Diabetes & Metabolism Journal

Review

Metabolic Risk/Epidemiology
Hepatic Fibrosis and Cancer: The Silent Threats of Metabolic Syndrome: Scott L. Friedman; Diabetes Metab J. 2024;48(2):161-169. Published online January 26, 2024; DOI: https://doi.org/10.4093/dmj.2023.0240

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Metabolic dysfunction-associated steatotic (fatty) liver disease (MASLD), previously termed non-alcoholic fatty liver disease, is a worldwide epidemic that can lead to hepatic inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The disease is typically a component of the metabolic syndrome that accompanies obesity, and is often overlooked because the liver manifestations are clinically silent until late-stage disease is present (i.e., cirrhosis). Moreover, Asian populations, including Koreans, have a higher fraction of patients who are lean, yet their illness has the same prognosis or worse than those who are obese. Nonetheless, ongoing injury can lead to hepatic inflammation and ballooning of hepatocytes as classic features. Over time, fibrosis develops following activation of hepatic stellate cells, the liver’s main fibrogenic cell type. The disease is usually more advanced in patients with type 2 diabetes mellitus, indicating that all diabetic patients should be screened for liver disease. Although there has been substantial progress in clarifying pathways of injury and fibrosis, there no approved therapies yet, but current research seeks to uncover the pathways driving hepatic inflammation and fibrosis, in hopes of identifying new therapeutic targets. Emerging molecular methods, especially single cell sequencing technologies, are revolutionizing our ability to clarify mechanisms underlying MASLD-associated fibrosis and HCC.

Citations

Citations to this article as recorded by

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Original Articles

Matrix Metalloproteinase-3 Gene Polymorphism is Associated with Coronary Artery Calcification Scores in Patients with Type 2 Diabetes Mellitus.: Sang Wook Kim, Eun Hee Cho; Korean Diabetes J. 2009;33(2):113-123. Published online April 1, 2009; DOI: https://doi.org/10.4093/kdj.2009.33.2.113

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Abstract PDF: BACKGROUND
Matrix metalloproteinase-3 (MMP-3) is expressed in human coronary atherosclerotic lesions and is known to be involved in the degradation of plaque. This study examines the association of MMP-3 gene promoter 5A/6A and -709A>G polymorphisms with coronary artery calcium scores in type 2 diabetes patients. METHODS: The study comprises 140 type 2 diabetes patients aged 34~85 years, who showed no evidence of clinical cardiovascular disease before recruitment. Recruitment was based on patient's coronary artery calcium (CAC) scores and polymorphisms were identified. RESULTS: Multiple regression analysis showed that the CAC scores were significantly associated with age (P = 0.008), waist circumference (P = 0.03), duration of diabetes (P = 0.003) and the serum creatinine level (P = 0.012). MMP-3 5A/6A and -709A>G polymorphisms were not associated with CAC across all subjects. However, in the subgroup with a duration of diabetes over 10 years, MMP-3 -709A>G were significantly associated with CAC (P = 0.037) adjusted for age, body mass index, waist circumference and duration of diabetes. CONCLUSION: Our data suggest that the CAC scores in patients with type 2 diabetes were related with age, waist circumference, duration of diabetes and higher serum creatinine levels. MMP-3 polymorphisms with -709A>G are associated with high CAC in patients with a duration of diabetes over 10 years.

In Vitro Expansion and Differentiation of Islet Precursor Cells from Cultured Neonatal Porcine Pancreatic Tissue.: Yu Bae Ahn, Kun Ho Yoon, Sun Hee Seo, Seung Hyun Ko, Ki Ho Song, Je Ho Han, Soon Jip Yoo, Hyun Sik Son, Moo Il Kang, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang; Korean Diabetes J. 2000;24(3):310-322. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Neonatal porcine pancreas is an attractive alternative source for islet transplantation because of its growth potential and availability. Porcine neonatal pancreatic cell clusters (NPCCs) consist mainly of protodifferentiated cells expressing both the duct cell marker pancytokeratin and islet hormones. In this study, we investigated to expand and mature the pancreas duct cells contained in porcine NPCCs with extracellular matrix. METHODS: For NPCCs, pancreas obtained from neonatal pigs were minced, digested with collagenase and cultured overnight. Then NPCCs were further dispersed to small cell groups and cultured on HTB-9 extracellular matrix: the tissue attached and formed monolayer patches. At the 3rd and 8th days, tissue was fixed, immunostained for pancytokeratin (panCK), vimentin (VT) and islet hormones. RESULTS: During 5 days culture, the total cell numbers increased 3.2 fold on the matrix, and 1.6 fold on the sticky dish, respectively. Insulin positive cells (Ins+) were 6.0% of total cells at day 3 and increased 1.6 fold in numbers at day 8. There was significant increase in DNA content of NPCCs in monolayers on both sticky dishes and HTB-9 matrix. In contrast, insulin content of both groups decreased during culture periods. Until 8 days of culture after dispersion of porcine NPCC, most duct cells costained with panCK and VT. CONCLUSION: We observed NPCCs were composed of many of duct cells which were known to be endocrine precursor cells and monolayer culture of NPCC withextracellular matrix resulted in the proliferation and differentiation of pancreatic duct cells.

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