Sarcolipin trumps β-adrenergic receptor signaling as the favored mechanism for muscle-based diet-induced thermogenesis
Sarcolipin trumps β-adrenergic receptor signaling as the favored mechanism for muscle-based diet-induced thermogenesis
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DOI：
10.1096/fj.13-230631
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发表时间：
2013-09-01
期刊：
影响因子：
4.8
通讯作者：
Tupling, A. Russell
中科院分区：
文献类型：
--
作者：
Bombardier, Eric;Smith, Ian C.;Tupling, A. Russell
Sarcolipin（SLN）调节基于肌肉的非颤抖性产热，并在高脂喂养（HFF）中上调。为了研究其他基于肌肉的产热系统是否补偿Sln的缺乏，并牢固地建立SLN作为饮食诱导的产热（DIT）的介体，我们测量了普通饲料和高脂肪喂养的Sln（-/-）和野生型（WT）小鼠的肌肉和全身能量消耗。在HFF之后，WT的静息肌肉代谢率（Vo（2），l/g/s）类似地增加（0.28 +/- 0.02对比0.31 +/- 0.03）和Sln（-/-）（0.23 +/- 0.03对比0.35 +/- 0.02）小鼠，由于Sln（-/-）小鼠中交感神经系统激活增加;然而，在HFF后，与WT小鼠相比，Sln（-/-）的全身代谢率（Vo（2），ml/kg/h）较低，但仅在小鼠在其笼中活动的时期（WT，2894 +/- 87 vs. Sln（-/-），2708 +/- 61）。在HFF期间用β-肾上腺素能受体（-AR）拮抗剂普萘洛尔治疗完全防止了Sln（-/-）小鼠中基于肌肉的DIT;然而，它对WT小鼠没有影响，导致全身代谢率和饮食诱导的体重增加差异更大。我们的研究结果表明，AR信号部分补偿了SLN的缺乏，以激活基于肌肉的DIT，但SLN是主要的和更有效的调解人。史密斯岛C.的方法，Gamu，D.，法哈尔多，弗吉尼亚州，Vigna，C.，塞耶河一、古普塔河C.的方法，Bal，N. C.的方法，Periasamy，M.，图普林A. R.肉脂素胜过肾上腺素能受体信号传导作为基于肌肉的饮食诱导产热的有利机制。
Sarcolipin (SLN) regulates muscle-based nonshivering thermogenesis and is up-regulated with high-fat feeding (HFF). To investigate whether other muscle-based thermogenic systems compensate for a lack of Sln and to firmly establish SLN as a mediator of diet-induced thermogenesis (DIT), we measured muscle and whole-body energy expenditure in chow- and high-fat-fed Sln(-/-) and wild-type (WT) mice. Following HFF, resting muscle metabolic rate (Vo(2), l/g/s) was increased similarly in WT (0.28 +/- 0.02 vs. 0.31 +/- 0.03) and Sln(-/-) (0.23 +/- 0.03 vs. 0.35 +/- 0.02) mice due to increased sympathetic nervous system activation in Sln(-/-) mice; however, whole-body metabolic rate (Vo(2), ml/kg/h) was lower in Sln(-/-) compared with WT mice following HFF but only during periods when the mice were active in their cages (WT, 2894 +/- 87 vs. Sln(-/-), 2708 +/- 61). Treatment with the -adrenergic receptor (-AR) antagonist propranolol during HFF completely prevented muscle-based DIT in Sln(-/-) mice; however, it had no effect in WT mice, resulting in greater differences in whole-body metabolic rate and diet-induced weight gain. Our results suggest that -AR signaling partially compensates for a lack of SLN to activate muscle-based DIT, but SLN is the primary and more effective mediator.Bombardier, E., Smith, I. C., Gamu, D., Fajardo, V. A., Vigna, C., Sayer, R. A., Gupta, S. C., Bal, N. C., Periasamy, M., Tupling, A. R. Sarcolipin trumps -adrenergic receptor signaling as the favored mechanism for muscle-based diet-induced thermogenesis.