Aiswarya Yalamanchi, Shivaprasad Channabasappa, Anish Kolly, Sridevi Atluri, Anupam Biswas, Amit Goel
Department of Endocrinology, Vydehi Institute of Medical Sciences and Research Centre, Bangalore, India.
Diabetes Metab Syndr Obes. 2019 May 22;12:779-788. doi: 10.2147/DMSO.S204254. eCollection 2019.
Fibrocalculous pancreatic diabetes (FCPD) is a secondary form of diabetes seen in patients with tropical chronic pancreatitis. Insulin deficiency plays a major role in the etiopathogenesis of FCPD. Limited data suggest a possible role of insulin resistance (IR) in the pathogenesis of FCPD. Sparse data exist on measures of insulin sensitivity (IS) and secretion in patients with FCPD and its comparison to type 2 diabetes mellitus (T2D) patients. Eighty patients with FCPD, 36 patients with T2D and 36 healthy subjects were included. A 75 g oral glucose tolerance test (OGTT) was performed in the morning after an overnight fast. We evaluated IS and secretion using indices derived from fasting (homeostasis model assessment of insulin resistance [HOMA-IR], quantitative insulin sensitivity check index [QUICKI] and homeostasis model assessment of beta-cell function [HOMA-ß]) and OGTT (Matsuda, insulin sensitivity index by Kanauchi [ISI-K], oral glucose insulin sensitivity index [OGIS], Stumvoll, insulinogenic index and oral disposition index [ODI]) measurements of glucose and insulin. HOMA-IR was significantly higher and QUICKI significantly lower in patients with FCPD and T2D than in healthy controls (<0.001). Matsuda, ISI-K, OGIS and Stumvoll were significantly lower in patients with FCPD and T2D than in healthy controls (<0.001), indicating reduced IS in both FCPD and T2D patients. HOMA-ß, insulinogenic index and ODI were significantly lower in patients with FCPD and T2D compared to healthy controls (<0.001). FCPD is associated with reduced IS as assessed by fasting and OGTT-based indices. FCPD is also associated with a greater degree of impairment in insulin secretion than in T2D. IR may play a role in the pathogenesis of FCPD.
纤维钙化性胰腺糖尿病(FCPD)是热带慢性胰腺炎患者中出现的一种继发性糖尿病形式。胰岛素缺乏在FCPD的病因发病机制中起主要作用。有限的数据表明胰岛素抵抗(IR)在FCPD发病机制中可能发挥作用。关于FCPD患者胰岛素敏感性(IS)和分泌的测量及其与2型糖尿病(T2D)患者的比较,现有数据稀少。纳入了80例FCPD患者、36例T2D患者和36名健康受试者。在过夜禁食后的早晨进行75克口服葡萄糖耐量试验(OGTT)。我们使用基于空腹(胰岛素抵抗稳态模型评估 [HOMA-IR]、定量胰岛素敏感性检查指数 [QUICKI] 和β细胞功能稳态模型评估 [HOMA-β])和OGTT(松田指数、金内胰岛素敏感性指数 [ISI-K]、口服葡萄糖胰岛素敏感性指数 [OGIS]、施图姆沃尔指数、胰岛素生成指数和口服处置指数 [ODI])的葡萄糖和胰岛素测量指标来评估IS和分泌。FCPD和T2D患者的HOMA-IR显著高于健康对照组,QUICKI显著低于健康对照组(<0.001)。FCPD和T2D患者的松田指数、ISI-K、OGIS和施图姆沃尔指数显著低于健康对照组(<0.001),表明FCPD和T2D患者的IS均降低。与健康对照组相比,FCPD和T2D患者的HOMA-β、胰岛素生成指数和ODI显著降低(<0.001)。根据基于空腹和OGTT的指标评估,FCPD与IS降低有关。FCPD还与胰岛素分泌受损程度比T2D更大有关。IR可能在FCPD的发病机制中起作用。