Brown Adipose Tissue and Seasonal Variation in Humans

Au-Yong, Iain; Thorn, Natasha; Ganatra, Rakesh; Perkins, Alan C.; Symonds, Michael

doi:10.2337/db09-0833

Cited by 232 publications

(220 citation statements)

References 26 publications

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“…The detectability of BAT by [ 18 F]fluorodeoxyglucose-PET-CT imaging at room temperature follows a circannual cycle, both in the northern and southern hemispheres (31)(32)(33), with low detectability of BAT in summer (i.e., short day) compared with winter (i.e., long day). Although differences in outside temperature over the year would be a likely explanation for this phenomenon, the detectability of BAT showed a stronger correlation with day length than with outside temperature (31). Based on our present data, the daily light exposure may thus well explain the circannual cycle of BAT detectability.…”

Section: Discussionmentioning

confidence: 99%

Prolonged daily light exposure increases body fat mass through attenuation of brown adipose tissue activity

Kooijman¹,

Berg²,

Ramkisoensing

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

121

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Disruption of circadian rhythmicity is associated with obesity and related disorders, including type 2 diabetes and cardiovascular disease. Specifically, prolonged artificial light exposure associates with obesity in humans, although the underlying mechanism is unclear. Here, we report that increasing the daily hours of light exposure increases body adiposity through attenuation of brown adipose tissue (BAT) activity, a major contributor of energy expenditure. Mice exposed to a prolonged day length of 16-and 24-h light, compared with regular 12-h light, showed increased adiposity without affecting food intake or locomotor activity. Mechanistically, we demonstrated that prolonged day length decreases sympathetic input into BAT and reduces β3-adrenergic intracellular signaling. Concomitantly, prolonging day length decreased the uptake of fatty acids from triglyceride-rich lipoproteins, as well as of glucose from plasma selectively by BAT. We conclude that impaired BAT activity is an important mediator in the association between disturbed circadian rhythm and adiposity, and anticipate that activation of BAT may overcome the adverse metabolic consequences of disturbed circadian rhythmicity. M odern world society is subjected to disturbances of circadian rhythms by shift work, sleep deprivation, and environmental light pollution. Importantly, the increasing prevalence of obesity is associated with a disrupted sleep-wake pattern in humans (1) and coincides with the availability of artificial light (2, 3). Additionally, a recent study revealed a relationship between exposure to light at night and obesity in a cross-sectional analysis of over 100,000 women (4). Light input is the most important cue for generation of circadian (∼24 h) rhythms by the master clock. Both in rodents and humans the master clock is situated in the suprachiasmatic nucleus (SCN) of the hypothalamus. The SCN is responsible for synchronization of peripheral clocks throughout the body, which is mediated by endocrine and neuronal signals (5). A causal role for a disturbed circadian rhythm in the development of obesity has been demonstrated by animal studies. Mice with genetically dysfunctional clock genes develop obesity and insulin resistance (6-9). Moreover, specific ablation of the SCN induces acute weight gain (10). These results indicate a crucial role for the SCN in the regulation of adiposity.Interestingly, we previously showed that prolonged light exposure only is sufficient to enhance weight gain in mice. Constant light disrupts the central circadian clock, evidenced by an immediate reduction in the circadian amplitude of SCN electrical activity. Moreover, constant light induces body weight gain and insulin resistance, even faster than high-fat diet, which was not caused by increased food intake or reduced locomotor activity (11). Therefore, disruption of the central biological clock likely induces weight gain by decreasing energy expenditure.Recently, it has been recognized that brown adipose tissue (BAT) importantly contributes to energy ...

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Section: Discussionmentioning

confidence: 99%

Prolonged daily light exposure increases body fat mass through attenuation of brown adipose tissue activity

Kooijman¹,

Berg²,

Ramkisoensing

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

121

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“…Body mass index (BMI) and body fat percentage is inversely related to BAT mass, and obese adult humans have low BAT mass, which increases following gastric banding surgery (57)(58)(59)(60). These findings have created significant interest in developing therapeutics that target BAT in humans for obesity therapy (27)(28)(29)(30)(31)(32).…”

Section: Discussionmentioning

confidence: 99%

Selective Kv1.3 channel blocker as therapeutic for obesity and insulin resistance

