scholarly journals MRI Reveals Human Brown Adipose Tissue Is Rapidly Activated in Response to Cold

2019 ◽  
Vol 3 (12) ◽  
pp. 2374-2384 ◽  
Author(s):  
Stephan M Oreskovich ◽  
Frank J Ong ◽  
Basma A Ahmed ◽  
Norman B Konyer ◽  
Denis P Blondin ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Time Course ◽  
Whole Body ◽  
Proton Density ◽  
Fat Percentage ◽  
Similar Time ◽  
Brown Adipose ◽  
Posterior Neck

Abstract Context In rodents, cold exposure induces the activation of brown adipose tissue (BAT) and the induction of intracellular triacylglycerol (TAG) lipolysis. However, in humans, the kinetics of supraclavicular (SCV) BAT activation and the potential importance of TAG stores remain poorly defined. Objective To determine the time course of BAT activation and changes in intracellular TAG using MRI assessment of the SCV (i.e., BAT depot) and fat in the posterior neck region (i.e., non-BAT). Design Cross-sectional. Setting Clinical research center. Patients or Other Participants Twelve healthy male volunteers aged 18 to 29 years [body mass index = 24.7 ± 2.8 kg/m2 and body fat percentage = 25.0% ± 7.4% (both, mean ± SD)]. Intervention(s) Standardized whole-body cold exposure (180 minutes at 18°C) and immediate rewarming (30 minutes at 32°C). Main Outcome Measure(s) Proton density fat fraction (PDFF) and T2* of the SCV and posterior neck fat pads. Acquisitions occurred at 5- to 15-minute intervals during cooling and subsequent warming. Results SCV PDFF declined significantly after only 10 minutes of cold exposure [−1.6% (SE: 0.44%; P = 0.007)] and continued to decline until 35 minutes, after which time it remained stable until 180 minutes. A similar time course was also observed for SCV T2*. In the posterior neck fat (non-BAT), there were no cold-induced changes in PDFF or T2*. Rewarming did not result in a change in SCV PDFF or T2*. Conclusions The rapid cold-induced decline in SCV PDFF suggests that in humans BAT is activated quickly in response to cold and that TAG is a primary substrate.

Rapid changes in metabolic cold defense and GDP binding to brown adipose tissue mitochondria of rat pups

1993 ◽  
Vol 264 (5) ◽  
pp. R1017-R1023 ◽  
Author(s):  
G. Kortner ◽  
K. Schildhauer ◽  
O. Petrova ◽  
I. Schmidt
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Time Course ◽  
Developmental Changes ◽  
Whole Body ◽  
Rat Pups ◽  
Brown Adipose ◽  
Rapid Changes ◽  
Whole Body Metabolism

To determine developmental changes of brown adipose tissue (BAT) thermogenic activity at defined circadian and thermal states, we evaluated the time course of cold-induced increases of in vitro guanosine 5'-diphosphate (GDP) binding in parallel with whole body metabolism (oxygen consumption, VO2) and core temperature (Tc) in 1- to 11-day-old rat pups. During the maximum phase of the juvenile diurnal cycle, Tc of littermates was recorded continuously and VO2 alternately until 2 min before animals were killed for removal of interscapular BAT. GDP binding after 1.5 h at thermoneutrality and its increase during physiologically comparable cold loads were significantly lower in 1-day-old pups than in 5- and 11-day-old pups. Cold defense was activated more rapidly in the older pups, but GDP binding in even the 1-day-old pups was significantly increased during the second 10-min period of cold exposure. We conclude that rapid changes in thermogenic activity, in connection with the known developmental changes in the dependence of the suckling rat's metabolic cold defense on maternal and sibling contact and circadian phase, will distort longitudinal studies of any fast-changing BAT parameter when the conditions immediately before tissue removal are not thoroughly controlled.

scholarly journals Cold exposure regulates the norepinephrine uptake transporter in rat brown adipose tissue

1999 ◽  
Vol 276 (1) ◽  
pp. R143-R151 ◽  
Author(s):  
Victoria L. King ◽  
Linda P. Dwoskin ◽  
Lisa A. Cassis
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Kinetic Parameters ◽  
Cold Exposure ◽  
Time Course ◽  
Neuronal Uptake ◽  
Interscapular Brown Adipose Tissue ◽  
High Affinity ◽  
Brown Adipose ◽  
And Control

The neuronal uptake of norepinephrine (NE) in sympathetically innervated tissues is mediated by a high-affinity NE uptake transporter (NET). Rat interscapular brown adipose tissue (ISBAT) is densely innervated by the sympathetic nervous system for the control of cold- and diet-induced thermogenesis. To determine if cold exposure regulates the NET, kinetic parameters for [3H]NE uptake and [3H]nisoxetine (Nis) binding were determined in ISBAT from 7-day cold-exposed (CE) and control rats. Uptake of [3H]NE in ISBAT slices was of high affinity (1.6 μM). After 7 days of cold exposure the affinity for [3H]NE uptake was not altered; however, the uptake capacity was decreased (38%) in ISBAT slices from CE rats. Kinetic parameters for [3H]Nis binding demonstrated a single high-affinity site in ISBAT from CE and control rats with similar affinity. The density of [3H]Nis sites in ISBAT was decreased (38%) following cold exposure. A time course (2 h-7 days) for cold exposure demonstrated downregulation of [3H]Nis binding density by day 3, which remained through day 7. The affinity for [3H]Nis binding was transiently decreased at 2 h of cold exposure. Similarly, ISBAT NE content was decreased at 2 h of cold exposure. Pair feeding CE rats to food intake of controls normalized plasma NE content; however, [3H]Nis binding density in ISBAT remained decreased in pair-fed rats. These results demonstrate that the ISBAT NET is downregulated following cold exposure. Reductions in ISBAT NE content precede alterations in NET density; however, plasma NE content is not related to regulation of the NET.

