Sains Malaysiana 54(1)(2025): 255-263

http://doi.org/10.17576/jsm-2025-5401-20

 

Ameliorative Effects of Betanin in Mice with Trimethyltin-Induced Pancreatic and Hepatocytic Alterations

(Kesan Amelioratif Betanin pada Tikus dengan Perubahan Pankreas dan Hepatosit Terinduksi Trimethyltin)

 

Wachiryah Thong-asa*, Yanisa Detpakdee & Kanlayawadee Srisoonthon

 

Animal Toxicology and Physiology Specialty Research Unit (ATPSRU), Department of Zoology, Faculty of Science, Kasetsart University, Bangkok 10900 Thailand

 

Diserahkan: 28 Mei 2024/Diterima: 4 November 2024

 

Abstract

The effects of TMT on metabolic alteration are on the rise, including obesity and diabetes. In the present study, we aimed to investigate the protective effect of betanin (Bet) against TMT-induced glycemic disturbance and pancreatic and hepatocytic alterations, expanding on TMT’s and Bet’s effects on metabolic diseases. Fifty male Institute of Cancer Research (ICR) mice were randomly divided into Sham-veh, TMT-L-veh, TMT-H-veh, TMT-L-Bet100, and TMT-H-Bet100 groups. A low dose (L) (1 mg/kg) and high dose (H) (2.6 mg/kg) of TMT were given via one-time intraperitoneal (i.p.) injection before intragastric gavage administration of treatments for 4 consecutive weeks. A weekly oral glucose tolerance test (OGTT) was conducted for glycemic control capacity evaluation with serum insulin assessment. Pancreatic and hepatic tissues were collected to analyze islet number and beta cell density, glycogen content, and histopathology. TMT exposure did not significantly change glycemic control capacity or serum insulin level (p > 0.05). TMT significantly reduced pancreatic beta cell density, and this was accompanied by a decrease in hepatic glycogen content and an increase in hepatosteatosis and inflammation (p < 0.05). Treatment with Bet significantly alleviated all these alterations (p < 0.05). Bet showed alleviative effects against TMT-induced pancreatic and hepatocytic alterations, including preventing pancreatic beta cell damage, maintaining the liver’s glycogen content, anti-hepatosteatosis, and anti-inflammation.

 

Keywords: Betanin; glycemic control; hepatosteatosis; pancreatic beta cell; trimethyltin

 

Abstrak

Kesan TMT pada perubahan metabolik semakin meningkat, termasuk obesiti dan diabetes. Dalam kajian ini, kami berhasrat untuk mengkaji kesan perlindungan betanin (Bet) terhadap gangguan glisemik aruhan-TMT dan perubahan pankreas dan hepatosit, mengembangkan kesan TMT dan Bet pada penyakit metabolik. Lima puluh tikus jantan Institut Penyelidikan Kanser (ICR) secara rawak dibahagikan kepada kumpulan Sham-veh, TMT-L-veh, TMT-H-veh, TMT-L-Bet100 dan TMT-H-Bet100. Dos rendah (L) (1 mg/kg) dan dos tinggi (H) (2.6 mg/kg) TMT diberikan melalui satu suntikan intraperitoneal (i.p.) sebelum diberikan rawatan gavage intragastrik selama 4 minggu berturut-turut. Ujian toleransi glukosa oral secara mingguan (OGTT) telah dijalankan untuk penilaian kapasiti kawalan glisemik dengan penilaian insulin serum. Tisu pankreas dan hati dikumpul untuk analisis nombor kelompok dan ketumpatan sel beta, kandungan glikogen dan histopatologi. Pendedahan TMT tidak banyak mengubah kapasiti kawalan glisemik atau aras insulin serum (p > 0.05). TMT mengurangkan ketumpatan sel beta pankreas dengan ketara dan menurunkan kandungan glikogen hepatik dan peningkatan dalam hepatosteatosis dan keradangan (p <0.05). Rawatan dengan Bet telah mengurangkan semua perubahan ini dengan ketara (p < 0.05). Bet menunjukkan kesan pengurangan terhadap perubahan pankreas dan hepatosit aruhan TMT, termasuk mencegah kerosakan sel beta pankreas, mengekalkan kandungan glikogen hati, anti-hepatosteatosis dan anti-keradangan.

 

Kata kunci: Betanin; kawalan glisemik; hepatosteatosis; sel beta pankreas; trimetiltin

 

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*Pengarang untuk surat-menyurat; email: fsciwyth@ku.ac.th

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

   

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