BACKGROUND: Gitelman syndrome (GS) is an autosomal recessive disease of renal tubulopathy, primarily characterized by hypokalemic metabolic alkalosis with significant hypomagnesemia, low urinary calcium, secondary aldosteronism and normal blood pressure. Both hypokalemia and hypomagnesemia were reported to cause impaired glucose tolerance and/or insulin resistance, but it is unclear whether impaired glucose tolerance and/or insulin resistance are common in GS patients. METHODS: An oral glucose tolerance test was performed among 16 GS patients and 12 healthy adults as control subjects. Fasting glucose and serum insulin levels were measured and the values of glucose and serum insulin after 30, 60, 120 and 180 min were also measured after an oral glucose load. The area under curve (AUC) of glucose and insulin was calculated. RESULTS: One patient had isolated impaired fasting glucose, 2 had isolated impaired glucose tolerance, and 1 had combined impaired fasting glucose and glucose tolerance. Six patients were diagnosed with type 2 diabetes mellitus. Compared with a healthy normal control group, GS patients showed a higher AUC glucose level [16.1 (IQR 12.5-25.4 mEq · h/l) vs. 13.0 (IQR 11.9-13.7 mEq · h/l); p < 0.05] and AUC insulin level [81.0 (IQR 58.9-138 µU · h/ml) vs. 46.4 (IQR 35.6-63.3 µU · h/ml); p < 0.01]. GS patients showed a delay of insulin secretion peak which was observed 120 min after a glucose load. Homeostasis model assessment of insulin resistance in GS patients was significantly higher than in control volunteers. Quantitative insulin sensitivity check index and insulin sensitivity index composite in the GS group were significantly lower than in the control group. CONCLUSION: Abnormal glucose metabolism and insulin secretion is common in GS patients. It is speculated that hypokalemia and hypomagnesemia may be the main cause.
BACKGROUND:Gitelman syndrome (GS) is an autosomal recessive disease of renal tubulopathy, primarily characterized by hypokalemic metabolic alkalosis with significant hypomagnesemia, low urinary calcium, secondary aldosteronism and normal blood pressure. Both hypokalemia and hypomagnesemia were reported to cause impaired glucose tolerance and/or insulin resistance, but it is unclear whether impaired glucose tolerance and/or insulin resistance are common in GSpatients. METHODS: An oral glucose tolerance test was performed among 16 GSpatients and 12 healthy adults as control subjects. Fasting glucose and serum insulin levels were measured and the values of glucose and serum insulin after 30, 60, 120 and 180 min were also measured after an oral glucose load. The area under curve (AUC) of glucose and insulin was calculated. RESULTS: One patient had isolated impaired fasting glucose, 2 had isolated impaired glucose tolerance, and 1 had combined impaired fasting glucose and glucose tolerance. Six patients were diagnosed with type 2 diabetes mellitus. Compared with a healthy normal control group, GSpatients showed a higher AUC glucose level [16.1 (IQR 12.5-25.4 mEq · h/l) vs. 13.0 (IQR 11.9-13.7 mEq · h/l); p < 0.05] and AUC insulin level [81.0 (IQR 58.9-138 µU · h/ml) vs. 46.4 (IQR 35.6-63.3 µU · h/ml); p < 0.01]. GSpatients showed a delay of insulin secretion peak which was observed 120 min after a glucose load. Homeostasis model assessment of insulin resistance in GSpatients was significantly higher than in control volunteers. Quantitative insulin sensitivity check index and insulin sensitivity index composite in the GS group were significantly lower than in the control group. CONCLUSION:Abnormal glucose metabolism and insulin secretion is common in GSpatients. It is speculated that hypokalemia and hypomagnesemia may be the main cause.