scholarly journals Brown adipose tissue is involved in the seasonal variation of cold-induced thermogenesis in humans

2016 ◽  
Vol 310 (10) ◽  
pp. R999-R1009 ◽  
Author(s):  
Takeshi Yoneshiro ◽  
Mami Matsushita ◽  
Satoshi Nakae ◽  
Toshimitsu Kameya ◽  
Hiroki Sugie ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Multivariate Regression Analysis ◽  
Tympanic Temperature ◽  
Whole Body ◽  
Dependent Manner ◽  
Significant Interaction Effect ◽  
Brown Adipose ◽  
The Impact

Brown adipose tissue (BAT) contributes to whole body energy expenditure (EE), especially cold-induced thermogenesis (CIT), in humans. Although it is known that EE and CIT vary seasonally, their relationship with BAT has not been investigated. In the present study, we examined the impact of BAT on seasonal variations of EE/CIT and thermal responses to cold exposure in a randomized crossover design. Forty-five healthy male volunteers participated, and their BAT was assessed by positron emission tomography and computed tomography. CIT, the difference of EE at 27°C and after 2-h cold exposure at 19°C, significantly increased in winter compared with summer, being greater in subjects with metabolically active BAT (High BAT, 185.6 kcal/day vs. 18.3 kcal/day, P < 0.001) than those without (Low BAT, 90.6 kcal/day vs. −46.5 kcal/day, P < 0.05). Multivariate regression analysis revealed a significant interaction effect between season and BAT on CIT ( P < 0.001). The cold-induced drop of tympanic temperature (Tty) and skin temperature (Tskin) in the forehead region and in the supraclavicular region close to BAT deposits were smaller in the High BAT Group than in the Low BAT Group in winter but not in summer. In contrast, the drop of Tskin in the subclavicular and peripheral regions distant from BAT was similar in the two groups in both seasons. In conclusion, CIT increased from summer to winter in a BAT-dependent manner, paralleling cold-induced changes in Tty/Tskin, indicating a role of BAT in seasonal changes in the thermogenic and thermal responses to cold exposure in humans.

scholarly journals Chronic cold exposure induces autophagy to promote fatty acid oxidation, mitochondrial turnover, and thermogenesis in brown adipose tissue

iScience ◽  
2021 ◽  
pp. 102434
Author(s):  
Winifred W. Yau ◽  
Kiraely Adam Wong ◽  
Jin Zhou ◽  
Nivetha Kanakaram Thimmukonda ◽  
Yajun Wu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Fatty Acid Oxidation ◽  
Cold Exposure ◽  
Acid Oxidation ◽  
Brown Adipose ◽  
Mitochondrial Turnover

Reduced brown adipose tissue activity during cold exposure is a metabolic feature of the human thrifty phenotype

Metabolism ◽  
2021 ◽  
Vol 117 ◽  
pp. 154709 ◽  
Author(s):  
Tim Hollstein ◽  
Karyne Vinales ◽  
Kong Y. Chen ◽  
Aaron M. Cypess ◽  
Alessio Basolo ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Thrifty Phenotype ◽  
Brown Adipose ◽  
Metabolic Feature ◽  
Brown Adipose Tissue Activity

scholarly journals The Role of AMPK Signaling in Brown Adipose Tissue Activation

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1122
Author(s):  
Jamie I. van der van der Vaart ◽  
Mariëtte R. Boon ◽  
Riekelt H. Houtkooper
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Whole Body ◽  
Ampk Signaling ◽  
Mitochondrial Homeostasis ◽  
Brown Adipose ◽  
Metabolic Stresses ◽  
Amp Activated Protein Kinase ◽  
Body Energy

Obesity is becoming a pandemic, and its prevalence is still increasing. Considering that obesity increases the risk of developing cardiometabolic diseases, research efforts are focusing on new ways to combat obesity. Brown adipose tissue (BAT) has emerged as a possible target to achieve this for its functional role in energy expenditure by means of increasing thermogenesis. An important metabolic sensor and regulator of whole-body energy balance is AMP-activated protein kinase (AMPK), and its role in energy metabolism is evident. This review highlights the mechanisms of BAT activation and investigates how AMPK can be used as a target for BAT activation. We review compounds and other factors that are able to activate AMPK and further discuss the therapeutic use of AMPK in BAT activation. Extensive research shows that AMPK can be activated by a number of different kinases, such as LKB1, CaMKK, but also small molecules, hormones, and metabolic stresses. AMPK is able to activate BAT by inducing adipogenesis, maintaining mitochondrial homeostasis and inducing browning in white adipose tissue. We conclude that, despite encouraging results, many uncertainties should be clarified before AMPK can be posed as a target for anti-obesity treatment via BAT activation.

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