Hepatology Research
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Insulin resistance increases the risk of incident type 2 diabetes mellitus in patients with non‐alcoholic fatty liver disease Aim Type 2 diabetes mellitus (T2DM) is a major complication of patients with non‐alcoholic fatty liver disease (NAFLD). The aim of this retrospective study is to determine the risk factors for development of T2DM in patients with biopsy‐proven NAFLD. Methods One hundred and sixty two consecutive patients with biopsy‐proven NAFLD who received a 75‐g oral glucose tolerance test were enrolled as the total cohort. Among them, we analyzed 89 patients without T2DM diagnosed by oral glucose tolerance test to estimate the cumulative rate for development of T2DM as the follow‐up cohort. Results Of 162 patients, the glucose tolerance pattern were DM in 45 patients (27.8%), impaired glucose tolerance in 68 (42.0%), and normal glucose tolerance in 49 (30.2%). Patients with NAFL tended to be more likely to have normal glucose tolerance than those with non‐alcoholic steatohepatitis (NASH). The serum levels of pre‐ and post‐load insulin were significantly higher in the NASH group. Of 89 patients without T2DM, 13 patients newly developed T2DM during a follow‐up period of 5.2 years. The cumulative rate of T2DM incidence was 8.8% at the end of the 5th year and 23.4% at the end of the 10th year. Multivariate analysis identified homeostasis model of assessment – insulin resistance (≥3.85, hazard ratio 40.1, P = 0.033) as an independent risk factor for development of T2DM. Conclusions Patients with NASH have an underlying potential of glucose intolerance. In NAFLD patients, insulin resistance is the most important risk factor for the incidence of T2DM. Appropriate therapy against insulin resistance could be needed for patients with NAFLD to prevent development of T2DM.
Hepatology Research - Tập 48 Số 3 - 2018
Preoperative assessment of multicentric occurrence in synchronous small and multiple hepatocellular carcinoma based on image-patterns and histological grading of non-cancerous region
Hepatology Research - Tập 29 Số 1 - Trang 24-30 - 2004
Ethanol upregulates pro-fibrogenic connective tissue growth factor (CTGF) gene expression in HepG2 cells via cytochrome P450 2E1-mediated ethanol oxidation
Hepatology Research - Tập 28 - Trang 102-108 - 2004
The role of oxidative stress in NASH and fatty liver model
Hepatology Research - Tập 33 Số 2 - Trang 128-131 - 2005
The influence of marginal zinc deficient diet on post-vaccination immune response against hepatitis B in rats
Hepatology Research - Tập 35 Số 1 - Trang 26-30 - 2006
Amino acid substitutions in PKR-eIF2 phosphorylation homology domain (PePHD) of hepatitis C virus E2 protein in genotype 2a/2b and 1b in Japan and interferon efficacy
Hepatology Research - Tập 26 - Trang 268-274 - 2003
Eosionophilic pseudotumor of the liver due to Ascaris suum infection
Hepatology Research - Tập 23 - Trang 306-314 - 2002
Occurrence of portal vein tumor thrombus in hepatocellular carcinoma affects prognosis and survival. A retrospective clinical study of 150 cases
Hepatology Research - Tập 24 Số 1 - Trang 50-59 - 2002
Prognostic indicators estimated by Tc-GSA in acute liver damage
Hepatology Research - Tập 31 - Trang 153-159 - 2005
Prolonged engraftment of human hepatocytes in mice transgenic for the deleted form of human hepatocyte growth factor Aim: Small animal models chimeric for human hepatocytes have provided valuable insights into the biology of hepatotropic viral infection and provided a platform for the study of therapeutic agents. Existing models of human hepatocyte transplantation are limited by phenotypic fragility and impaired immunity. We hypothesized that mice transgenic for human hepatocyte growth factor (HGF), a potent human hepatocyte mitogen, would engraft human hepatocytes in the absence of immunodeficiency.Methods: A plasmid construct containing the 2.3 kb coding region of the 723 amino acid isoform of HGF cDNA under the transcriptional control of the mouse albumin promoter/enhancer was used to generate transgenic mice. Cryopreserved human hepatocytes were transplanted into nine transgenic and six non‐transgenic mice. Engraftment of human hepatocytes was followed for a period of 12 weeks by immunoblotting for human albumin in mouse serum samples.Results: In six out of the nine transgenic mice, abundance of human albumin, following an initial decline, increased andpeaked at > 70 days post transplantation, demonstrating sustained engraftment of transplanted human hepatocytes. In all the non‐transgenic mice, post‐transplant human albumin levels declined sequentially without evidence of sustained engraftment. Immunostaining of mouse liver sections indicated the presence of human hepatocytes adjacent to clusters of non‐staining murine hepatocytes.Conclusion: These results demonstrate that sustained engraftment of human hepatocytes in mice is facilitated by expression of the human dHGF transgene. Human hepatocyte engraftment in this model has been achieved on an immunocompetent strain background and merits further study as a candidate for the study of hepatotropic viral infections.
Hepatology Research - Tập 37 Số 10 - Trang 854-862 - 2007
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