondrial protein or nanomoles per pad.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Lkb1 controls brown adipose tissue growth and thermogenesis by regulating the intracellular localization of CRTC3

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Tizhong Shan ◽  
Yan Xiong ◽  
Pengpeng Zhang ◽  
Zhiguo Li ◽  
Qingyang Jiang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Intracellular Localization ◽  
Tissue Growth ◽  
Brown Adipose

Characteristics of diet-induced brown adipose tissue growth and thermogenesis in rats

Life Sciences ◽  
1982 ◽  
Vol 30 (18) ◽  
pp. 1525-1530 ◽  
Author(s):  
Orien L. Tulp ◽  
Mark H. Gregory ◽  
Ellio Danforth
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Tissue Growth ◽  
Brown Adipose

Trophic response of hamster brown adipose tissue: roles of norepinephrine and pineal gland

1984 ◽  
Vol 247 (6) ◽  
pp. E793-E799
Author(s):  
J. Triandafillou ◽  
W. Hellenbrand ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Muscular Dystrophy ◽  
Pineal Gland ◽  
Brown Adipose Tissue ◽  
Environmental Temperature ◽  
Tissue Growth ◽  
Short Photoperiod ◽  
Experimental Conditions ◽  
Brown Adipose ◽  
Tissue Size

The objective was to find out whether the reduced amount of brown adipose tissue in myopathic hamsters [Am. J. Physiol. 239 (Cell Physiol. 8): C18–C22, 1980] was secondary to a refractoriness to the trophic influence of norepinephrine. However, no evidence for any trophic influence of norepinephrine on brown adipose tissue of either normal or myopathic hamsters could be detected under experimental conditions that have demonstrated such an influence in rats. A mediator other than norepinephrine, melatonin, secreted by the pineal gland, is known to mediate the control of brown adipose tissue growth induced in hamsters by short photoperiod. Further studies of intact or pinealectomized hamsters showed that the pineal gland was not required for either cold- or diet-induced growth of brown adipose tissue. It is concluded that the defect in control of brown adipose tissue size in the hamster with muscular dystrophy is not due either to abnormal control by norepinephrine or to the pineal gland since neither of these appears to participate in the normal regulation of brown adipose tissue size in relation to environmental temperature or to diet.

Thyroxine 5'-deiodinase in hamster and rat brown adipose tissue: effect of cold and diet

1986 ◽  
Vol 251 (1) ◽  
pp. E1-E7 ◽  
Author(s):  
J. Kopecky ◽  
L. Sigurdson ◽  
I. R. Park ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Specific Activity ◽  
Total Activity ◽  
Tissue Growth ◽  
Endogenous Production ◽  
Deiodinase Activity ◽  
Brown Adipose ◽  
Lag Period ◽  
Palatable Diet

Thyroxine 5'-deiodinase (type II) is present in a microsomal fraction of brown adipose tissue (BAT) of Syrian hamsters. Cold exposure increased specific activity in homogenates after a lag period of approximately 2 h to reach a maximum by 1-3 days. Total activity increased 80 times in cold-acclimated hamsters. During deacclimation, a rapid decrease occurred again after a lag period of approximately 2 h. The increase did not parallel increases in protein or in thermogenic state of mitochondria (mitochondrial GDP binding), which occurred more slowly. Changes in serum 3,5,3'-triiodothyronine concentration paralleled changes in BAT 5'-deiodinase during both acclimation to cold and deacclimation. The cold-induced increase in BAT 5'-deiodinase activity occurred more slowly but was much larger in hamsters than in rats. Eating a palatable diet increased BAT protein content and thermogenic activity in both hamsters and rats but did not alter total 5'-deiodinase activity in either species. We conclude that the trophic response of brown adipose tissue to cold in both hamsters and rats is accompanied by an enhanced endogenous production of triiodothyronine that may play a role in control of tissue growth. The trophic response to a palatable diet differs in that enhanced endogenous production of triiodothyronine is not an obligatory accompaniment. Specific stimulation of 5'-deiodinase by cold might modify thermogenesis in tissues other than BAT by providing triiodothyronine and be of greater significance in hamsters than in rats.

scholarly journals Both proliferation and lipogenesis of brown adipocytes contribute to postnatal brown adipose tissue growth in mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Steven G. Negron ◽  
A. Gulhan Ercan-Sencicek ◽  
Jessica Freed ◽  
Madeline Walters ◽  
Zhiqiang Lin
Keyword(s):  
Cell Cycle ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Molecular Mechanisms ◽  
Tissue Growth ◽  
The Body ◽  
Brown Adipocytes ◽  
Volume Increase ◽  
Brown Adipose ◽  
Developmental Dynamics

AbstractBrown adipose tissue (BAT) is the primary non-shivering thermogenesis organ in mammals, which plays essential roles in maintaining the body temperature of infants. Although the development of BAT during embryogenesis has been well addressed in rodents, how BAT grows after birth remains unknown. Using mouse interscapular BAT (iBAT) as an example, we studied the cellular and molecular mechanisms that regulate postnatal BAT growth. By analyzing the developmental dynamics of brown adipocytes (BAs), we found that BAs size enlargement partially accounts for iBAT growth. By investigating the BAs cell cycle activities, we confirmed the presence of proliferative BAs in the neonatal mice. Two weeks after birth, most of the BAs exit cell cycle, and the further expansion of the BAT was mainly due to lipogenesis-mediated BAs volume increase. Microscopy and fluorescence-activated cell sorting analyses suggest that most BAs are mononuclear and diploid. Based on the developmental dynamics of brown adipocytes, we propose that the murine iBAT has two different growth phases between birth and weaning: increase of BAs size and number in the first two weeks, and BAs size enlargement thereafter. In summary, our data demonstrate that both lipogenesis and proliferation of BAs contribute to postnatal iBAT growth in mice.

Sign in / Sign up

Export Citation Format

Share Document