Publications by authors named "Zhiyan Weng"

Article Synopsis
  • Identifying dysregulation of -cells in type 2 diabetes mellitus (T2DM) is essential, as weight changes during treatment can impact islet cell function, yet this connection is not well-studied.
  • A longitudinal study of 775 T2DM patients over approximately 2.29 years measured various body composition metrics and assessed insulin, C-peptide, and glucose levels post-glucose load.
  • Findings showed no significant changes in BMI, but those at readmission had increased fat mass and insulin resistance; specifically, higher fat mass was linked to worsening insulin resistance, while greater appendicular skeletal muscle mass was associated with better insulin function.
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Gastric cancer is a significant global health concern with complex molecular underpinnings influencing disease progression and patient outcomes. Various molecular drivers were reported, and these studies offered potential avenues for targeted therapies, biomarker discovery, and the development of precision medicine strategies. However, it was posed that the heterogeneity of the disease and the complexity of the molecular interactions are still challenging.

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Objective: Non-healing diabetic foot ulcers are a leading cause of disability and death in diabetic patients, which often results in lower limb amputation. This study aimed to investigate the impact of biomarkers on the healing of diabetic foot ulcers by utilizing dynamic serum proteomics and skin proteomic analysis, combined with clinical case follow-up studies.

Methods: To analyze dynamic serum proteomic changes in four groups, age-matched normal subjects, diabetic patients, pretreatment diabetic foot ulcer patients, and healed diabetic foot ulcer patients were selected.

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Metabolic inflammatory damage, characterized by Toll-like receptor 4 (TLR4) signaling activation, is a major mechanism underlying lipotoxicity-induced -cell damage. The present study is aimed at determining whether G protein-coupled receptor 4 (GPR40) agonist can improve -cell lipotoxicity-induced damage by inhibiting the TLR4-NF-B pathway. Lipotoxicity, inflammation-damaged -cells, obese SD, and TLR4 rat models were used in the study.

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