scholarly journals Metabolic syndrome and nonalcoholic fatty liver disease. The role of endothelial progenitor cells♦

2013 ◽  
Vol 12 (6) ◽  
pp. 908-914 ◽  
Author(s):  
Ylse Gutiérrez-Grabe ◽  
Juan G. Gavilanes-Espinar ◽  
Felipe A. Masso-Rojas ◽  
Vicente Sánchez-Valle ◽  
Araceli Páez-Arenas ◽  
...  
2011 ◽  
Vol 140 (5) ◽  
pp. S-989-S-990
Author(s):  
Nahum Mendez-Sanchez ◽  
Ylse Gutierrez-Grobe ◽  
Ramón A. Kobashi-Margáin ◽  
Juan G. Gavilanes-Espinar ◽  
Angel A. Gutiérrez-Jiménez ◽  
...  

Metabolism ◽  
2016 ◽  
Vol 65 (8) ◽  
pp. 1196-1207 ◽  
Author(s):  
Nancy E. Aguilar-Olivos ◽  
Paloma Almeda-Valdes ◽  
Carlos A. Aguilar-Salinas ◽  
Misael Uribe ◽  
Nahum Méndez-Sánchez

2021 ◽  
Vol 22 (12) ◽  
pp. 6627
Author(s):  
Teoman Dogru ◽  
Ali Kirik ◽  
Hasan Gurel ◽  
Ali A. Rizvi ◽  
Manfredi Rizzo ◽  
...  

Nonalcoholic fatty liver disease (NAFLD) is strongly associated to the features of metabolic syndrome which can progress to cirrhosis, liver failure and hepatocellular carcinoma. However, the most common cause of mortality in people with NAFLD is not liver-related but stems from atherosclerotic cardiovascular disease (CVD). The prevalence of NAFLD is on the rise, mainly as a consequence of its close association with two major worldwide epidemics, obesity and type 2 diabetes (T2D). The exact pathogenesis of NAFLD and especially the mechanisms leading to disease progression and CVD have not been completely elucidated. Human fetuin-A (alpha-2-Heremans Schmid glycoprotein), a glycoprotein produced by the liver and abundantly secreted into the circulation appears to play a role in insulin resistance, metabolic syndrome and inflammation. This review discusses the links between NAFLD and CVD by specifically focusing on fetuin-A’s function in the pathogenesis of NAFLD and atherosclerotic CVD.


2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Kei Nakajima

Nonalcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are multidisciplinary liver diseases that often accompany type 2 diabetes or metabolic syndrome, which are characterized by insulin resistance. Therefore, effective treatment of type 2 diabetes and metabolic syndrome should target not only the cardiometabolic abnormalities, but also the associated liver disorders. In the last decade, it has been shown that metformin, thiazolidinediones, vitamin E, ezetimibe, n-3 polyunsaturated fatty acids, renin-angiotensin system (RAS) blockers, and antiobesity drugs may improve hepatic pathophysiological disorders as well as clinical parameters. Accordingly, insulin sensitizers, antioxidative agents, Niemann-Pick C1-like 1 (NPC1L1) inhibitors, RAS blockers, and drugs that target the central nervous system may represent candidate pharmacotherapies for NAFLD and possibly NASH. However, the efficacy, safety, and tolerability of long-term treatment (potentially for many years) with these drugs have not been fully established. Furthermore, clinical trials have not comprehensively examined the efficacy of lipid-lowering drugs (i.e., statins, fibrates, and NPC1L1 inhibitors) for the treatment of NAFLD. Although clinical evidence for RAS blockers and incretin-based agents (GLP-1 analogs and dipeptidyl peptidase-4 inhibitors) is also lacking, these agents are promising in terms of their insulin-sensitizing and anti-inflammatory effects without causing weight gain.


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