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<p>Glucose-sensing neurons in the hypothalamus play a pivotal role in maintaining glucose homeostasis in vivo and in detecting hypoglycemia. Leptin, a key hormone regulating body weight and energy balance, has been shown to modulate these glucose-sensing neurons, thereby enhancing glucose uptake. However, the precise mechanism by which leptin regulates K<sub>ATP</sub> channels to influence glucose responsiveness remains unclear. In this study, we employed a comprehensive approach combining electrophysiological techniques, biotinylation assays, and immunofluorescence—using the GT1-7 mouse hypothalamic cell line to elucidate this mechanism. We found that leptin enhances K<sub>ATP</sub> channel currents, resulting in hyperpolarization. This effect is attributable to the increased surface expression of the SUR1 subunit of K<sub>ATP</sub> channels. Importantly, leptin receptors are required in whole process. Consequently, leptin alters the glucose responsiveness of GT1-7 cells by modulating the surface expression of K<sub>ATP</sub> channels and enhancing their activity.</p>

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Leptin increases KATP channels’ surface expression of GT1-7 cells to regulate low glucose response

  • 期刊论文

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  • 发表日期：

    2026年1月8日

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  • Yi Wu,
  • Yanyan Zhang,
  • Hui Wang,
  • Huoyan Xu,
  • Fangling Peng

摘要

Glucose-sensing neurons in the hypothalamus play a pivotal role in maintaining glucose homeostasis in vivo and in detecting hypoglycemia. Leptin, a key hormone regulating body weight and energy balance, has been shown to modulate these glucose-sensing neurons, thereby enhancing glucose uptake. However, the precise mechanism by which leptin regulates KATP channels to influence glucose responsiveness remains unclear. In this study, we employed a comprehensive approach combining electrophysiological techniques, biotinylation assays, and immunofluorescence—using the GT1-7 mouse hypothalamic cell line to elucidate this mechanism. We found that leptin enhances KATP channel currents, resulting in hyperpolarization. This effect is attributable to the increased surface expression of the SUR1 subunit of KATP channels. Importantly, leptin receptors are required in whole process. Consequently, leptin alters the glucose responsiveness of GT1-7 cells by modulating the surface expression of KATP channels and enhancing their activity.