ArticleJournal of gastroenterology2013
Decreased expression of insulin and increased expression of pancreatic transcription factor PDX-1 in islets in patients with liver cirrhosis: a comparative investigation using human autopsy specimens.
Article in Journal of gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Effects of Liver Fibrosis on Islet Function in Patients with Chronic Hepatitis B Complicated with Impaired Fasting Glucose.International journal of general medicine · 2023Article
- Hepatogenous diabetes: Knowledge, evidence, and skepticism.World journal of hepatology · 2022Review
- Potential Effect of DPP-4 Inhibitors Towards Hepatic Diseases and Associated Glucose Intolerance.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Review
- Short-Term SGLT2 Inhibitor Administration Does Not Alter Systemic Insulin Clearance in Type 2 Diabetes.Biomedicines · 2021Article
- Salvianolate Reduces Glucose Metabolism Disorders in Dimethylnitrosamine-Induced Cirrhotic Rats.Chinese journal of integrative medicine · 2018Article
- Pancreatic congestion in liver cirrhosis correlates with impaired insulin secretion.Journal of gastroenterology · 2015Article
- The morbidity and associated risk factors of cancer in chronic liver disease patients with diabetes mellitus: a multicenter field survey.Journal of gastroenterology · 2015Article
- Dipeptidyl peptidase-4: a key player in chronic liver disease.World journal of gastroenterology · 2013Review
- Hepatogenous Diabetes - Let us Shun the Neglect!Indian journal of endocrinology and metabolismArticle
- Insulin Resistance and Beta Cell Function in Hepatogenous Diabetes.Indian journal of endocrinology and metabolismArticle
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10 authors at 2 institutions in 1 country.
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Abstract
backgroundGlucose intolerance in patients with liver cirrhosis (LC), known as hepatogenous diabetes, is thought to be distinct from type 2 diabetes (T2DM) in some aspects. Hyperinsulinemia and/or insulin resistance in liver disease is associated with hepatocarcinogenesis, growth of hepatocellular carcinoma, and poor prognosis. However, the pathophysiological processes in islets that are responsible for hyperinsulinemia in LC are still not precisely known. Therefore, we investigated the histopathological differences in islets of Langerhans cells between LC and T2DM.
methodsA total of 35 human autopsy pancreatic tissue samples were used in this study (control, n = 18; T2DM, n = 6; LC, n = 11). The expression of insulin, glucagon, somatostatin, pancreatic duodenal homeobox-1 (PDX-1), proliferating cell nuclear antigen (PCNA), and Ki-67 was examined using immunohistochemistry and quantitated by image analysis.
resultsIslet hypertrophy and a significant increase in PCNA-positive cells in islets were observed in the tissues from LC cases. The insulin-positive areas in islets were significantly decreased in LC cases compared with control and T2DM cases (P = 0.001, P = 0.035, respectively), whereas the PDX-1-positive area was significantly increased in LC cases (P = 0.001) compared with the control. Furthermore, disorganization of pancreatic endocrine cells and nucleocytoplasmic translocation of PDX-1 were both seen in the LC subjects.
conclusionsIn LC, islets undergo hypertrophy and exhibit paradoxical expression of insulin and PDX-1. In the subjects autopsied, insulin expression was decreased, whereas expression of the pancreatic transcription factor PDX-1 was increased in LC. These results point to important distinctions between LC and T2DM.
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