Effect of Acute Cold Exposure on the Expression of the Adiponectin, Resistin and Leptin Genes in Rat White and Brown Adipose Tissues

2002 ◽  
Vol 34 (11/12) ◽  
pp. 629-634 ◽  
Author(s):  
M. Puerta ◽  
M. Abelenda ◽  
M. Rocha ◽  
P. Trayhurn
Keyword(s):  
Cold Exposure ◽  
Adipose Tissues ◽  
Acute Cold Exposure ◽  
Brown Adipose

Changes in brown adipose tissues and coxsackievirus B pathogenesis in mice on acute and chronic cold exposure

1970 ◽  
Vol 16 (9) ◽  
pp. 833-839 ◽  
Author(s):  
E. I. Grodums ◽  
G. Dempster
Keyword(s):  
Cold Exposure ◽  
Morphological Changes ◽  
Myocardial Damage ◽  
Adipose Tissues ◽  
Clear Cut ◽  
Acute Cold Exposure ◽  
Coxsackievirus B ◽  
Brown Adipose ◽  
The Brain ◽  
Adipose Cells

On acute cold exposure the normal brown adipose cells in the mouse interscapular pad underwent morphological changes apparently as a result of loss and redistribution of the intracellular lipid globules; on continued cold exposure the globules increased in numbers and size. If adult female mice were inoculated with coxsackievirus B-3 during acute cold exposure and returned to normal room temperature soon afterwards, the viral damage in the brown adipose tissues was seriously aggravated; if on the other hand they were left in the cold for the duration of the infection, the damage was aggravated to a lesser degree. Finally, if cold-acclimated mice were inoculated the lesion was localized in one area of the pad.In contrast, the myocardial damage was aggravated only in those mice which were inoculated during acute cold exposure and left in the cold. The cox. B-3 pathogenesis in the brain showed no clear-cut variations resulting from changes in the ambient temperature. The infectious amount of virus recovered from the heart and brain appeared to be greater and persist longer, if the mice were subjected to a prolonged cold exposure.The cold exposure, however, failed completely to increase the age susceptibility of mice to cox. B-2.

scholarly journals Treatment with atrial natriuretic peptide induces adipose tissue browning and exerts thermogenic actions in vivo

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Haruka Kimura ◽  
Tomohisa Nagoshi ◽  
Yuhei Oi ◽  
Akira Yoshii ◽  
Yoshiro Tanaka ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Hepatic Steatosis ◽  
Cold Exposure ◽  
Lipid Droplets ◽  
Adipose Tissues ◽  
Brown Adipose ◽  
Ucp1 Expression ◽  
Tissue Browning

AbstractIncreasing evidence suggests natriuretic peptides (NPs) coordinate inter-organ metabolic crosstalk with adipose tissues and play a critical role in energy metabolism. We recently reported A-type NP (ANP) raises intracellular temperature in cultured adipocytes in a low-temperature-sensitive manner. We herein investigated whether exogenous ANP-treatment exerts a significant impact on adipose tissues in vivo. Mice fed a high-fat-diet (HFD) or normal-fat-diet (NFD) for 13 weeks were treated with or without ANP infusion subcutaneously for another 3 weeks. ANP-treatment significantly ameliorated HFD-induced insulin resistance. HFD increased brown adipose tissue (BAT) cell size with the accumulation of lipid droplets (whitening), which was suppressed by ANP-treatment (re-browning). Furthermore, HFD induced enlarged lipid droplets in inguinal white adipose tissue (iWAT), crown-like structures in epididymal WAT, and hepatic steatosis, all of which were substantially attenuated by ANP-treatment. Likewise, ANP-treatment markedly increased UCP1 expression, a specific marker of BAT, in iWAT (browning). ANP also further increased UCP1 expression in BAT with NFD. Accordingly, cold tolerance test demonstrated ANP-treated mice were tolerant to cold exposure. In summary, exogenous ANP administration ameliorates HFD-induced insulin resistance by attenuating hepatic steatosis and by inducing adipose tissue browning (activation of the adipose tissue thermogenic program), leading to in vivo thermogenesis during cold exposure.

