Background: Patients with chronic hepatitis B (CHB) and cirrhosis often have impaired fasting glucose (IFG). This study sought to investigate the impact of liver fibrosis on islet function in individuals diagnosed with CHB and IFG.
Material And Methods: Patients with chronic hepatitis B (CHB) and impaired fasting glucose (IFG) were selected for this study. They were divided into low-risk (L-R), intermediate-risk (M-R), and high-risk (H-R) liver fibrosis groups based on the FIB-4 score. The study compared islet function among different risk groups of liver fibrosis and analyze the correlation between liver fibrosis and islet function. Additionally, the patients were divided into a diabetes mellitus (DM) group and a non-DM (NDM) group based on the development of DM. The cumulative risk of progression to DM in patients with L-R, M-R, and H-R liver fibrosis was analyzed using the Kaplan-Meier method. Hazard ratios (HRs) and confidence intervals (CIs) were calculated for DM development through Cox regression analysis.
Results: In this study of 228 individuals, higher FIB-4 scores were observed in the DM group compared to the NDM group. Patients with H-R liver fibrosis displayed lower islet function and had a significantly higher risk of developing DM. The FIB-4 score and fasting plasma glucose (FPG) were identified as independent risk factors for DM progression in CHB patients with IFG.
Conclusion: Among patients with CHB and IFG, the severity of liver fibrosis is associated with islet function, and the FIB-4 score is a significant risk factor for DM development.
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http://dx.doi.org/10.2147/IJGM.S429455 | DOI Listing |
Hepatol Commun
November 2024
Department of Cell Biology, New York University School of Medicine, New York, New York, USA.
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD, formerly known as NAFLD) is a major driver of cirrhosis and liver-related mortality. However, therapeutic options for MASLD, including prevention of liver steatosis, are limited. We previously described that vasoactive intestinal peptide-producing neurons (VIP-neurons) regulate the efficiency of intestinal dietary fat absorption and IL-22 production by type 3 innate lymphoid cells (ILC3) in the intestine.
View Article and Find Full Text PDFHepatol Commun
November 2024
Paediatric Liver, GI and Nutrition Centre and Mowatlabs, King's College Hospital, London, UK.
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View Article and Find Full Text PDFHepatol Commun
November 2024
Department of Medicine, University of California, San Diego, La Jolla, California, USA.
Background: Liver fibrosis is caused by chronic toxic or cholestatic liver injury. Fibrosis results from the recruitment of myeloid cells into the injured liver, the release of inflammatory and fibrogenic cytokines, and the activation of myofibroblasts, which secrete extracellular matrix, mostly collagen type I. Hepatic myofibroblasts originate from liver-resident mesenchymal cells, including HSCs and bone marrow-derived CD45+ collagen type I+ expressing fibrocytes.
View Article and Find Full Text PDFClin J Gastroenterol
January 2025
Department of Medicine, Division of Gastroenterology and Hepatology, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano, 390-8621, Japan.
Although steatotic liver onset after natural menopause has been reported, evidence on the clinical course and treatment options for steatotic liver after surgical menopause is scarce. A 34-year-old woman with a history of severe obesity presented to our department with liver dysfunction following total hysterectomy and bilateral oophorectomy. Her serum estradiol level was notably low at 22 pg/mL, and a liver biopsy revealed significant fatty degeneration, lobular inflammation, hepatocyte ballooning, and stage F1 fibrosis.
View Article and Find Full Text PDFBull Exp Biol Med
January 2025
N. N. Burdenko Voronezh State Medical University, Voronezh, Russia.
A method of intraoperative modeling of liver cirrhosis in an experiment has been developed. Mature male Wistar rats underwent typical liver resection (~70% of the initial volume). After resection, intrahepatic injection of 1 ml ademetionine was performed (controls received 0.
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