Brown Adipose Tissue Exhibits a Glucose-Responsive Thermogenic Biorhythm in Humans
High abundance of brown adipose tissue (BAT) is linked to lower glycaemia in humans, leading to the belief that BAT may protect against diabetes. The relationship between BAT glucose utilization and systemic glucose homeostasis has not been defined. In this paper we have characterized glycaemic excu...
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Published in | Cell metabolism Vol. 23; no. 4; pp. 602 - 609 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
12.04.2016
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Subjects | |
Online Access | Get full text |
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Summary: | High abundance of brown adipose tissue (BAT) is linked to lower glycaemia in humans, leading to the belief that BAT may protect against diabetes. The relationship between BAT glucose utilization and systemic glucose homeostasis has not been defined. In this paper we have characterized glycaemic excursions and BAT thermogenic responses in human brown adipocytes, BAT explants, and healthy adults through supraclavicular temperature profiling, revealing their circadian coupling in vivo and in vitro, orchestrated by UCP1, GLUT4, and Rev-erbα biorhythms. Extent of glycated haemoglobin also correlated positively with environmental temperature among community-dwelling patients. These data uncover potential crosstalk between BAT and glucose regulatory pathways, evident on cellular, tissue, individual, and population levels, and provide impetus to search for BAT harnessing strategies for therapeutic purposes.
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•Brown fat utilizes glucose as substrate fuel to produce heat in humans•Human brown fat exhibits a thermogenic circadian rhythm•Brown fat circadian rhythm is glucose responsive•Low brown fat abundance is associated with greater glycaemic fluctuations
Lee et al. reveal how glucose utilization by brown fat in humans is coupled with heat production in a circadian manner. Higher brown fat abundance correlates with lesser glycemia variability, suggesting that brown fat may help buffer glucose fluctuations and maintain whole-body glucose homeostasis over time. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1550-4131 1932-7420 |
DOI: | 10.1016/j.cmet.2016.02.007 |