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Brown adipose tissue: function and physiological significance.
TLDR
The development of brown adipose tissue with its characteristic protein, uncoupling protein-1 (UCP1), was probably determinative for the evolutionary success of mammals, as its thermogenesis enhances neonatal survival and allows for active life even in cold surroundings.
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Chronic Peroxisome Proliferator-activated Receptor γ (PPARγ) Activation of Epididymally Derived White Adipocyte Cultures Reveals a Population of Thermogenically Competent, UCP1-containing Adipocytes…
TLDR
It is reported here that chronic treatment with the peroxisome proliferator-activated receptor γ agonist rosiglitazone promotes not only the expression of PGC-1α and mitochondriogenesis in these cells but also a norepinephrine-augmentable UCP1 gene expression in a significant subset of the cells, providing these cells with a genuine thermogenic capacity.
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Unexpected evidence for active brown adipose tissue in adult humans.
TLDR
It is concluded that a substantial fraction of adult humans possess active brown adipose tissue that thus has the potential to be of metabolic significance for normal human physiology as well as to become pharmaceutically activated in efforts to combat obesity.
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UCP1 ablation induces obesity and abolishes diet-induced thermogenesis in mice exempt from thermal stress by living at thermoneutrality.
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Nonshivering thermogenesis and its adequate measurement in metabolic studies
Summary Alterations in nonshivering thermogenesis are presently discussed as being both potentially causative of and able to counteract obesity. However, the necessity for mammals to defend their…
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The presence of UCP1 demonstrates that metabolically active adipose tissue in the neck of adult humans truly represents brown adipose tissue
TLDR
It is demonstrated that human adults indeed possess BAT and thus imply possibilities of future therapeutic strategies for the treatment of obesity, including maintenance of brown adipocytes and stimulation of the growth of preexisting brown precursors.
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Only UCP1 can mediate adaptive nonshivering thermogenesis in the cold
TLDR
Not even during prolonged and enhanced demand for extra heat production was any endogenous hormone or neurotransmitter able to recruit any UCP1‐independent adaptive nonshivering thermogenic process in muscle or in any other organ, and no proteins other than U CP1—not even UCP2 or UCP3—therefore have the ability to mediate adaptive nonsHivering thermogenesis in the cold.
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UCP1 in brite/beige adipose tissue mitochondria is functionally thermogenic.
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The browning of white adipose tissue: some burning issues.
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Recruited vs. nonrecruited molecular signatures of brown, "brite," and white adipose tissues.
TLDR
The effect of physiologically induced recruitment of thermogenic function (cold acclimation) on the expression pattern of the genes was quantified; in general, the depot pattern dominated over the recruitment effects.
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