The development of insulin resistance in brown adipose tissue may impair the acute cold-induced activation of thermogenesis in genetically obese (ob/ob) mice

1984 ◽  
Vol 4 (11) ◽  
pp. 933-940 ◽  
Author(s):  
Stewart W. Mercer ◽  
Paul Trayhurn
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Brown Fat ◽  
Acute Cold Exposure ◽  
Brown Adipose

Genetically obese (ob/ob) mice develop insulin resistance in brown adipose tissue during the fifth week of life. Prior to this, at 26 days of age, oh/oh mice show a substantial increase in GDP binding to brownadipose-tissue mitochondria during acute cold exposure. When insulin resistance in brown fat develops, by 35 days of age, the increase in GDP binding in response to cold is markedly reduced. Studies with 2-deoxyglucose suggest that insulin resistance in brown adipose tissue could impair thermogenic responsiveness during acute cold exposure by limiting the ability of the tissue to take up glucose.

scholarly journals Melatonin deficiency decreases brown adipose tissue acute thermogenic capacity in rats measured by 18F-FDG PET

2020 ◽  
Author(s):  
Bruno Halpern ◽  
Marcio C Mancini ◽  
Caroline Mendes ◽  
Camila Maria Longo Machado ◽  
Silvana Prando ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Mrna Expression ◽  
Cold Exposure ◽  
Fdg Pet ◽  
Room Temperature ◽  
Bat Activity ◽  
Acute Cold Exposure ◽  
Brown Adipose ◽  
Thermogenic Capacity

Abstract Objective: Melatonin has been shown to increase brown adipose tissue (BAT) mass, which can lead to important metabolic effects, such as bodyweight reduction and glycemic improvement. However, BAT mass can only be measured invasively and. the gold standard for non-invasive measurement of BAT activity is positron emission tomography with 2-deoxy-2-[fluorine-18] fluoro-D-glucose (18F-FDG PET). There is no study, to our knowledge, that has evaluated if melatonin influences BAT activity, measured by this imaging technique in animals. Methods: Three experimental groups of Wistar rats (control, pinealectomy, and pinealectomy replaced with melatonin) had an 18F-FDG PET performed at room temperature and after acute cold exposure. The ratio of increased BAT activity after cold exposure/room temperature was called “acute thermogenic capacity” (ATC) We also measured UCP-1 mRNA expression to correlate with the 18F-FDG PET results. Results: Pinealectomy led to reduced acute thermogenic capacity, compared with the other groups, as well as reduced UCP1 mRNA expression.Conclusion: Melatonin deficiency impairs BAT response when exposed to acute cold exposure. These results can lead to future studies of the influence of melatonin on BAT, in animals and humans, without needing an invasive evaluation of BAT.

Relationship between cold-induced thermoregulation and spontaneous rapid body weight loss of aging F344 rats

1996 ◽  
Vol 271 (5) ◽  
pp. R1115-R1122 ◽  
Author(s):  
R. B. McDonald ◽  
M. Florez-Duquet ◽  
C. Murtagh-Mark ◽  
B. A. Horwitz
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Physiological State ◽  
Rapid Weight Loss ◽  
Acute Cold Exposure ◽  
Brown Adipose ◽  
F344 Rats

