Diabetes research and clinical practice · 2025
Hypomagnesemia induces impaired glucose metabolism and insulin resistance in patients with Gitelman syndrome.
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Xin Yu, Yin Yaqi, Zhu Lili, Wang Yuepeng, Wu Ting, Xu Junjie, Zang Li
Аннотация
AIMS: To investigate the contributing factors of impaired glucose metabolism in patients with Gitelman syndrome (GS).
METHODS: This study collected clinical data and conducted oral glucose tolerance tests (OGTT) on 44 GS patients, with 60 non-functioning adrenal incidentaloma (NFAI) patients serving as controls.
RESULTS: Compared to NFAI patients, GS patients exhibited a significantly higher prevalence of impaired glucose metabolism (P < 0.001), with markedly higher homeostasis model assessment of insulin resistance (HOMA-IR), lower quantitative insulin sensitivity check index, and lower Matsuda index compared to NFAI patients (all P < 0.001). The homeostasis model assessment for β cells was elevated (P = 0.003) and the insulin secretion sensitivity index-2 was reduced (P = 0.007) in GS patients relative to NFAI patients. Logistic regression identified hypomagnesemia (P = 0.042) and hypokalemia (P = 0.046) as risk factors for dysregulated glucose metabolism in GS patients. Additionally, higher body mass index (BMI) (P = 0.016) and hypomagnesemia (P = 0.045) were significant contributors to IR. Notably, GS patients had a steeper linear regression slope between BMI and HOMA-IR compared to NFAI patients (P = 0.016). A negative linear correlation between plasma magnesium and BMI (R = 0.54, P < 0.001) was found in GS patients.
CONCLUSIONS: Hypomagnesemia may contribute to increased BMI, exacerbating impaired glucose metabolism and IR in GS patients.
METHODS: This study collected clinical data and conducted oral glucose tolerance tests (OGTT) on 44 GS patients, with 60 non-functioning adrenal incidentaloma (NFAI) patients serving as controls.
RESULTS: Compared to NFAI patients, GS patients exhibited a significantly higher prevalence of impaired glucose metabolism (P < 0.001), with markedly higher homeostasis model assessment of insulin resistance (HOMA-IR), lower quantitative insulin sensitivity check index, and lower Matsuda index compared to NFAI patients (all P < 0.001). The homeostasis model assessment for β cells was elevated (P = 0.003) and the insulin secretion sensitivity index-2 was reduced (P = 0.007) in GS patients relative to NFAI patients. Logistic regression identified hypomagnesemia (P = 0.042) and hypokalemia (P = 0.046) as risk factors for dysregulated glucose metabolism in GS patients. Additionally, higher body mass index (BMI) (P = 0.016) and hypomagnesemia (P = 0.045) were significant contributors to IR. Notably, GS patients had a steeper linear regression slope between BMI and HOMA-IR compared to NFAI patients (P = 0.016). A negative linear correlation between plasma magnesium and BMI (R = 0.54, P < 0.001) was found in GS patients.
CONCLUSIONS: Hypomagnesemia may contribute to increased BMI, exacerbating impaired glucose metabolism and IR in GS patients.