甲狀腺疾病造成的碳水化合物代謝影響, 可能會導致糖尿病失控, 雖然不是每次血糖都受影響, 但甲亢患者有可能因為血糖上升過快, 造成葡萄糖耐受試驗異常, 過多的甲狀腺素會增加消化道吸收. 增加胰島素阻抗及胰島素降解.
The effect on carbohydrate metabolism can potentially lead to disruptions in diabetes control. Although the glucose level does not always change, there can be an abnormal response to glucose tolerance testing in hyperthyroidism because glucose rises faster than normal.7 Additionally, excessive thyroid hormones increase the rate of digestive tract absorption and thyroid hormone levels and therefore increase insulin resistance and insulin degradation.
甲亢症肝醣合成與降解增加, 造成肝醣貯積下降, 葡萄糖吸收增加, 葡萄糖利用率與產生增加, 周邊組織攝入葡萄糖速率增加, 導致葡萄糖試驗時峰值上升. 胰島素需求量增加, 如果沒有適當解決, 會失去代償. 導致DKA, 此外, 尚未被診斷的DM患者, 甲亢症會增加胰島素阻抗而出現糖尿病, 在甲亢症治療過程, 可能需增加血糖藥物, 直到甲狀腺功能穩定且血糖穩定.
In hyperthyroidism, glycogen synthesis and degradation increase, leading to decreased glycogen levels.3 Glucose absorption is increased, as well as utilization and production. Peripheral tissues have increased rates of glucose uptake that can lead to the aforementioned exaggerated glucose peak during a timed glucose test. Insulin requirements are increased, and, if not addressed adequately, control can decompensate, leading to diabetic ketoacidosis. Additionally, in patients with undetected diabetes, hyperthyroidism can unmask diabetes because glucose levels can be abnormally elevated because of increased insulin resistance.3 Increased dosages of diabetes medications may be necessary in those already treated, until thyroid function is stabilized and resultant glucose stabilization occurs.
甲狀腺低下症, 肝臟分泌肝醣減少, 降解也減少, 導致肝醣貯積增加, 腸胃道吸收葡萄糖下降, 周邊組織葡萄糖利用率下降, 葡萄糖新生的受質減少. 胰島素半衰期增加, 胰島素濃度下降, 胰島素分泌下降. 導致胰島素需求量降低, 如果外源性胰島素沒有減少, 會導致低血糖.
甲狀腺低下症治療過程, 血糖可能呈現穩定狀態, 但經過治療之後, 當甲狀腺功能正常, 可能導致血糖濃度上升, 影響血糖控制
In hypothyroidism, liver secretion of glycogen decreases, but so does degradation, leading to increased levels of glycogen. Absorption of glucose from the gastrointestinal tract is slowed, and glucose utilization is slowed in the peripheral tissues. The availability of gluconeogenic substrate is decreased. Additionally, the insulin half-life is prolonged, insulin levels are lower, and insulin secretion is reduced, which may lead to reduced insulin requirements. If exogenous insulin is not decreased, hypoglycemia may occur. It is likely that glucose levels will stabilize during hypothyroidism treatment. But when thyroid function is normalized, this may lead to higher blood glucose levels and adverse effects on glycemic control.