We previously showed that, although cold-induced thermoregulation is attenuated in 26-mo-old male Fischer 344 (F344) rats, not all rats this age exhibit the same degree of cold-exposed hypothermia or diminished brown adipose tissue nonshivering thermogenic capacity. Examination of this heterogeneity suggested the hypothesis that it was associated with a difference in the physiological state between aged rats that were maintaining stable body weight versus those showing the rapid weight loss often occurring near the end of the rat's natural life span. To test this, we acutely exposed male F344 rats to cold (4 h at 6 degrees C) beginning at 24 mo of age. This exposure was weekly for the first 2 wk and then on alternate weeks as long as the rat's body weight was stable. If body weight progressively declined for 3-5 consecutive days, the rat's response to the acute cold exposure was again measured, as was that of two additional rats not displaying this rapid loss in body weight. If body temperature decreased during the cold exposure to intraperitoneal temperatures < or = 32.5 degrees C, the rat was killed with pentobarbital sodium and interscapular brown adipose tissue was removed. One of the age-matched controls was also killed at this time. The age at which body weight showed a spontaneous rapid decline ranged from 24.5 to 29 mos. All eight rats displaying spontaneous rapid weight loss had significant hypothermia during the acute cold exposure, whereas none of the eight weight-stable rats did. The development of hypothermia in the spontaneous rapid weight loss group was not, in general, observed before their weight loss. The weight loss and hypothermia were associated with lower levels of brown fat uncoupling protein and significant changes in body fat and protein. These data suggest that the development of senescence-related hypothermia occurs rapidly and is not a simple function of chronological age or the median life span of the animals. Furthermore, these data imply that the rate of aging in terms of maintenance of thermoregulatory homeostasis has both a gradual and rapid component, the latter being associated with a different physiological state than the former.

Thermogenic effect of triiodothyroacetic acid at low doses in rat adipose tissue without adverse side effects in the thyroid axis

2008 ◽  
Vol 294 (4) ◽  
pp. E688-E697 ◽  
Author(s):  
G. Medina-Gomez ◽  
R. M. Calvo ◽  
M.-J. Obregon
Keyword(s):  
Adipose Tissue ◽  
Cold Exposure ◽  
Uncoupling Protein ◽  
Thyroid Stimulating Hormone ◽  
Low Doses ◽  
Adipose Tissues ◽  
Brown Adipose ◽  
Thyroid Axis ◽  
Rat Adipose Tissue

Triiodothyroacetic acid (TRIAC) is a physiological product of triiodothyronine (T3) metabolism, with high affinity for T3 nuclear receptors. Its interest stems from its potential thermogenic effects. Thus this work aimed 1) to clarify these thermogenic effects mediated by TRIAC vs. T3 in vivo and 2) to determine whether they occurred predominantly in adipose tissues. To examine this, control rats were infused with equimolar T3 or TRIAC doses (0.8 or 4 nmol·100 g body wt−1·day−1) or exposed for 48 h to cold. Both T3 doses and only the highest TRIAC dose inhibited plasma and pituitary thyroid-stimulating hormone (TSH) and thyroxine (T4) in plasma and tissues. Interestingly, the lower TRIAC dose marginally inhibited plasma T4. T3 infusion increased plasma and tissue T3 in a tissue-specific manner. The highest TRIAC dose increased TRIAC concentrations in plasma and tissues, decreasing plasma T3. TRIAC concentrations in tissues were <10% those of T3. Under cold exposure or high T3 doses, TRIAC increased only in white adipose tissue (WAT). Remarkably, only the lower TRIAC dose activated thermogenesis, inducing ectopic uncoupling protein (UCP)-1 expression in WAT and maximal increases in UCP-1, UCP-2, and lipoprotein lipase (LPL) expression in brown adipose tissue (BAT), inhibiting UCP-2 in muscle and LPL in WAT. TRIAC, T3, and cold exposure inhibited leptin secretion and mRNA in WAT. In summary, TRIAC, at low doses, induces thermogenic effects in adipose tissues without concomitant inhibition of TSH or hypothyroxinemia, suggesting a specific role regulating energy balance. This selective effect of TRIAC in adipose tissues might be considered a potential tool to increase energy metabolism.

