Potential mechanistic pathways underlying intestinal and hepatic effects of kefir in high-fructose-fed rats.

Akar F., Sumlu E., Alçığır M. E., Bostancı A., Sadi G.

Food research international (Ottawa, Ont.), cilt.143, ss.110287, 2021 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 143
  • Basım Tarihi: 2021
  • Doi Numarası: 10.1016/j.foodres.2021.110287
  • Dergi Adı: Food research international (Ottawa, Ont.)
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED)
  • Sayfa Sayıları: ss.110287
  • Anahtar Kelimeler: Dietary fructose, Kefir, Microbiota, Permeability factors, Lipogenesis, Insulin signaling, NF-KAPPA-B, GUT MICROBIOTA, INSULIN-RESISTANCE, EXOPOLYSACCHARIDE KEFIRAN, DIET, MICE, EXPRESSION, STEATOSIS, LIPOGENESIS, MODULATION
  • Gazi Üniversitesi Adresli: Evet

Özet

Excess intake of fructose may contribute to the high prevalence of metabolic disorder. In this study, we investigated the effects of kefir supplementation on the intestine-liver-adipose tissue axis in metabolic disorder induced by high-fructose diet in rats to describe mechanistic action and potential therapeutic value of kefir. Fructose was given to the rats as a 20% solution in drinking water for 15 weeks. Kefir was administrated by gastric gavage once a day during the final six weeks. Kefir supplementation improved metabolic parameters, including plasma triglyceride and insulin levels; hepatic weight, triglyceride content and fatty degeneration; omental fat mass in fructose-fed rats. Kefir supplementation decreased the ratio of Firmicutes/Bacteroidetes in feces, as well as necrotic degeneration, expression levels of nuclear factor-kappa B (NF-kappa B), and inducible nitric oxide synthase (iNOS), but increased expression of tight-junction proteins occludin and claudin-1, in the ileum of the fructose-fed rats. Kefir treatment also reduced the mRNA levels of key lipogenic genes sterol regulatory element-binding protein (SREBP-1c) and fatty acid synthase (FASN) together with a decline in expression of tumor necrosis factor-alpha (TNF-alpha), NF-kappa B, and glycosylated glycoprotein (CD68) in the liver. Moreover, kefir treatment improved insulin signaling at the level of insulin receptor substrate 1 (IRS-1) and phospho-endothelial nitric oxide synthase (peNOS) as well as fructose transporters (GLUT2 and GLUT5) in the liver, but not in the adipose tissue, of high-fructose-fed rats. Consequently, kefir supplementation suppresses hepatic lipogenesis and inflammatory status, but promotes insulin signaling, in association with a change of the fecal microbiota and attenuation of the intestinal permeability factors in high-fructose-fed rats. Thus, we propose that kefir has favorable effects on the hepatic and intestinal irregularities induced by fructose overconsumption.