Human Postprandial Nutrient Metabolism and Low-Grade Inflammation: A Narrative Review

Abstract

The importance of the postprandial state has been acknowledged, since hyperglycemia and hyperlipidemia are linked with several chronic systemic low-grade inflammation conditions. Humans spend more than 16 h per day in the postprandial state and the postprandial state is acknowledged as a complex interplay between nutrients, hormones and diet-derived metabolites. The purpose of this review is to provide insight into the physiology of the postprandial inflammatory response, the role of different nutrients, the pro-inflammatory effects of metabolic endotoxemia and the anti-inflammatory effects of bile acids. Moreover, we discuss nutritional strategies that may be linked to the described pathways to modulate the inflammatory component of the postprandial response.

Keywords: bile acids; low-grade inflammation; microbiome; nutrients; postprandial inflammation.

Figure 1

The postprandial period as an endocrine, metabolic and inflammatory framework. Meal ingestion results in a complex and multifactorial endocrine and metabolic response, which influences postprandial inflammation via different pathways. Ingestion of glucose and lipids induces postprandial inflammation, whereas amino acids have pro- and anti-inflammatory effects. During the postprandial period, the enterokines insulin, bile acids, fibroblast growth factor 19 (FGF19), glucagon-like peptide- 1 (GLP-1) and ghrelin are released and exert anti-inflammatory effects on postprandial metabolism. Leptin mediates negative effects in adipose tissue. Insulin also has pro-inflammatory effects. Furthermore, as a result of nutrient ingestion, several mechanisms (i.e., lipopolysaccharide (LPS), Toll-like receptor 4 (TLR4), nuclear factor kappa-light-chain-enhancer-of activated B cells (Nf-κB), reactive oxygen species (ROS), complement component factor 3 (C3), interleukins, Tumor Necrosis factor (TNF)-α and soluble CD14 are activated or produced, and stimulate postprandial inflammation.

Figure 2

The role of Farnesoid X Receptor (FXR) in postprandial inflammation. FXR activation exerts several anti-inflammatory effects via different pathways: FXR activation suppresses interferon gamma (IFNγ)-related genes in macrophages and inhibits Tumor necrosis Factor-α (TNF-α) production in immune cells, inhibits nuclear factor kappa-light-chain-enhancer-of activated B cells (Nf-κB) activity and the pro-inflammatory enzyme inducible nitric oxide synthase (iNOS) in vascular smooth muscle cells, maintains intestinal barrier integrity and induces antibacterial gene expression, decreases endoplasmatic reticulum (ER) stress-induced NLRP3 inflammasome activation assessed with interleukin-1beta (IL-1β) and increases the gene expression of complement component factor 3 (C3). FXR not only has anti-inflammatory effects, but is also affected by the inflammatory response itself. Inflammatory stimuli TNF-α and IL-1β activate FXR via Nf-κB expression and IFNγ, Toll-like receptor 4 (TLR4), bile acids, fibroblast factor 19 (FGF19) and synthetic ligands also stimulate FXR.