Pancreatic β-cell dysfunction is central to the development and progression of type 2 diabetes. Dysregulation of microRNAs (miRNAs) has been associated with pancreatic islet dysfunction in type 2 diabetes. Previous study has shown that miR-483 is expressed relatively higher in β-cells than in α-cells. To explore the physiological function of miR-483, we generated a β-cell-specific knockout mouse model of miR-483. Loss of miR-483 enhances high-fat diet-induced hyperglycemia and glucose intolerance by the attenuation of diet-induced insulin release. Intriguingly, mice with miR-483 deletion exhibited loss of β-cell features, as indicated by elevated expression of aldehyde dehydrogenase family 1, subfamily A3 (Aldh1a3), a marker of β-cell dedifferentiation. Moreover, Aldh1a3 was validated as a direct target of miR-483 and overexpression of miR-483 repressed Aldh1a3 expression. Genetic ablation of miR-483 also induced alterations in blood lipid profile. Collectively, these data suggest that miR-483 is critical in protecting β-cell function by repressing the β-cell disallowed gene Aldh1a3. The dysregulated miR-483 may impair insulin secretion and initiate β-cell dedifferentiation during the development of type 2 diabetes.
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http://dx.doi.org/10.1210/endocr/bqab031 | DOI Listing |
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December 2024
Division of Joint Surgery and Sports Medicine, Department of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
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December 2024
School of Science, Xi'an Technological University, Xi'an, 710021, PR China.
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December 2024
Longyan First Affiliated Hospital of Fujian Medical University, Longyan, 364000, Fujian, China.
The monocyte-to-Apolipoprotein A1 ratio (MAR) emerges as a potentially valuable inflammatory biomarker indicative of metabolic dysfunction-associated fatty liver disease (MASLD). Accordingly, this investigation primarily aims to assess the correlation between MAR and MASLD risk. A cohort comprising 957 individuals diagnosed with type 2 diabetes mellitus (T2DM) participated in this study.
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December 2024
Computer Science Department, Indiana University, Bloomington, IN, USA.
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December 2024
Institute of Physiology, iCBR, Faculty of Medicine, University of Coimbra, Subunit 1, polo 3, Azinhaga de Santa Comba, Celas, 3000-548, Coimbra, Portugal.
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