Loss of Slc39a5 in α-cells impairs glucose metabolism by chronically increasing glucagon

These results demonstrate that Slc39a5 deficiency in α-cells leads to chronic glucagon elevation, which directly impairs hepatic glucose metabolism and promotes insulin resistance and hyperglycemia. This study thus establishes a causal role for α-cells Slc39a5 in prediabetes progression, highlighting sustained glucagon excess as a key contributor of metabolic dysfunction.

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Publication Details

Journal
Journal of Advanced Research
Published
2025-11-01
DOI
https://doi.org/10.1016/j.jare.2025.11.013
Primary Topic
Pancreatic function and diabetes
Type
article
Field-Weighted Citation Impact
0.00
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article

Loss of Slc39a5 in α-cells impairs glucose metabolism by chronically increasing glucagon

Jing Ren, Rui‐Ping Xiao, Xiuqin Zhang, Xueting Sun et al.
Journal of Advanced Research
Pancreatic function and diabetes
article

Loss of Slc39a5 in α-cells impairs glucose metabolism by chronically increasing glucagon

Jing Ren, Rui‐Ping Xiao, Xiuqin Zhang, Xueting Sun, Wenyong Xiong, Ning Hou, Xuelian Wang, Wenli Chen, Yan Xu, Weiyi Cui
article en

Abstract

These results demonstrate that Slc39a5 deficiency in α-cells leads to chronic glucagon elevation, which directly impairs hepatic glucose metabolism and promotes insulin resistance and hyperglycemia. This study thus establishes a causal role for α-cells Slc39a5 in prediabetes progression, highlighting sustained glucagon excess as a key contributor of metabolic dysfunction.

Journal of Advanced Research
Yunnan University (CN), Peking University (CN)
Openalex Percentile: Top 47%
Pancreatic function and diabetes
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