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Tangshen Formula Alleviates Hepatic Steatosis by Inducing Autophagy Through the AMPK/SIRT1 Pathway
Conclusion In conclusion, the present study demonstrated that autophagy was involved in relieving the effects of TSF against NAFLD, which were mediated by the AMPK/SIRT1 pathway (Figure 7D). These findings may improve our current understanding of the role of TSF in treating hepatic steatosis and provide an experimental basis for the clinical application of TSF in NAFLD and its related metabolic syndrome. Ethics Statement This study was carried out in accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. The protocol was approved by the Ethics Co...
Source: Frontiers in Physiology - April 25, 2019 Category: Physiology Source Type: research

Activation of AMP-activated protein kinase inhibits ER stress and renal fibrosis.
In conclusion, AMPK may serve as a promising therapeutic target through reducing ER stress and renal fibrosis. PMID: 25428127 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Renal Physiology - November 26, 2014 Category: Physiology Authors: Kim H, Moon SY, Kim JS, Baek CH, Kim M, Min JY, Lee SK Tags: Am J Physiol Renal Physiol Source Type: research

Metformin promotes irisin release from murine skeletal muscle independently of AMP‐activated protein kinase activation
ConclusionMetformin promotes irisin release from murine skeletal muscle into blood, independently of AMPK pathway activation. Our results suggest that stimulation of irisin may be a novel molecular mechanism of metformin which is widely used for treatment of metabolic disorders.
Source: Acta Physiologica - November 24, 2014 Category: Physiology Authors: D.‐J. Li, F. Huang, W.‐J. Lu, G.‐J. Jiang, Y.‐P. Deng, F.‐M. Shen Tags: Original Article Source Type: research

Metformin promotes irisin release from murine skeletal muscle independently of AMPK activation
ConclusionMetformin promotes irisin release from murine skeletal muscle into blood, independently of AMPK pathway activation. Our results suggest that stimulation of irisin may be a novel molecular mechanism of metformin which is widely used for treatment of metabolic disorders.This article is protected by copyright. All rights reserved.
Source: Acta Physiologica - November 11, 2014 Category: Physiology Authors: Dong‐Jie Li, Fang Huang, Wen‐Jie Lu, Guo‐Jun Jiang, Ya‐ping Deng, Fu‐Ming Shen Tags: Regular Paper Source Type: research

Polycystin-1 but not polycystin-2 deficiency causes upregulation of the mTOR pathway and can be synergistically targeted with rapamycin and metformin.
Abstract Autosomal dominant polycystic kidney disease (ADPKD) is caused by loss-of-function mutations in either PKD1 or PKD2 genes, which encode polycystin-1 (TRPP1) and polycystin-2 (TRPP2), respectively. Increased activity of the mammalian target of rapamycin (mTOR) pathway has been shown in PKD1 mutants but is less documented for PKD2 mutants. Clinical trials using mTOR inhibitors were disappointing, while the AMP-activated kinase (AMPK) activator, metformin is not yet tested in patients. Here, we studied the mTOR activity and its upstream pathways in several human and mouse renal cell models with either siRNA ...
Source: Pflugers Archiv : European Journal of Physiology - November 6, 2013 Category: Physiology Authors: Mekahli D, Decuypere JP, Sammels E, Welkenhuyzen K, Schoeber J, Audrezet MP, Corvelyn A, Dechênes G, Ong AC, Wilmer MJ, van den Heuvel L, Bultynck G, Parys JB, Missiaen L, Levtchenko E, De Smedt H Tags: Pflugers Arch Source Type: research

AMP-activated protein kinase inhibits TGF-β-, angiotensin II-, aldosterone-, high glucose- and albumin-induced epithelial-mesenchymal transition.
In conclusion, AMPK activation might be beneficial in attenuating the tubulointerstitial fibrosis induced by TGF-β, angiotensin II, aldosterone, high glucose and urinary albumin. PMID: 23324179 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Renal Physiology - January 16, 2013 Category: Physiology Authors: Lee JH, Kim JH, Kim JS, Chang JW, Kim SB, Park JS, Lee SK Tags: Am J Physiol Renal Physiol Source Type: research