Short Chain Fatty Acids and Fecal Microbiota Abundance in Humans with Obesity: A Systematic Review and Meta-Analysis

Abstract

There have been mixed results regarding the relationship among short chain fatty acids (SCFAs), microbiota, and obesity in human studies. We selected studies that provided data on SCFA levels or fecal microbiota abundance in obese and nonobese individuals and then combined the published estimates using a random-effects meta-analysis. Obese individuals had significantly higher fecal concentrations of acetate (SMD (standardized mean differences) = 0.87, 95% CI (confidence interva) = 0.24–1.50, I2 (I–squared) = 88.5), propionate (SMD = 0.86, 95% CI = 0.35–1.36, I2 = 82.3%), and butyrate (SMD = 0.78, 95% CI = 0.29–1.27, I2 = 81.7%) than nonobese controls. The subgroup analyses showed no evidence of heterogeneity among obese individuals with a BMI >30 kg/m2 (I2 = 0.0%). At the phylum level, the abundance of fecal microbiota was reduced in obese compared to nonobese individuals, but the difference was not statistically significant (Bacteroidetes phylum, SMD = −0.36, 95% CI = −0.73–0.01; Firmicutes phylum, SMD = −0.10, 95% CI = −0.31–0.10). The currently available human case-control studies show that obesity is associated with high levels of SCFA but not gut microbiota richness at the phylum level. Additional well-designed studies with a considerable sample size are needed to clarify whether this association is causal, but it is also necessary to identify additional contributors to SCFA production, absorption, and excretion in humans.

Timing of complementary feeding is associated with gut microbiota diversity and composition and short chain fatty acid concentrations over the first year of life

“…Although we found that infants given early complementary foods had higher butyrate concentrations at 12 months of age, we cannot discern whether this is the result of SCFA production vs. excretion, for which there is a measurable trade off [24]. Higher fecal concentrations of butyrate and propionate in humans has been associated with worse metabolic outcomes like obesity and hypertension, while higher serum SCFAs have been associated with better health [25,52,53]. Inflammation in the gut could be triggered by the early displacement of infant-associated microbes and metabolites, subsequently reducing the absorption of butyrate and increasing its excretion in the feces [54].…”

“…Still, the majority of human studies on SCFAs and immunometabolic conditions have been performed in adults, making it unclear if these relationships hold true for infants [20][21][22]. As the nutritional requirements for infants change significantly across the first year of life to support rapid growth during this period, there could be differences in the role of the gut microbiota and subsequent production of SCFAs on metabolism [53,55]. More research is warranted to determine if higher fecal SCFA concentrations in infants are associated with development of health outcomes later in life.…”

Detection of Early Disease Risk Factors Associated with Metabolic Syndrome: A New Era with the NMR Metabolomics Assessment

“…It is derived from intestinal microbial fermentation of dietary fibers in the colon [219] and acts as signaling ligand between host metabolism and the gut microbiome at different levels [220]. Acetate contribution leads to energy harvest participating in the human energy balance, with an important role in lipogenesis, cholesterol synthesis and accumulation in adipocytes [221]. Acetate affects substrate metabolism and host energy via an increase in energy expenditure and fat oxidation [222].…”

Short Chain Fatty Acids Commonly Produced by Gut Microbiota Influence Salmonella enterica Motility, Biofilm Formation, and Gene Expression

“…mediates resistance to Salmonella colonization by producing propionate [9]. Diverse studies have observed total SFCAs concentrations ranging between 60 and 85 mM with levels of acetate between 40 and 50 mM, propionate around 15 mM, and butyrate around 10 mM [11,12]. A dysregulation of SCFAs levels can facilitate the colonization of intestine by pathogens.…”