冷気は体重を減少させる

先行して、日本人の研究で、17度1日2時間暴露×６週間で体重減少の報告あったとのこと
今回は、6時間×10日間で、熱産生・カロリー消費褐色脂肪増加させ、15度程度で、快適に寒気なくこの効果があったとのこと。

若年・中年では、寒気なしの熱産生は数パーセントから30％へエネルギー負債増加させることができる。

Cold exposure – an approach to increasing energy expenditure in humans
Wouter van Marken Lichtenbelt, et.al.
Trends in Endocrinology & Metabolism

(pdf)

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http://www.sciencedirect.com/science/article/pii/S1043276013002099

Fuel utilization in brown adipocytes. 
The schematic shows a summary of fatty acid (FA) sensing, uptake and oxidation pathways, as well as glucose uptake and downstream metabolism pathways in a typical brown adipocyte.
Shown are glucose uptake by glucose transporters (GLUT), including GLUT translocation stimulated by adrenergic signaling, and the fate of glucose in de novo lipogenesis, storage as glycogen, or conversion to pyruvate and mitochondrial oxidation.
 FAs are sensed by G protein-coupled receptors (GPCRs) and possibly also CD36, and are taken up by CD36 and fatty acid transport proteins (FATPs).
Lipoprotein lipase (LPL) produced and secreted by adipocytes after adrenergic stimulation is also able to break down triglyceride (TG)-rich lipoproteins (TRLs), providing additional lipid fuel for uptake.
FAs activate mitochondrial UCP1 (uncoupling protein 1), as does activation from the sympathetic nervous system and adrenergic signaling [via adrenergic receptors (Rs)], enabling energy expenditure via thermogenesis.
FAs also become available from the lipolysis of lipid droplets (which is partially regulated by lipid droplet-associated proteins).
FAs may be elongated and/or converted to acyl-carnitine for transport into the mitochondria via the carnitine shuttle, where they become fuel for β-oxidation.
Fatty acid binding proteins (FABPs) also contribute to intracellular FA handling. Additional abbreviation: CPT1, carnitine palmityl-transferase 1.