Absence of CD47 maintains brown fat thermogenic capacity and protects mice from aging-related obesity and metabolic disorder

2021 ◽  
Author(s):  
Dong Li ◽  
Taesik Gwag ◽  
Shuxia Wang
Keyword(s):  
Metabolic Disorder ◽  
Brown Fat ◽  
Thermogenic Capacity

Hyperprolactinemia prevents short photoperiod-induced changes in brown fat

1989 ◽  
Vol 256 (1) ◽  
pp. R174-R180
Author(s):  
K. S. Kott ◽  
B. J. Moore ◽  
L. Fournier ◽  
B. A. Horwitz
Keyword(s):  
Protein Content ◽  
Fat Mass ◽  
Carcass Composition ◽  
Brown Fat ◽  
Short Photoperiod ◽  
Necessary Condition ◽  
Tissue Mass ◽  
The Right ◽  
Induced Changes ◽  
Thermogenic Capacity

Previous studies demonstrated that short photoperiod exposure significantly decreases circulating prolactin levels. The present study investigated the possibility that concomitant changes in brown fat tissue mass, protein content, thermogenic capacity, and carcass composition are dependent on this change in prolactin levels. Male golden (Syrian) hamsters were sham operated and exposed to a short (10L:14D) or long (14L:10D) photoperiod. A third group was implanted with exogenous pituitaries under the right kidney capsule and exposed to a short photoperiod. In experiment I, 4 wk of short- vs. long-photoperiod exposure did not result in significant changes in circulating prolactin levels, nor was there an increase in brown fat mass, protein content, or thermogenic capacity. Four weeks of short-photoperiod exposure did significantly increase carcass lipid content. However, this increase did not occur in hamsters exposed to 4 wk of short photoperiod but made hyperprolactinemic (implanted with two exogenous pituitaries). Ten weeks of short photoperiod significantly reduced circulating prolactin levels. Concomitantly, brown fat mass, protein content, and thermogenic capacity, as well as carcass fat, were increased. These short-photoperiod-induced changes were not observed in similarly exposed hamsters that were made hyperprolactinemic via two implanted pituitaries. In experiment II, similar changes in brown fat and body composition occurred in sham-operated hamsters exposed to 10 wk of short photoperiod. These changes were prevented in hamsters exposed to 10 wk of short photoperiod but made hyperprolactinemic via only one implanted pituitary. These results suggest that decreased prolactin is a necessary condition for the increased brown fat mass, protein content, and thermogenic capacity that occurs when golden hamsters are exposed to short photoperiod.

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.

GDP binding to hamster brown fat mitochondria is reduced during hibernation

1985 ◽  
Vol 249 (6) ◽  
pp. R689-R693 ◽  
Author(s):  
B. A. Horwitz ◽  
J. S. Hamilton ◽  
K. S. Kott
Keyword(s):  
Binding Sites ◽  
Mitochondrial Protein ◽  
Substantial Reduction ◽  
Brown Fat ◽  
Short Photoperiod ◽  
Syrian Hamsters ◽  
Hydroxyacyl Coa Dehydrogenase ◽  
Brown Fat Mitochondria ◽  
Important Site ◽  
Thermogenic Capacity

Preparation for hibernation is accompanied by increased thermogenic capacity of brown fat (BAT), an important site of thermogenesis during arousal from hibernation. This study examined whether that thermogenic capacity is reduced in hibernation and reactivated during arousal. In one set of experiments, Syrian hamsters were exposed to short photoperiod (10:14 light-dark) and cold (7 degrees C). Those not hibernating at death (n = 10) served as controls for those that were (n = 9). A third group (n = 10) was killed 80–90 min after arousal was initiated by manual perturbation. Mitochondrial GDP binding (nmol/mg mitochondrial protein) was used to estimate thermogenic capacity. In a second experimental series, BAT citrate (si)-synthase and 3-hydroxyacyl-CoA dehydrogenase activities were measured in hibernating and nonhibernating hamsters. Although there were no differences in the maximum activities of these enzymes, GDP binding was markedly lower in the hibernators relative to the nonhibernators (0.214 +/- 0.031 vs. 0.535 +/- 0.039). However, in the partially aroused hamsters, GDP binding had doubled (0.438 +/- 0.04). Thus hibernation is accompanied by a substantial reduction of BAT thermogenic capacity (as manifested by GDP binding), which is reversed during arousal. The rapidity of this reversal indicates that it does not involve the synthesis of new GDP binding sites.

