Maternal quercetin intake during lactation attenuates renal inflammation and modulates autophagy flux in high fructose-fed female rat offspring exposed to maternal malnutrition

Maternal restriction of dietary protein during pregnancy and lactation is known to induce renal disease in later life. High fructose intake causes metabolic syndrome, which results in an increased risk of chronic kidney disease development. We investigated whether quercetin intake during lactation affects high fructose-induced inflammation and autophagy flux in the kidneys of high-fructose diet-fed adult female offspring exposed to maternal normal (NP)- or low (LP)-protein diets. Pregnant Wistar rats received diets containing 20% (NP) or 8% (LP) casein, as well as 0 or 0.2%- quercetin containing NP diets (NP/NP or NP/NPQ) in Experiment (Expt.) 1, 0 or 0.2%- quercetin containing LP diets (LP/LP or LP/LPQ) diets in Expt. 2 during lactation. At weaning, pups that received a diet of distilled water (Wa) or 10% fructose solution (Fr) were divided into six groups: NP/NP/Wa, NP/NP/Fr, NP/NPQ/Fr in Expt. 1, and LP/LP/Wa, LP/LP/Fr, LP/LPQ/Fr in Expt. 2, respectively. At week 12, macrophage infiltration, mRNA levels of TNF-α and IL-6, and markers of autophagy flux in the kidneys of male offspring were examined. We found that macrophage number and, TNF-α and IL-6 mRNA levels increased in the kidneys of the NP/NP/Fr or LP/LP/Fr, respectively. Conversely, macrophage number and IL-6 levels in the NP/NPQ/Fr or LP/LPQ/Fr decreased. LC3B-II levels were downregulated in the NP/NP/Fr or LP/LP/Fr rats. In contrast, LC3B-II levels were upregulated while p62 levels were downregulated in NP/NPQ/Fr and LP/LPQ/Fr rats. In conclusion, maternal quercetin intake during lactation may cause long-term alterations in inflammation and autophagy flux in the kidneys of high fructose-fed adult female offspring.