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Hepatic expression and cellular distribution of the glucose transporter family

World Journal of Gastroenterology 2012年第46期18卷 6771-6781页

作者： sumera karim David H Adams Patricia F Lalor Centre for Liver Research and NIHR Biomedical Research Unit Institute of Biomedical Research University of Birmingham

Glucose and other carbohydrates are transported into cells using members of a family of integral membrane glucose transporter (GLUT) molecules. To date 14 members of this family, also called the solute carrier 2A proteins have been identified which are divided on the basis of transport characteristics and sequence similarities into several families (Classes 1 to 3). The expression of these different receptor subtypes varies between different species, tissues and cellular subtypes and each has differential sensitivities to stimuli such as insulin. The liver is a contributor to metabolic carbohydrate homeostasis and is a major site for synthesis, storage and redistribution of carbohydrates. Situations in which the balance of glucose homeostasis is upset such as diabetes or the metabolic syndrome can lead metabolic disturbances that drive chronic organ damage and failure, confirming the importance of understanding the molecular regulation of hepatic glucose homeostasis. There is a considerable literature describing the expression and function of receptors that regulate glucose uptake and release by hepatocytes, the most import cells in glucose regulation and glycogen storage. However there is less appreciation of the roles of GLUTs expressed by non parenchymal cell types within the liver, all of which require carbohydrate to function. A better understanding of the detailed cellular distribution of GLUTs in human liver tissue may shed light on mechanisms underlying disease pathogenesis. This review summarises the available literature on hepatocellular expression of GLUTs in health and disease and highlights areas where further investigation is required.

关键词： Hepatic Liver Glucose transporters Glucose Transport Hepatocyte

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Inhibition of vascular adhesion protein-1 modifies hepatic steatosis in vitro and in vivo

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World Journal of Hepatology 2020年第11期12卷 931-948页

作者： Emma L Shepherd sumera karim Philip N Newsome Patricia F Lalor Centre for Liver and Gastroenterology Research Birmingham National Institute for Health ResearchBirmingham Biomedical Research CentreInstitute of Immunology and ImmunotherapyUniversity of BirminghamBirmingham B152TTWest MidlandsUnited Kingdom Liver Unit Queen Elizabeth HospitalUniversity Hospitals BirminghamBirmingham B152TTWest MidlandsUnited Kingdom

BACKGROUND Non-alcoholic fatty liver disease(NAFLD)is associated with obesity,insulin resistance and dyslipidaemia and currently is estimated to affect up to a third of all individuals in developed *** standard of care for patients varies according to disease stage,but includes lifestyle interventions common insulin sensitizers,antioxidants and lipid ***,to date specific therapies have shown little histological or fibrosis stage improvement in large clinical trials,and there is still no licensed therapy for *** the high prevalence,limited treatment options and significant screening costs for the general population,new treatments are urgently *** To assess the potential for inhibition of the amine oxidase enzyme vascular adhesion protein-1(VAP-1)to modify hepatic lipid accumulation in *** We have used immunochemical and qPCR analysis to document expression of VAP-1 and key functional proteins and transporters across the NAFLD *** then utilised hepatocytes in culture and human precision cut liver slices in concert with selective enzyme activity inhibitors to test the effects of activating the semicarbazide-sensitive amine oxidase activity of VAP-1 on hepatic lipid uptake and triglyceride export.A murine model of NAFLD was also used to determine the consequences of VAP-1 knockout and gene expression arrays were used to quantify the effects of VAP-1 activity on key lipid modifying and proinflammatory gene *** We confirmed that increasing severity of NAFLD and progression to cirrhosis was associated with a significant increase in hepatocellular VAP-1 *** in vitro exposed to recombinant VAP-1 and its substrate methylamine showed increased lipid accumulation as determined by quantification of Oil Red O *** was recapitulated using hydrogen peroxide,and lipid accumulation was accompanied by changes in expression of the lipid transporter molecules FABP3,FATP6,insulin recep

关键词： Non-alcoholic fatty liver disease Hepatocyte Lipid Cell biology Vascular adhesion protein-1 Steatosis

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