저칼륨혈증이 인슐린 분비를 감소시킨다는 내용

저칼륨혈증이 인슐린 분비를 감소시킨다는 내용은 primary hyperaldosteronism에서 나옵니다.
Primary aldosteronism 환자의 약 25%는 hypokalemia로 인한 인슐린 분비 저하로 fasting glucose가 약간 상승합니다.

또한 이 내용은 thiazide-associated diabetes에서도 중요한 역할을 합니다.  그러나 이뇨제 이외 혈압약들이 많아 저용량 thiazide(12.5 ~25 mg)를 사용하는 현대에서는 예전만큼 악화되는 glucose tolerance가 흔하지 않습니다.

Dose dependence of thiazide-induced side effects

Metabolic complications induced by bendrofluazide in relation to daily dose (multiply by 10 to get equivalent doses of hydrochlorothiazide). Increasing the dose led to progressive hypokalemia and hyperuricemia and a greater likelihood of a mild elevation in the FBG, all without a further reduction in the systemic blood pressure. Each treatment group contained approximately 52 patients.
Data from: Carlsen JE, Kober L, Torp-Pedersen C, Johansen P. Relation between dose of bendrofluazide, antihypertensive effect, and adverse biochemical effects. BMJ 1990; 300:975.

Concurrent hypokalemia appears to play an important role, as evidenced by a small study showing no change in glucose tolerance if urinary losses are replaced by potassium supplements. Subsequent analyses of larger trials confirmed the association between hypokalemia and a higher probability of developing type 2 diabetes. As an example, in the Systolic Hypertension in Elderly Program trial, the risk of diabetes with use of a thiazide (chlorthalidone) was significantly attenuated when adjusted for changes in serum potassium. Each 0.5 mEq/L decrease in serum potassium was associated with a 45 percent higher risk of new diabetes. The putative mechanism for this association is a failure of potassium channels to close in response to rising plasma glucose concentrations, with a resultant decrease in insulin secretion.

REF. UpToDate 2018.09.07