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hepatic inflammation ( 15 ). Another central question is whether the hepatic improvements by FGF21 are related directly or indirectly. The literature is controversial as direct signaling in hepatocytes in vitro ( 72 ) and liver in vivo ( 73 ) are
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Institute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Duesseldorf, Germany
German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany
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hepatic inflammation is the component most strongly associated with IR. Several pathophysiological processes might explain these findings. In obesity-related IR, diminished inhibition of hormone-sensitive lipase will lead to enhanced efflux of FFA from
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and increasing hepatic glycogen contents. This finding is in agreement to previous reports on the effects of oleuropein in reducing blood glucose of other GDM models, such as alloxan-induced and obesity-induced diabetic rats ( 15 ). Inflammation and
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electrical stimulation (MES) attenuates metabolic abnormalities such as glucose intolerance, insulin resistance, chronic inflammation, enhanced hepatic gluconeogenesis, and steatosis in mouse models of diabetes as well as in patients with metabolic syndrome
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-IV could effectively ameliorate GDM in genetic mouse model of GDM by inhibiting NLRP3 inflammasome in the pancreas ( 13 ). We also found that AS-IV remarkably reduced hepatic gluconeogenesis, hepatic inflammation and oxidative stress to alleviate GDM in
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precedes inflammation in the liver, indicating that the liver does not play a role in the initial development of metabolic inflammation. Moreover, hepatic inflammation is of lesser importance in the development of insulin resistance compared to adipose
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DZHK (German Centre for Cardiovascular Research), Greifswald, Germany
DZD (German Center for Diabetes Research), Greifswald, Germany
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Institute and Policlinic for Radiology and Interventional Radiology, University Hospital, Carl-Gustav-Carus University Dresden, Dresden, Germany
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DZHK (German Centre for Cardiovascular Research), Greifswald, Germany
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DZHK (German Centre for Cardiovascular Research), Greifswald, Germany
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DZHK (German Centre for Cardiovascular Research), Greifswald, Germany
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Introduction In industrialized countries, the prevalence and incidence of hepatic steatosis have steadily increased over the past decades ( 1 ). Besides excessive alcohol consumption, obesity and other metabolic disorders have been frequently
Department of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, People’s Republic of China
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Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Guangzhou, People’s Republic of China
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Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Guangzhou, People’s Republic of China
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HFD mice To further confirm the expression of hub genes in the mice model, C57BL/6J mice were fed with HFD for 0, 4, and 8 weeks. H & E staining showed that HFD induced hepatic SS in mice without obvious inflammation ( Fig. 6A ). Moreover, hepatic TG
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Diabetes Center, Faculty of Medicine, University of Geneva, Geneva, Switzerland
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increased flux of hepatic FFAs induces the accumulation of TG, which cause mitochondrial dysfunction and ER stress. Intestinal permeability participates in the activation of hepatic inflammation and ER stress. Altogether these multiple parallel hits lead to
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-characterized as a mediator of hepatic lipotoxicity ( 30 ). Accumulating evidence has revealed that palmitoyl acid can activate proapoptotic signaling and trigger oxidative stress, leading to hepatocellular death and hepatic inflammation during the progression of