Combining a β3 adrenergic receptor agonist with alpha-lipoic acid reduces inflammation in male mice with diet-induced obesity.
Combining a β3 adrenergic receptor agonist with alpha-lipoic acid reduces inflammation in male mice with diet-induced obesity.
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DOI:
10.1002/oby.23309
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发表时间:
2022-01
期刊:
影响因子:
--
通讯作者:
Cypess AM
中科院分区:
文献类型:
--
作者:
Abdul Sater Z;Cero C;Pierce AE;Lea HJ;Abdul Sater H;Zhu KY;Liu N;Ma Y;Gavrilova O;Cypess AM
β3-adrenoceptors (β3-AR) stimulate lipolysis and thermogenesis in white and brown adipose tissue. Obesity increases oxidative stress and inflammation that attenuate adipose tissue (AT) β3-AR signaling. To test the hypothesis that the combination of the β3-AR agonist CL-316,243 (CL) and the antioxidant alpha-lipoic acid (ALA) would lower inflammation in diet-induced obesity (DIO) and improve β3-AR function. A total of 40 DIO mice were separated into four groups: Control (per os [PO] and intraperitoneal [IP] vehicle); CL alone (0.01 mg/kg IP daily); ALA alone (250 mg/kg in drinking water); or ALA+CL combination, all for 5 weeks. Food intake was similar in all groups, yet mice receiving ALA+CL showed improved body composition and inflammation: lower body weight [+1.7g Control vs. −2.5g ALA+CL (−7%); P<0.01] and % body fat (−9%, P < 0.001). Systemic and epididymal WAT (epiWAT) inflammation was lower with ALA+CL than all other groups, with enhanced recruitment of epiWAT anti-inflammatory CD206+ M2-macrophages. β3-AR signaling in WAT was enhanced in the combination-treatment group, with higher mRNA and protein levels of thermogenic uncoupling protein 1 (UCP1) and AT lipases. Chronic treatment with ALA and a β3-AR agonist reduces DIO-induced inflammation. AT immune modulation could be a therapeutic target in patients with obesity.
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影响因子:
4.9
作者:
Ravussin, Y.;Gutman, R.;LeDuc, C. A.;Leibel, R. L.
通讯作者:
Leibel, R. L.
影响因子:
4.1
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DOI:
10.1016/j.bbalip.2010.04.012
发表时间:
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期刊:
Biochimica et biophysica acta
影响因子:
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作者:
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通讯作者:
Granneman JG
影响因子:
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作者:
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通讯作者:
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影响因子:
5.6
作者:
Kim, Seung-Jin;Choi, Youngshim;Park, Taesun
通讯作者:
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