Publications by authors named "Xiafang Lin"
Article Synopsis
- - The study explores the role of Fam3a in pancreatic α-cell function, particularly its impact on glucagon and GLP-1 levels, using both global and α-cell-specific knockout models.
- - Researchers conducted experiments on αTC1.9 cells to determine how Fam3a influences the expression of PCSK1, which is crucial for converting proglucagon into GLP-1, revealing a regulatory pathway involving the proteins Nr4a2 and Foxa2.
- - Results indicated that Fam3a knockout enhanced GLP-1 levels in mice, while human islet data suggested an inverse relationship between FAM3A and PCSK1, highlighting Fam3a's potential role as a negative regulator of GL
Article Synopsis
- SGLT2 inhibitors (SGLT2i) show promise as a treatment for non-alcoholic fatty liver disease (NAFLD) by improving metabolic indexes and reducing liver fat and fibrosis in mouse models.
- The study found that SGLT2i treatment decreased inflammation and promoted a shift in macrophage types from M1 (pro-inflammatory) to M2 (anti-inflammatory) in liver tissues.
- Researchers identified PFKFB3, an enzyme involved in glycolysis, as a key target for SGLT2i action, indicating a new therapeutic approach for treating NAFLD by inhibiting lipogenesis in liver cells through macrophage interaction.
Sodium-glucose cotransporter 2 inhibitors, efficacious antidiabetic agents that have cardiovascular and renal benefits, can promote pancreatic β-cell regeneration in type 2 diabetic mice. However, the underlying mechanism remains unclear. In this study, we aimed to use multiomics to identify the mediators involved in β-cell regeneration induced by dapagliflozin.
View Article and Find Full Text PDFUnlabelled: Dysfunction of glucagon-secreting α-cells participates in the progression of diabetes, and glucagon receptor (GCGR) antagonism is regarded as a novel strategy for diabetes therapy. GCGR antagonism upregulates glucagon and glucagon-like peptide 1 (GLP-1) secretion and, notably, promotes β-cell regeneration in diabetic mice. Here, we aimed to clarify the role of GLP-1 receptor (GLP-1R) activated by glucagon and/or GLP-1 in the GCGR antagonism-induced β-cell regeneration.
View Article and Find Full Text PDFAims: Sodium-glucose co-transporter 2 inhibitors, including dapagliflozin, improve ß cell function in type 2 diabetic individuals. Whether dapagliflozin can protect islet microvascular endothelial cells (IMECs) and thus contribute to the improvement of ß cell function remains unknown.
Materials And Methods: The db/db mice were treated with dapagliflozin or vehicle for 6 weeks.
Aims: To investigate whether treatment with γ-aminobutyric acid (GABA) alone or in combination with glucagon receptor (GCGR) monoclonal antibody (mAb) exerted beneficial effects on β-cell mass and α-cell mass, and to explore the origins of the regenerated β-cells in mice with type 1 diabetes (T1D).
Methods: Streptozotocin (STZ)-induced T1D mice were treated with intraperitoneal injection of GABA (250 μg/kg per day) and/or REMD 2.59 (a GCGR mAb, 5 mg/kg per week), or IgG dissolved in PBS for 8 weeks.