Review reveals pharmacological strategies targeting gut microbiota and endotoxemia in metabolic syndrome, highlighting novel therapeutic avenues against systemic inflammation and cardiometabolic risk.
Central obesity, atherogenic dyslipidaemia, insulin resistance, and hypertension are among the metabolic dysregulations associated with metabolic syndrome (MetS). Insulin resistance and chronic low-grade inflammation are two of the many acquired and genetic components that make up the pathophysiology of MetS. MetS is strongly linked to a greater risk of diabetes and CVD in the absence of effective treatment. To create effective intervention strategies and preventative techniques, the MetS process needs to be thoroughly examined. Recent research has emphasised the critical roles that metabolic endotoxemia and the gut microbiota play in the pathophysiology of MetS. The manipulation of gut microbiota‒host metabolism interactions has been linked to several factors, including bile acid metabolism, short-chain fatty acid metabolism, and inflammation caused by malfunction of the gut barrier. Pharmacological treatments for the gut microbiota are becoming increasingly popular as treatment alternatives. This brief message highlights some of the most recent developments in pharmaceutical strategies for preventing both gut dysbiosis and systemic low-grade inflammation caused by endotoxemia. Antibiotics, prebiotics, probiotics, synbiotics, postbiotics, and metabolite modulators produced from the microbiota are all used in these tactics. Particular focus is placed on next-generation treatments such as small chemical inhibitors of microbial‒host interactions, bacteriophage therapy, and tailored probiotics.
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Dimeji et al. (2025) studied this question.
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