Resveratrol intervention attenuates chylomicron secretion via repressing intestinal FXR-induced expression of scavenger receptor SR-B1

Juan Pang, Fitore Raka, Alya Abbas Heirali, Weijuan Shao, Dinghui Liu, Jianqiu Gu, Jia Nuo Feng, Chieko Mineo, Philip W. Shaul, Xiaoxian Qian, Bryan Coburn, Khosrow Adeli (), Wenhua Ling () and Tianru Jin ()
Additional contact information
Juan Pang: Sun Yat-sen University
Fitore Raka: The Hospital for Sick Children
Alya Abbas Heirali: University Health Network
Weijuan Shao: University Health Network
Dinghui Liu: The Third Affiliated Hospital of Sun Yat-sen University
Jianqiu Gu: The First Hospital of China Medical University
Jia Nuo Feng: University Health Network
Chieko Mineo: University of Texas Southwestern Medical Center
Philip W. Shaul: University of Texas Southwestern Medical Center
Xiaoxian Qian: The Third Affiliated Hospital of Sun Yat-sen University
Bryan Coburn: University Health Network
Khosrow Adeli: The Hospital for Sick Children
Wenhua Ling: Sun Yat-sen University
Tianru Jin: University Health Network

Nature Communications, 2023, vol. 14, issue 1, 1-18

Abstract: Abstract Two common features of dietary polyphenols have hampered our mechanistic understanding of their beneficial effects for decades: targeting multiple organs and extremely low bioavailability. We show here that resveratrol intervention (REV-I) in high-fat diet (HFD)-challenged male mice inhibits chylomicron secretion, associated with reduced expression of jejunal but not hepatic scavenger receptor class B type 1 (SR-B1). Intestinal mucosa-specific SR-B1-/- mice on HFD-challenge exhibit improved lipid homeostasis but show virtually no further response to REV-I. SR-B1 expression in Caco-2 cells cannot be repressed by pure resveratrol compound while fecal-microbiota transplantation from mice on REV-I suppresses jejunal SR-B1 in recipient mice. REV-I reduces fecal levels of bile acids and activity of fecal bile-salt hydrolase. In Caco-2 cells, chenodeoxycholic acid treatment stimulates both FXR and SR-B1. We conclude that gut microbiome is the primary target of REV-I, and REV-I improves lipid homeostasis at least partially via attenuating FXR-stimulated gut SR-B1 elevation.

Date: 2023
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DOI: 10.1038/s41467-023-38259-1

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