Alginate Oligosaccharide and Gut Microbiota: Exploring the Key to Health

Abstract

Alginate oligosaccharide (AOS), a degradation product of alginate derived from marine brown algae, has attracted significant attention due to its potent ability to modulate gut microbiota and enhance human health. This review aims to systematically introduce current evidence on the interactions between AOS and gut microbial communities, focusing on how AOS improves health through regulating gut microbiota. Initially, the structural factors of AOS that influence their functions are highlighted, including molecular weight, monomer composition, terminal structure, and chemical modifications. Importantly, AOS primarily exerts beneficial effects by adjusting gut microbiota community and outputs, which include the promotion of probiotics, the inhibition of pathogens, the balance of microbiota composition, and the increase of short-chain fatty acid production. Moreover, the discovered mechanisms underlying AOS-mediated health promotion via microbiota modulation are detailed comprehensively, specifically emphasizing intestinal barrier maintenance, antioxidation, dual-regulation of immune and inflammatory responses, pathogenic infection inhibition, metabolic improvement, uric acid excretion promotion, anti-tumor effects, and anti-skin aging. Such beneficial effects make AOS valuable in keeping healthy, preventing disorders, and intervening in diseases. Despite these findings and research progress, there are yet limitations in studying AOS-gut microbiota interactions, such as precise microbiota-targeted structural optimization, personalized nutritional interventions based on microbial characteristics, and broadening the horizon of microbiota-derived metabolic metabolomic profiles. In conclusion, advancing our understanding of the gut microbiota-centered mechanisms of AOS would probably facilitate novel nutritional strategy development for health promotion.

Keywords: alginate; gut microbiota; intestinal health; oligosaccharide; prebiotics; short-chain fatty acids; α-L-guluronic acid; β-D-mannuronic acid.

Figure 1

The structure of AOS. (A) β-d-mannuronic acid (M) and α-l-guluronic acid (G) units, along with one of their oligomers, “M-G-M”, as an example; (B) terminal structures of unsaturated, saturated, and carboxyl AOS. The red color highlights the difference of terminal structures.

Figure 2

Mechanism of AOS in promoting health through gut microbiota, including maintenance of intestinal barrier integrity (involving upregulating the expression of intestinal tight junction and increasing the thickness of intestinal mucus layer), antioxidation (involving regulating the oxidative and antioxidative system homeostasis), dual regulation of inflammation and immune responses, anti-tumor effects (involving improving inflammation as well as oxidative stress), inhibiting pathogen infections (involving regulating pH, promoting the secretion of immune globulin, maintaining the integrity of biofilm, etc.), regulation of lipid and glucose metabolism (involving promoting lipolysis and glycolysis, while inhibiting lipid synthesis and gluconeogenesis), promotion of uric acid excretion, and anti-skin aging. “+” and “↑” indicate increasing, upregulating, promoting, accelerating, activating, or maintaining effects of AOS, while “−” and “↓” indicate decreasing, downregulating, inhibiting, or suppressing effects of AOS. AMPs: antimicrobial peptides; SCFAs: short-chain fatty acids; AMPK: adenosine 5′-monophosphate-activated protein kinase; NF-κB: nuclear factor-κB; Akt: protein kinase B; IL-1β: interleukin-1β; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; IFN-γ: interferon-γ; COX-2: cyclooxygenase-2; ROS: reactive oxygen species; MDA: malondialdehyde; SOD: superoxide dismutase; GSH: glutathione; CAT: catalase; STX: Shiga toxin; ST: heat-stable toxin; LT: heat-labile toxin; LPS: lipopolysaccharide; LDL: low-density lipoprotein; TC: total cholesterol; TG: triacylglycerol; FFAs: free fatty acids; AhR: aryl hydrocarbon receptor; SMCT: sodium-coupled monocarboxylate transporter; URAT1: urate transporter 1; GLUT9: glucose transporter 9; ABCG2: ATP-binding cassette superfamily G member 2; ABCG5: ATP-binding cassette superfamily G member 5; PYGL: phosphorylase glycogen lyase; PCK2: phosphoenolpyruvate carboxykinase 2; Fasn: fatty acid synthase; ACC1: acetyl-CoA carboxylase 1; SIRT1: sirtuin 1; Srebp1: sterol responsive element-binding protein 1; PGC1α: peroxisome proliferator-activated receptor γ coactivator 1α; chREBP: carbohydrate response element-binding protein; G6pase: glucose-6-phosphatase; GSK3α: glycogen synthase kinase 3α; GSK3β: glycogen synthase kinase 3β; GYS2: glycogen synthase 2; HK2: hexokinase 2; PFK1: phosphofructokinase 1.