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在肝的 G6PT-H6PDH-11HsD1 三个一组和它在新陈代谢的症候群的 pathomechanism 的含意

World Journal of Hepatology 2012年第4期4卷 129-138页

作者： Ibolya Czegle miklós csala József Mandl Angelo Benedetti István Karádi Gábor Bánhegyi 3rd Department of Internal Medicine Semmelweis University 1125 Budapest Hungary Pathobiochemistry Research Group Hungarian Academy of Sciences 1094 Budapest Hungary Department of Medical Chemistry Molecular Biology and Pathobiochemistry Semmelweis University 1094 Budapest Hungary Department of Pathophysiology Experimental Medicine and Public Health University of Siena 53100 Siena Italy

The metabolic syndrome, one of the most common clinical conditions in recent times, represents a combination of cardiometabolic risk determinants, including central obesity, glucose intolerance, insulin resistance, dyslipidemia, non-alcoholic fatty liver disease and hypertension. Prevalence of the metabolic syndrome is rapidly increasing worldwide as a consequence of common overnutrition and consequent obesity. Although a unifying picture of the pathomechanism is still missing, the key role of the pre-receptor glucocorticoid activation has emerged recently. Local glucocorticoid activation is catalyzed by a triad composed of glucose-6-phosphate-transporter, hexose-6-phosphate dehydrogenase and 11β-hydroxysteroid dehydrogenase type 1 in the endoplasmic reticulum. The elements of this system can be found in various cell types, including adipocytes and hepatocytes. While the contribution of glucocorticoid activation in adipose tissue to the pathomechanism of the metabolic syndrome has been well established, the relative importance of the hepatic process is less understood. This review summarizes the available data on the role of the hepatic triad and its role in the metabolic syndrome, by confronting experimental findings with clinical observations.

关键词： Metabolic syndrome Liver Glucocorticoid Glucose-6-phosphate-transporter Hexose-6-phosphate dehydrogenase 11β-hydroxysteroid dehydrogenase type 1

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Lipotoxicity in the liver

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World Journal of Hepatology 2013年第10期5卷 550-557页

作者： Veronika Zámbó Laura simon-szabó Péter szelényi va Kereszturi Gábor Bánhegyi miklós csala Department of Medical Chemistry Molecular Biology and PathobiochemistrySemmelweis University

Obesity due to excessive food intake and the lack of physical activity is becoming one of the most serious public health problems of the 21stcentury. With the increasing prevalence of obesity, non-alcoholic fatty liver disease is also emerging as a pandemic. While previously this pathophysiological condition was mainly attributed to triglyceride accumulation in hepatocytes,recent data show that the development of oxidative stress, lipid peroxidation, cell death, inflammation and fibrosis are mostly due to accumulation of fatty acids,and the altered composition of membrane phospholipids. In fact, triglyceride accumulation might play a protective role, and the higher toxicity of saturated or trans fatty acids seems to be the consequence of a blockade in triglyceride synthesis. Increased membrane saturation can profoundly disturb cellular homeostasis by impairing the function of membrane receptors,channels and transporters. However, it also inducesendoplasmic reticulum stress via novel sensing mechanisms of the organelle's stress receptors. The triggered signaling pathways in turn largely contribute to the development of insulin resistance and apoptosis. These findings have substantiated the lipotoxic liver injury hypothesis for the pathomechanism of hepatosteatosis.This minireview focuses on the metabolic and redox aspects of lipotoxicity and lipoapoptosis, with special regards on the involvement of endoplasmic reticulum stress responses.

关键词： saturated fatty acid Lipotoxicity steatosis Lipoapoptosis Endoplasmic reticulum stress

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