Why the study?
Hypercaloric diet-induced dyslipidemia and obesity lead to kidney damage, prompting investigation into whether curcumin modulates related inflammation, fibrosis, lipid metabolism, and morphological changes.
Does curcumin prevent renal damage, inflammation, fibrosis, and lipid metabolism alterations in mice fed high-fat and/or high-fructose diets?
Does curcumin prevent renal damage, inflammation, fibrosis, and lipid metabolism alterations in mice fed high-fat and/or high-fructose diets?
Curcumin prevents renal structural damage and modulates renal injury in mice fed hypercaloric diets.
Curcumin may attenuate diet-induced renal changes in mice; leaves open any clinical role in human obesity-related kidney disease.
BACKGROUND: Dyslipidemia and obesity hypercaloric diet-induced lead to kidney damage. We investigated the effect of curcumin on the expression of proteins related to inflammation, fibrosis, fatty acids metabolism, kidney damage, and morphological changes in the kidneys of mice hypercaloric diets-fed. METHODS: Groups of 5-week-old C57BL/6 mice (n=6) were formed: Control (C), High-fructose diet (F), Highfructose diet and curcumin (F+Cur), High-fat diet (HFD), High-fat diet and curcumin (HFD+Cur), High-fat diet and fructose (HFD+F), High-fat diet, fructose and curcumin (HFD+F+Cur), treated for 16 weeks with 30% (w/v) fructose, 60% (w/w) fat and 0.75% (w/w) curcumin. Kidneys were obtained for histomorphological and Western blot analysis. RESULTS: Curcumin prevented TNF-α overexpression in the F and HFD+F groups. VLCAD expression was higher in the F, HFD, and HFD+F groups. PPARγ expression was lower in the F+Cur, HFD+Cur, and HFD+F+Cur groups. Curcumin prevented overexpression of CPT1 and KIM1 in the HFD+F and HFD groups. Curcumin prevented morphological lesions, fibrosis, and lipid deposition that were hypercaloric diet-induced. CONCLUSION: Chronic consumption of hypercaloric diets causes inflammation, fibrosis, and lipid deposition in the kidney. It is suggested that curcumin prevents renal structural damage, limits tissue lipid deposition, and differentially modulates renal injury depending on diet composition in mice fed high-fat and/or high-fructose diets.
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Meléndez-Salcido et al. (2024) studied this question.
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