Lactobacillus plantarum improves lipogenesis and IRS-1/AKT/eNOS signalling pathway in the liver of high-fructose-fed rats

Sumlu E., Bostanci A., SADİ G., ALÇIĞIR M. E., AKAR F.

ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY, cilt.128, sa.3, ss.786-794, 2022 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 128 Sayı: 3
  • Basım Tarihi: 2022
  • Doi Numarası: 10.1080/13813455.2020.1727527
  • Dergi Adı: ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, Food Science & Technology Abstracts, MEDLINE, Veterinary Science Database
  • Sayfa Sayıları: ss.786-794
  • Anahtar Kelimeler: Dietary fructose, fatty liver, insulin signalling, Lactobacillus plantarum, Lactobacillus helveticus, INSULIN-RESISTANCE, HIGH-FAT, DIETARY FRUCTOSE, MESSENGER-RNA, EXPRESSION, DYSFUNCTION, ACTIVATION, DISEASE, CHREBP, GENES
  • Gazi Üniversitesi Adresli: Evet

Özet

In the present study, we investigated the influence of Lactobacillus plantarum and Lactobacillus helveticus supplementation on lipogenesis, insulin signalling and glucose transporters in liver of high-fructose-fed rats. Fructose was given to the rats as a 20% solution in drinking water for 15 weeks. Lactobacillus plantarum and L. helveticus supplementations were performed by gastric gavage once a day during final 6 weeks. Dietary high-fructose increased hepatic weight, lipid accumulation and FASN expression as well as caused a significant reduction in IRS-1 expression, pAKT/total AKT and peNOS/total eNOS ratios, but an elevation in GLUT2 and GLUT5 mRNAs in the liver. Lactobacillus plantarum supplementation decreased hepatic weight, triglyceride content and FASN expression as well as improved IRS-1/AKT/eNOS pathway and GLUT2 expression in the liver of high-fructose-fed rats. However, L. helveticus supplementation exerted a restoring effect on lipid accumulation by decreasing FASN expression, and regulating effect on IRS-1 and GLUT2 expressions.