Does daily fasting shielding kidney on hyperglycemia-related inflammatory cytokine via TNF-α, NLRP3, TGF-β1 and VCAM-1 mRNA expression

Int J Biol Macromol. 2021 Nov 1:190:911-918. doi: 10.1016/j.ijbiomac.2021.08.216. Epub 2021 Sep 4.

Abstract

This study aimed to investigate the effects of blood glucose control and the kidneys' functions, depending on fasting, in the streptozotocin-induced diabetes model in rats via TNF-α, NLRP-3, TGF-β1 and VCAM-1 mRNA expression in the present study. 32 Wistar albino rats were allocated randomly into four main groups; H (Healthy, n = 6), HF (Healthy fasting, n = 6), D (Diabetes, n = 10), DF (Diabetes and fasting, n = 10). Blood glucose and HbA1c levels significantly increased in the D group compared to the healthy ones (p < 0.05). However, the fasting period significantly improved blood glucose and HbA1c levels 14 days after STZ induced diabetes in rats compared to the D group. Similar findings we obtained for serum (BUN-creatinine) and urine samples (creatinine and urea levels). STZ induced high glucose levels significantly up-regulated TNF-α, NLRP-3, TGF-β1 and VCAM-1 mRNA expression and fasting significantly decreased these parameters when compared to diabetic rats. Histopathological staining also demonstrated the protective effects of fasting on diabetic kidney tissue. In conclusion, intermittent fasting regulated blood glucose level as well as decreasing harmful effects of diabetes on kidney tissue. The fasting period significantly decreased the hyperglycemia-related inflammatory cytokine damage on kidneys and also reduced apoptosis in favor of living organisms.

Keywords: Diabetes; Fasting; Kidney; Rat.

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Blood Glucose / metabolism
  • Blood Urea Nitrogen
  • Caspase 9 / metabolism
  • Creatinine / blood
  • Creatinine / urine
  • Diabetes Mellitus, Experimental / blood
  • Diabetes Mellitus, Experimental / genetics
  • Diabetes Mellitus, Experimental / urine
  • Fasting / blood
  • Fasting / metabolism*
  • Glycated Hemoglobin / analysis
  • Hyperglycemia / blood
  • Hyperglycemia / genetics*
  • Hyperglycemia / pathology
  • Hyperglycemia / urine
  • Inflammation / genetics*
  • Inflammation / pathology
  • Kidney / pathology*
  • NLR Family, Pyrin Domain-Containing 3 Protein / genetics*
  • NLR Family, Pyrin Domain-Containing 3 Protein / metabolism
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Wistar
  • Transforming Growth Factor beta1 / genetics*
  • Transforming Growth Factor beta1 / metabolism
  • Tumor Necrosis Factor-alpha / genetics*
  • Tumor Necrosis Factor-alpha / metabolism
  • Urea / urine
  • Vascular Cell Adhesion Molecule-1 / genetics*
  • Vascular Cell Adhesion Molecule-1 / metabolism

Substances

  • Blood Glucose
  • Glycated Hemoglobin A
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • RNA, Messenger
  • Transforming Growth Factor beta1
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • Urea
  • Creatinine
  • Caspase 9