Indian journal of endocrinology and metabolism · 2025
Assessment of the Relationship of Cationic Trypsinogen (PRSS1) Gene Polymorphism with Prediabetes and Type 2 Diabetes in the Bangladeshi Population.
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Parial Ramendu, Siddika Ayesha, Chowdhury Md Maruf H, Das Manisha
Аннотация
INTRODUCTION: Cationic trypsinogen (PRSS1) 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 PRSS1 (A16V, R122C and R122H) gene polymorphism in the Bangladeshi population, categorized as normal glucose tolerant (NGT), prediabetes (PD) and type 2 diabetes (T2D).
METHODS: 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.
RESULTS: For the PRSS1 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/P, 7.256/0.027). A significant positive correlation was observed with the A16V genotype for the abdominal pain (P = 0.008) and DBP (P = 0.026) of the study subjects.
CONCLUSION: PRSS1 A16V, R122C and R122H variants have no relationship with prediabetic and/or type 2 diabetic subjects of Bangladesh. However, abdominal pain was significantly related to the PRSS1 A16V variant.
METHODS: 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.
RESULTS: For the PRSS1 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/P, 7.256/0.027). A significant positive correlation was observed with the A16V genotype for the abdominal pain (P = 0.008) and DBP (P = 0.026) of the study subjects.
CONCLUSION: PRSS1 A16V, R122C and R122H variants have no relationship with prediabetic and/or type 2 diabetic subjects of Bangladesh. However, abdominal pain was significantly related to the PRSS1 A16V variant.