Abstract
Gut microbiota-mediated inflammation promotes obesity-associated low-grade inflammation, which represents a hallmark of metabolic syndrome. To investigate if lifestyle-induced weight loss (WL) may modulate the gut microbiome composition and its interaction with the host on a functional level, we analyzed the fecal metaproteome of 33 individuals with metabolic syndrome in a longitudinal study before and after lifestyle-induced WL in a well-defined cohort. The 6-month WL intervention resulted in reduced BMI (−13.7%), improved insulin sensitivity (HOMA-IR, −46.1%), and reduced levels of circulating hsCRP (−39.9%), indicating metabolic syndrome reversal. The metaprotein spectra revealed a decrease of human proteins associated with gut inflammation. Taxonomic analysis revealed only minor changes in the bacterial composition with an increase of the families Desulfovibrionaceae, Leptospiraceae, Syntrophomonadaceae, Thermotogaceae and Verrucomicrobiaceae. Yet we detected an increased abundance of microbial metaprotein spectra that suggest an enhanced hydrolysis of complex carbohydrates. Hence, lifestyle-induced WL was associated with reduced gut inflammation and functional changes of human and microbial enzymes for carbohydrate hydrolysis while the taxonomic composition of the gut microbiome remained almost stable. The metaproteomics workflow has proven to be a suitable method for monitoring inflammatory changes in the fecal metaproteome.
Highlights
IntroductionThe development of obesity and metabolic syndrome depends to a large extent on an individual’s unique metabolic processing of foods, genetics, lifestyle, and gut microbiome
Taxonomic and functional alterations of the gut microbiome are typically observed in inflammatory gut diseases [2] and in metabolic diseases such as diabetes mellitus [3] or obesity [4,5]
Recent studies suggest that metabolic syndrome is associated with a maladaptive gut microbiome that promotes obesity-associated low-grade inflammation [1] leading to progression of diabetes mellitus and cardiovascular disease [5]
Summary
The development of obesity and metabolic syndrome depends to a large extent on an individual’s unique metabolic processing of foods, genetics, lifestyle, and gut microbiome. Experimental and observational evidence suggests that obesity-associated inflammation plays a central role in metabolic dysfunction and disease progression. Recent studies indicate that gut microbiome-mediated inflammation may promote metabolic disorders and obesity-associated low-grade inflammation [1]. Taxonomic and functional alterations of the gut microbiome are typically observed in inflammatory gut diseases [2] and in metabolic diseases such as diabetes mellitus [3] or obesity [4,5]. Close spatial and functional interactions of the host and gut microbiota require a welltuned balance. Gut microbiota may affect host physiology through metabolic activities and fermentation of nondigestible dietary components and synthesis of vitamins and signaling molecules [7]. The definition of the microbiome’s role in resolution of metabolic disease following lifestyleinduced WL remains elusive
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