Weight gain and brown fat composition of mice selected for high body weight fed a high-fat diet

1990 ◽  
Vol 258 (3) ◽  
pp. R608-R615 ◽  
Author(s):  
M. Desautels ◽  
R. A. Dulos
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Succinate Dehydrogenase ◽  
Body Weight Gain ◽  
Fat Deposition ◽  
Brown Fat ◽  
High Fat ◽  
High Body Weight ◽  
High Body ◽  
Thermogenic Capacity

Mice selected for high body weight (QL522) had increased food intake, body weight gain, and fat deposition relative to mice without weight selection (QL521). Brown adipose tissue (BAT) thermogenic capacity, as determined by the tissue content of protein, DNA, and succinate dehydrogenase and by mitochondrial uncoupling protein content was similar or slightly higher in 2- and 10-mo-old QL522 mice relative to age-matched QL521 mice. When food intake of QL522 mice was restricted to the level of QL521 mice, body weight gain and fat deposition over 28 days were then comparable to those of QL521 mice. Food restriction had no effect on BAT composition of QL522 mice. Both QL521 and QL522 mice increased calorie intake by 40-50% when offered a palatable high-fat supplement (HF), but only QL522 mice increased weight gain and fat deposition significantly. QL521 mice fed a high-fat supplement showed a significant increase in brown fat succinate dehydrogenase content, whereas QL522 mice showed significant increases in brown fat weight, protein, and succinate dehydrogenase content relative to mice fed stock diet. Nonshivering thermogenic capacity, as assessed by norepinephrine-stimulated oxygen uptake in anesthetized animals at 30 degrees C was similar between QL521 and QL522 mice eating stock diet and was significantly increased by the high-fat supplement in both strains. Thus mice selected for high body weight are very susceptible to diet-induced obesity, and we have no evidence that a reduction in brown fat thermogenic capacity contributes to the increased fat deposition of QL522 mice as they grow old or when they are offered palatable energy-dense supplements.

Increased thermogenic capacity in brown fat mitochondria during tumor growth in the rat

1988 ◽  
Vol 8 (3) ◽  
pp. 327-332 ◽  
Author(s):  
Edward Preston ◽  
Joan Triandafillou ◽  
Nicholas Haas
Keyword(s):  
Tumor Growth ◽  
Brown Fat ◽  
Brown Fat Mitochondria ◽  
Thermogenic Capacity

Parallel measurements of heat production and thermogenin content in brown fat cells during cold acclimation of rats

1986 ◽  
Vol 6 (1) ◽  
pp. 31-38 ◽  
Author(s):  
Erik Steen Hansen ◽  
Jens Knudsen
Keyword(s):  
Cold Acclimation ◽  
Heat Production ◽  
Continuous Flow ◽  
Specific Protein ◽  
Competitive Elisa ◽  
Brown Fat ◽  
Fat Cells ◽  
Two Parameters ◽  
Parallel Measurements ◽  
Thermogenic Capacity

The maximum thermogenic capacity of brown fat cells from control and cold acclimated rats was measured using a continuous-flow microcalorimetric system, The content of the 32.000 D, brown fat specific protein, thermogenin, was measured in the cells used for heat production measurements by competitive ELISA. The ratio between the maximal thermogenic capacity and the amount ofthermogenin for control and cold acclimated rats was compared. It was found that the ratio between the two parameters decreased during cold acclimation due to a decrease in maximal thermogenic capacity and an increase in the amount ofthermogenin, indicating regulation of heat production either at thermogenin or receptor level.

scholarly journals UCP1 inhibition in Cidea-overexpressing mice is physiologically counteracted by brown adipose tissue hyperrecruitment

2017 ◽  
Vol 312 (1) ◽  
pp. E72-E87 ◽  
Author(s):  
Alexander W. Fischer ◽  
Irina G. Shabalina ◽  
Charlotte L. Mattsson ◽  
Gustavo Abreu-Vieira ◽  
Barbara Cannon ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Brown Fat ◽  
Transcriptional Level ◽  
Compensatory Mechanism ◽  
Adipose Tissues ◽  
Protein Levels ◽  
Brown Adipose ◽  
Specific Regulation ◽  
Thermogenic Capacity

