Galectin-3 impairs calcium transients and β-cell function

Qian Jiang, Qijin Zhao, Yibing Chen, Chunxiao Ma, Xiaohong Peng, Xi Wu, Xingfeng Liu, Ruoran Wang, Shaocong Hou, Lijuan Kong, Yanjun Wan, Shusen Wang, Zhuo-Xian Meng, Bing Cui, Liangyi Chen and Pingping Li ()
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Qian Jiang: Chinese Academy of Medical Sciences and Peking Union Medical College
Qijin Zhao: Chinese Academy of Medical Sciences and Peking Union Medical College
Yibing Chen: Chinese Academy of Medical Sciences and Peking Union Medical College
Chunxiao Ma: Chinese Academy of Medical Sciences and Peking Union Medical College
Xiaohong Peng: Peking University
Xi Wu: Peking University
Xingfeng Liu: Chinese Academy of Medical Sciences and Peking Union Medical College
Ruoran Wang: Zhejiang University
Shaocong Hou: Chinese Academy of Medical Sciences and Peking Union Medical College
Lijuan Kong: Chinese Academy of Medical Sciences and Peking Union Medical College
Yanjun Wan: Chinese Academy of Medical Sciences and Peking Union Medical College
Shusen Wang: Nankai University
Zhuo-Xian Meng: Zhejiang University
Bing Cui: Chinese Academy of Medical Sciences and Peking Union Medical College
Liangyi Chen: Peking University
Pingping Li: Chinese Academy of Medical Sciences and Peking Union Medical College

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract In diabetes, macrophages and inflammation are increased in the islets, along with β-cell dysfunction. Here, we demonstrate that galectin-3 (Gal3), mainly produced and secreted by macrophages, is elevated in islets from both high-fat diet (HFD)-fed and diabetic db/db mice. Gal3 acutely reduces glucose-stimulated insulin secretion (GSIS) in β-cell lines and primary islets in mice and humans. Importantly, Gal3 binds to calcium voltage-gated channel auxiliary subunit gamma 1 (CACNG1) and inhibits calcium influx via the cytomembrane and subsequent GSIS. β-Cell CACNG1 deficiency phenocopies Gal3 treatment. Inhibition of Gal3 through either genetic or pharmacologic loss of function improves GSIS and glucose homeostasis in both HFD-fed and db/db mice. All animal findings are applicable to male mice. Here we show a role of Gal3 in pancreatic β-cell dysfunction, and Gal3 could be a therapeutic target for the treatment of type 2 diabetes.

Date: 2024
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DOI: 10.1038/s41467-024-47959-1

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