Upadhyay¹,

Eckel‐Mahan²,

Mirbolooki³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Obesity is an epidemic, calling for innovative and reliable pharmacological strategies. Here, we show that ShK-186, a selective and potent blocker of the voltage-gated Kv1.3 channel, counteracts the negative effects of increased caloric intake in mice fed a diet rich in fat and fructose. ShK-186 reduced weight gain, adiposity, and fatty liver; decreased blood levels of cholesterol, sugar, HbA1c, insulin, and leptin; and enhanced peripheral insulin sensitivity. These changes mimic the effects of Kv1.3 gene deletion. ShK-186 did not alter weight gain in mice on a chow diet, suggesting that the obesityinducing diet enhances sensitivity to Kv1.3 blockade. Several mechanisms may contribute to the therapeutic benefits of ShK-186. ShK-186 therapy activated brown adipose tissue as evidenced by a doubling of glucose uptake, and increased β-oxidation of fatty acids, glycolysis, fatty acid synthesis, and uncoupling protein 1 expression. Activation of brown adipose tissue manifested as augmented oxygen consumption and energy expenditure, with no change in caloric intake, locomotor activity, or thyroid hormone levels. The obesity diet induced Kv1.3 expression in the liver, and ShK-186 caused profound alterations in energy and lipid metabolism in the liver. This action on the liver may underlie the differential effectiveness of ShK-186 in mice fed a chow vs. an obesity diet. Our results highlight the potential use of Kv1.3 blockers for the treatment of obesity and insulin resistance.

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“…A higher percentage of individuals, as we might expect based on this hypothesis, present BAT-positive PET-FDG in winter (62,63,67), even when am bient temperature is controlled (63). Another fascinating theory that helps to explain this difference is that photoperiod could also interfere with BAT recruitment (63).…”

Section: What Is the Real Prevalence Of Brown Adipose Tissue? Conceptmentioning

confidence: 76%

“…In Brazil, there are no published studies on this subject, but unpublished data suggests even lower levels. Table 2 highlights differences in BAT uptake in different populations, in ambient temperature and after cold exposure (12,13,14,23,30,38,(62)(63)(64)(65)(66)(67) What could the reason be for such differences considering similar protocols?…”

Section: What Is the Real Prevalence Of Brown Adipose Tissue? Conceptmentioning

confidence: 99%

“…Another fascinating theory that helps to explain this difference is that photoperiod could also interfere with BAT recruitment (63). As the days start to get shorter, in anticipation of winter, BAT may slowly be recruited, in order to have sufficient levels ready for when the cold starts, and preventing body thermoneutrality from being reliant upon shivering.…”

Section: What Is the Real Prevalence Of Brown Adipose Tissue? Conceptmentioning

confidence: 99%

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Brown adipose tissue: what have we learned since its recent identification in human adults

Halpern

Mancini

Halpern

2014

Arq Bras Endocrinol Metab

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Brown adipose tissue, an essential organ for thermoregulation in small and hibernating mammals due to its mitochondrial uncoupling capacity, was until recently considered to be present in humans only in newborns. The identification of brown adipose tissue in adult humans since the development and use of positron emission tomography marked with 18-fluorodeoxyglucose (PET-FDG) has raised a series of doubts and questions about its real importance in our metabolism. In this review, we will discuss what we have learnt since its identification in humans as well as both new and old concepts, some of which have been marginalized for decades, such as diet-induced thermogenesis. Arq Bras Endocrinol Metab. 2014;58(9):889-99 Keywords Brown adipose tissue; obesity; thermogenesis; UCP-1; energy expenditure RESUMO O tecido adiposo marrom, órgão essencial para a termorregulação de animais hibernantes e pequenos devido à sua capacidade desacopladora, era até poucos anos considerado presente apenas em recém-nascidos na espécie humana. A identificação do tecido adiposo marrom em adultos com o desenvolvimento e uso da tomografia de emissão de pósitron marcado com 18-fluorodesoxiglicose (PET-FDG) gerou questões sobre sua real importância para nosso metabolismo. Nesta revisão, discutiremos o que aprendemos nesse tempo, assim como conceitos antigos e novos, alguns marginalizados por décadas, como a termogênese induzida por dieta. Arq Bras Endocrinol Metab. 2014;58(9):889-99 Descritores

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Brown Adipose Tissue and Seasonal Variation in Humans

Cited by 232 publications

References 26 publications

Prolonged daily light exposure increases body fat mass through attenuation of brown adipose tissue activity

Prolonged daily light exposure increases body fat mass through attenuation of brown adipose tissue activity

Selective Kv1.3 channel blocker as therapeutic for obesity and insulin resistance

Brown adipose tissue: what have we learned since its recent identification in human adults

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