An increase in inflammation and islet dysfunction is a feature of prediabetes

糖尿病前期 医学 炎症 内科学 内分泌学 抵抗素 糖尿病 小岛 2型糖尿病 胰岛素抵抗 脂肪因子
作者
Jessica R. Weaver,Justin J. Odanga,Erick K. Breathwaite,Michelle Treadwell,Angela C. Murchinson,Gary Walters,Danette P. Fuentes,Jung Bok Lee
出处
期刊:Diabetes-metabolism Research and Reviews [Wiley]
卷期号:37 (6) 被引量:20
标识
DOI:10.1002/dmrr.3405
摘要

Type 2 diabetes (T2D) is a global health problem that will be diagnosed in almost 300 million people by 2025 according to the World Health Organization. Before being diagnosed with T2D, individuals may have glucose levels above normal but below the diabetic range. This condition is known as prediabetes. Studies showed that people with prediabetes had an increase in several pro-inflammatory cytokines in their serum and in their fasting glucose levels. The answer remains unclear when inflammation begins in the pancreas and islets, and what is the extent of this inflammation.Subjects with haemoglobin A1c levels from 5.7% to 6.4% were classified as pre-diabetic. Sections of pancreas and isolated islets from normal donors and donors with prediabetes were tested for markers of inflammation and glucose-stimulated insulin secretion (GSIS).Gene and protein expression of the inflammatory markers resistin, interleukin-1 beta, tumour necrosis factor-alpha, interleukin-6, and monocyte chemoattractant protein-1 increased in donors with prediabetes compared to normal donors. GSIS response was significantly decreased in pre-diabetic islets compared to normal islets. Donors with prediabetes also had decreased expression of CD163+ cells but not CD68+ cells.Based on our findings, inflammation and islet dysfunction may be more significant than originally thought in people with prediabetes. Rather than being in a normal state before diabetes occurs, it appears that subjects are already in an early diabetic condition resembling more closely T2D.
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