Decoding dietary pectin: from structural complexity and microbial CAZyme–PUL networks to cross-feeding and host-beneficial metabolites
TL;DR
This review systematically examines the pathways through which pectin is degraded by the gut microbial consortia, with a central focus on the role of carbohydrate-active enzymes (CAZymes), and proposes that future efforts should focus on achieving a more comprehensive understanding of microbial and enzymatic mechanisms of pectin degradation.
Abstract
Abstract The interaction of pectin, as one of the most complex dietary glycans, with gut microbiota represents a typical pattern for shaping the gut microenvironment and human homeostasis. Pectin has a heterogeneous structure, characterized by homogalacturonan (HG), rhamnogalacturonan I (RG-I), and rhamnogalacturonan II (RG-II) domains, which dictate its fermentability and functional outcomes. This review systematically examines the pathways through which pectin is degraded by the gut microbial consortia, with a central focus on the role of carbohydrate-active enzymes (CAZymes). These enzymes, including glycoside hydrolases (GHs), polysaccharide lyases (PLs), and carbohydrate esterases (CEs), act synergistically to depolymerize pectin into oligosaccharides and monosaccharides. Specific microbial groups, notably Bacteroides and Bifidobacterium, utilize these breakdown products via specialized transport systems. Intracellular fermentation leads to the synthesis of a series of degradation products, such as acetate, propionate, and butyrate, which are crucial for maintaining gut barrier integrity, modulating immune responses, and regulating systemic metabolism. Finally, we summarize the multifaceted health effects of pectin-derived short-chain fatty acids (SCFAs) and propose that future efforts should focus on achieving a more comprehensive understanding of microbial and enzymatic mechanisms of pectin degradation, as well as complex cross-feeding networks, to inform the development of targeted nutritional interventions.