Cidea is a gene highly expressed in thermogenesis-competent (UCP1-containing) adipose cells, both brown and brite/beige. Here, we initially demonstrate a remarkable adipose-depot specific regulation of Cidea expression. In classical brown fat, Cidea mRNA is expressed continuously and invariably, irrespective of tissue recruitment. However, Cidea protein levels are regulated posttranscriptionally, being conspicuously induced in the thermogenically recruited state. In contrast, in brite fat, Cidea protein levels are regulated at the transcriptional level, and Cidea mRNA and protein levels are proportional to tissue “briteness.” Although routinely followed as a thermogenic molecular marker, Cidea function is not clarified. Here, we employed a gain-of-function approach to examine a possible role of Cidea in the regulation of thermogenesis. We utilized transgenic aP2-hCidea mice that overexpress human Cidea in all adipose tissues. We demonstrate that UCP1 activity is markedly suppressed in brown-fat mitochondria isolated from aP2-hCidea mice. However, mitochondrial UCP1 protein levels were identical in wild-type and transgenic mice. This implies a regulatory effect of Cidea on UCP1 activity, but as we demonstrate that Cidea itself is not localized to mitochondria, we propose an indirect inhibitory effect. The Cidea-induced inhibition of UCP1 activity (observed in isolated mitochondria) is physiologically relevant since the mice, through an appropriate homeostatic compensatory mechanism, increased the total amount of UCP1 in the tissue to exactly match the diminished thermogenic capacity of the UCP1 protein and retain unaltered nonshivering thermogenic capacity. Thus, we verified Cidea as being a marker of thermogenesis-competent adipose tissues, but we conclude that Cidea, unexpectedly, functions molecularly as an indirect inhibitor of thermogenesis.

scholarly journals The Hepatokine TSK does not affect brown fat thermogenic capacity, body weight gain, and glucose homeostasis

2019 ◽  
Vol 30 ◽  
pp. 184-191 ◽  
Author(s):  
Mathilde Mouchiroud ◽  
Étienne Camiré ◽  
Manal Aldow ◽  
Alexandre Caron ◽  
Éric Jubinville ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Glucose Homeostasis ◽  
Body Weight Gain ◽  
Brown Fat ◽  
Thermogenic Capacity

Decreased testosterone levels do not mediate short-photoperiod-induced brown fat changes

1986 ◽  
Vol 251 (5) ◽  
pp. R963-R970 ◽  
Author(s):  
K. S. Kott ◽  
B. J. Moore ◽  
B. A. Horwitz
Keyword(s):  
Testosterone Level ◽  
Citrate Synthase ◽  
Hormone Secretion ◽  
Gonadal Hormones ◽  
Brown Fat ◽  
Short Photoperiod ◽  
Gonadal Hormone ◽  
Hydroxyacyl Coa Dehydrogenase ◽  
Long Photoperiod ◽  
Thermogenic Capacity

Previous studies showed that short photoperiod increased brown fat (BAT) mass and reduced gonadal size and gonadal hormone secretion in hamsters. The present study investigated the possibility that the effects on BAT were dependent on reduced levels of gonadal hormones. BAT from male Syrian hamsters exposed to short photoperiod for 10 wk was significantly greater in mass, protein content, and total maximal citrate synthase and beta-hydroxyacyl-CoA dehydrogenase activities than was BAT from long-photoperiod hamsters, These differences between short- and long-photoperiod exposure were observed in hamsters housed at 21 as well as at 8 degrees C. Short photoperiod also increased the total recovered mitochondrial GDP binding, a finding consistent with increased BAT thermogenic capacity. These short-photoperiod effects were neither mimicked by castration of long-photoperiod hamsters nor prevented by high levels of testosterone administered to short-photoperiod animals. Castration did attenuate the effects of short photoperiod on BAT growth if, after surgery and prior to short-photoperiod exposure, the animals were housed at a long photoperiod for 2-3 wk. In contrast, in hamsters immediately placed at short photoperiod after surgery, castration did not inhibit short-photoperiod effects. The present three experiments demonstrate that, in addition to increasing BAT mass, short photoperiod elevates the thermogenic capacity of BAT, and this elevation does not require the absence or a much reduced testosterone level.

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