Hypomagnesemia induces impaired glucose metabolism and insulin resistance in patients with Gitelman syndrome.

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.