Parial Ramendu, Siddika Ayesha, Chowdhury Md Maruf H, Das Manisha
Department of Biochemistry and Molecular Biology, University of Chittagong, Chattogram 4331, Bangladesh.
Research and Publication Division, EuGEF Research Foundation, Chattogram, Bangladesh.
Indian J Endocrinol Metab. 2025 Jul-Aug;29(4):472-477. doi: 10.4103/ijem.ijem_546_24. Epub 2025 Aug 26.
Cationic trypsinogen () gene mutation is responsible for hereditary pancreatitis (HP) with clinical outcomes like abdominal pain, diabetes mellitus and pancreatic cancer. The present study aims to screen () gene polymorphism in the Bangladeshi population, categorized as normal glucose tolerant (NGT), prediabetes (PD) and type 2 diabetes (T2D).
Blood was collected from the study subjects with overnight fasting (8-10 h), and 2 h after 75 g glucose intake orally. Serum was used for biochemical analyses, and whole blood for genetic analysis. Biochemical parameters were measured following a standard procedure. Anthropometric, clinical and biochemical abnormalities were defined and classified as per World Health Organization (WHO) guidelines for the population from Asia. Genetic analysis was done following the polymerase chain reaction-restriction fragment length polymorphism method standardized in our laboratory. Data were analyzed with the SPSS Software (version 22), IBM Corporation, USA.
For the genotype, a total of 559 subjects were screened. R122H and R122C variant genotypes were absent in all subjects' categories. However, three heterozygous variant genotypes A16V (1.3%) in the trypsinogen gene were found in the NGT subjects group. Abdominal pain in the subjects was significantly higher in the A16V variant genotype compared to subjects with no abdominal pain (Fisher's exact/, 7.256/0.027). A significant positive correlation was observed with the genotype for the abdominal pain ( = 0.008) and DBP ( = 0.026) of the study subjects.
and variants have no relationship with prediabetic and/or type 2 diabetic subjects of Bangladesh. However, abdominal pain was significantly related to the A16V variant.
阳离子胰蛋白酶原（）基因突变是遗传性胰腺炎（HP）的病因，可导致腹痛、糖尿病和胰腺癌等临床症状。本研究旨在筛查孟加拉人群中正常糖耐量（NGT）、糖尿病前期（PD）和2型糖尿病（T2D）患者的（）基因多态性。
研究对象在空腹过夜（8 - 10小时）后及口服75克葡萄糖2小时后采集血液。血清用于生化分析，全血用于基因分析。按照标准程序测量生化参数。根据世界卫生组织（WHO）针对亚洲人群的指南对人体测量、临床和生化异常进行定义和分类。采用我们实验室标准化的聚合酶链反应 - 限制性片段长度多态性方法进行基因分析。使用美国IBM公司的SPSS软件（版本22）对数据进行分析。
共筛查了559名受试者的基因型。所有受试者类别中均未发现R122H和R122C变异基因型。然而，在NGT受试者组中发现了胰蛋白酶原基因的三种杂合变异基因型A16V（1.3%）。与无腹痛的受试者相比，A16V变异基因型受试者的腹痛发生率显著更高（Fisher确切概率法/，7.256/0.027）。研究对象的腹痛（ = 0.008）和舒张压（ = 0.026）与基因型呈显著正相关。
和变异与孟加拉的糖尿病前期和/或2型糖尿病患者无关。然而，腹痛与A16V变异显著相关。
