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Sustained Pro-Inflammatory Effects of Hypoglycemia in People with Type 2 Diabetes and in People Without Diabetes
Diabetes ( IF 6.2 ) Pub Date : 2022-07-18 , DOI: 10.2337/db22-0246
Clementine E M Verhulst 1 , Julia I P van Heck 1 , Therese W Fabricius 2 , Rinke Stienstra 1, 3 , Steven Teerenstra 4 , Rory J McCrimmon 5 , Cees J Tack 1 , Ulrik Pedersen-Bjergaard 2, 6 , Bastiaan E de Galan 1, 7, 8
Affiliation  

Iatrogenic hypoglycaemia activates the immune system and is associated with an increased risk for atherosclerotic disease. We determined acute and long-term effects of insulin-induced hypoglycemia on inflammatory markers in humans with or without type 2 diabetes. Fifteen adults with type 2 diabetes and 16 matched controls (M/F 17/14, age 59.6±7.1 years, BMI 28.5±4.3 kg/m2) underwent a hyperinsulinemic-euglycemic (5.31±0.32 mmol/L) hypoglycemic (2.80±0.12 mmol/L) glucose clamp. Blood was drawn during euglycemia and hypoglycemia and 1, 3 and 7 days later, to determine circulating immune cell composition, function, and inflammatory proteins. In response to hypoglycemia, absolute numbers of circulating lymphocytes and monocytes significantly increased and remained elevated for one week. The proportion of CD16+ -monocytes increased, and the proportion of CD14+ -monocytes decreased, which sustained for a week in people without diabetes. During hypoglycemia, ex vivo stimulated, monocytes released more TNF-α and IL-1β, and less IL-10, particularly in people with diabetes. Hs-CRP and 25 circulating inflammatory proteins increased, remaining significantly elevated one week after hypoglycemia. While levels at euglycemia differed, responses to hypoglycemia were broadly similar in people with or without type 2 diabetes. We conclude that hypoglycemia induces a pro-inflammatory response at the cellular and protein level that is sustained for one week in people with type 2 diabetes and controls.

中文翻译:


低血糖对 2 型糖尿病患者和非糖尿病患者的持续促炎症作用



医源性低血糖会激活免疫系统,并与动脉粥样硬化疾病的风险增加相关。我们确定了胰岛素引起的低血糖对患有或不患有 2 型糖尿病的人类炎症标志物的急性和长期影响。 15 名患有 2 型糖尿病的成人和 16 名匹配的对照者(男/女 17/14,年龄 59.6±7.1 岁,BMI 28.5±4.3 kg/m2)接受高胰岛素-正常血糖(5.31±0.32 mmol/L)低血糖(2.80±0.12)治疗。 mmol/L) 葡萄糖钳。在血糖正常和低血糖期间以及1、3和7天后抽血,以确定循环免疫细胞的组成、功能和炎症蛋白。作为对低血糖的反应,循环淋巴细胞和单核细胞的绝对数量显着增加,并在一周内保持升高状态。 CD16+单核细胞比例增加,CD14+单核细胞比例减少,这种情况在非糖尿病人群中持续一周。在低血糖期间,在离体刺激下,单核细胞释放更多的 TNF-α 和 IL-1β,以及更少的 IL-10,尤其是在糖尿病患者中。 Hs-CRP 和 25 种循环炎症蛋白增加,低血糖 1 周后仍显着升高。虽然正常血糖水平不同,但患有或不患有 2 型糖尿病的人对低血糖的反应大致相似。我们得出的结论是,低血糖会在细胞和蛋白质水平上诱导促炎症反应,这种反应在 2 型糖尿病患者和对照组中可持续一周。
更新日期:2022-07-18
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