Brown fat mediates increased energy expenditure of cold-exposed overfed neonatal rats

1986 ◽  
Vol 251 (3) ◽  
pp. R518-R524
Author(s):  
B. J. Moore ◽  
J. S. Stern ◽  
B. A. Horwitz
Keyword(s):  
Energy Expenditure ◽  
Cold Exposure ◽  
Rapid Onset ◽  
Brown Fat ◽  
O2 Consumption ◽  
Neonatal Rats ◽  
Ambient Temperatures ◽  
Rat Pups ◽  
Acute Cold Exposure ◽  
Brown Adipose

Genetically lean rat pups, overfed by being raised in small litters of three from day 1 postpartum, rapidly become obese compared with pups raised in standard sized litters of eight. Because of the rapid onset of their obesity, we expected that overfed pups would exhibit defective brown fat thermogenesis as is seen in neonatal genetically obese rodents. O2 consumption (VO2) was measured in 2-, 4-, 6-, and 8-day-old homozygous lean (Fa/Fa) Zucker pups from each treatment. We determined minimum rate of VO2 at thermoneutrality and maximum VO2 in response to progressively colder ambient temperatures. Overfed pups were fatter than standard-fed pups (P less than 0.001). But contrary to our prediction, overfed pups had a significantly increased maximum VO2 in response to acute cold exposure. To test the hypothesis that brown fat mediated the increased VO2 in the overfed pups, scapular brown fat lipectomies were performed on a new group of overfed pups at 2 days of age and compared with sham-operated littermate controls. On day 8, no differences in minimum VO2 were seen at thermoneutrality when brown fat is turned off. But maximum VO2 in response to cold, when brown fat is turned on maximally, was significantly reduced in the lipectomized overfed pups compared with sham-operated overfed littermates. These data suggest that manipulations of diet, accomplished by raising pups in small litters, can increase brown fat thermogenic function. The results of the lipectomy experiment imply that brown adipose tissue is a primary mediator of the increased energy expenditure in response to acute cold exposure in the overfed pups.

scholarly journals Cold Exposure Differentially Stimulates Angiogenesis in BAT and WAT of Mice: Implication in Adrenergic Activation

2017 ◽  
Vol 42 (3) ◽  
pp. 974-986 ◽  
Author(s):  
Xiao Luo ◽  
Ru Jia ◽  
Xiao-qin Luo ◽  
Guan Wang ◽  
Qiang-ling Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cold Exposure ◽  
Angiogenic Factors ◽  
Adipose Tissues ◽  
Interscapular Brown Adipose Tissue ◽  
White Adipocytes ◽  
Adrenoceptor Agonist ◽  
Brown Adipose

Background/Aims: To characterize the temporal profile of cold-induced angiogenesis in brown and white adipose tissues of mice in vivo and the temporal changes of angiogenic factors in primary mice brown (BA) and white adipocytes (WA) treated with β3-adrenoceptor agonist (CL316,243) in vitro. Methods: 8-week old male C57BL/6J mice were individually housed in conventional cages under cold exposure (4°C) for 1, 2, 3, 4 and 5 days. Interscapular brown adipose tissue (iBAT), inguinal subcutaneous (sWAT) and epididymal white adipose tissues (eWAT) were harvested for immunohistochemical and gene expression analysis. In vitro, primary mice BA and WA treated with or without CL316,243 were harvested for gene expression and protein secretion analysis. Results: A combination of morphological and genetic (Vegfa, Vegfr2, Hif-1α, Pai1 and Pedf) analyses demonstrated depot-specific angiogenesis in response to cold exposure. Upon CL316,243 treatment, angiogenic factors (Vegfa, Vegfr2, Hif-1α, Pai1 and Pedf) and secreted protein VEGFA were transiently increased in both BA and WA. Conclusion: Our results show that iBAT is highly responsive to cold-induced angiogenesis that is mainly supported by sWAT with a lesser extent by eWAT. Moreover, the angiogenesis is a transient process with the angiogenic factors may work in an autocrine/paracrine manner.

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