Pectin can not be digested and absorbed by the gastrointestinal tract, but it is available for gut microbiota.

Pectin increases the expression of G-protein coupled receptor and the levels of PYY and GLP-1.

The PYY and GLP-1 concentrations in plasma were increased by pectin supplementation, which assist to suppress the food intake and further reduce the body weight gain in mice supplied with pectin.

The occurrence of obesity is closely related to gut microbiota. A symbiotic relationship exists between gut microbiota and the host, and gut microbiota dysbiosis can disrupt energy balance homeostasis and cause metabolic syndrome including hyperglycemia, insulin resistance and obesity One of the important mechanisms by which gut microbiota affects the host health is its capacity to regulate glucose metabolism, gut immunity and other physiological processes through short-chain fatty acids (SCFAs) production.

Gut microbiota can ferment dietary fibers such as pectin and oligofructose that are not digested and absorbed by the host’s gastrointestinal tract to produce SCFAs. In the distal gut, SCFAs can enter the cells through diffusion or SLC5A8-mediated transport, and act as an energy source or trigger the hormone release by activating G-protein coupled receptor.

SCFAs are important signaling molecules in the host and they are involved in the processes such as gut immune regulation and gluconeogenesis. Many studies have shown that SCFAs serve as endogenous ligands for G-protein coupled receptors like GPR43 and GPR41,  and promote the release of gut hormones Peptide YY (PYY) and glucagon like peptide-1 (GLP-1).

Furthermore, PYY and GLP-1 can participate in the modulation of energy homeostasis through affecting the central nervous system and regulating the appetite of the host after entering the blood circulation.

Pectin has a good effect on reducing p,p′-DDE-induced obesity through regulating gut microbiota and provided a potential strategy for the treatment of environmental pollutant-caused health problems.

p,p′-Dichlorodiphenyldichloroethylene (p,p′-DDE), the main metabolite of dichlorodiphenyltrichloroethane (DDT) in organisms, is a typical environmental pollutant.

p,p′-DDE is persistent and difficult to be degraded. It can accumulate in the fat of organisms and transport along the food chain, thereby affecting human health. Previous research presented that exposure to p,p′-DDE could promote adipogenesis, induce lipid metabolism dysfunction and aggravate glucose intolerance and insulin resistance under a high-fat diet causing weight gain.

Pectins can influence the gastrointestinal immune barrier in a microbiota-dependent (indirect effects) and microbiota-independent (direct effects) manner. Direct effects include strengthening of the mucus layer, stimulation of epithelial integrity or modulation of immune responses. Pectins can exert direct effects through interaction with galectins or TLRs. Indirect effects include stimulation of microbial diversity, production of SCFAs, favoring adhesion of commensals to epithelial cells or anti-adhesive effects of pathogens to epithelial cells. SCFAs may stimulate epithelial integrity and mucus secretion by binding to GPR41, GPR43, or GPR109a. Immune responses are also influenced by SCFAs, which may interact with GPR41, GPR43, or GPR109a, activate or inhibit histone deacetylases or regulate transcription factors.

The composition of gut microbiota is highly linked with human health, and unhealthy lifestyles, in particular High Fat Diet, can induce chronic metabolic diseases by regulating gut microbiota. The plasticity of intestinal microbiota makes microbiome-targeted dietary intervention an important treatment for diseases. Natural polysaccharides are important components of human foods that are critical bidirectional regulators of gut microbiota. Gut microbiome ferments indigestible polysaccharides, and the fermented metabolites, in turn, affect intestinal microbiota composition and metabolites. Importantly, natural polysaccharides display probiotics-like activities in improving High Fat Diet-induced metabolic diseases.

Natural polysaccharides improve high-fat diet (HFD)-induced metabolic diseases through regulating gut microbiota. Plants or animals-derived polysaccharides are fermented by gut microorganism, and produce metabolites, such as short-chain fatty acids (SCFAs). In turn, these metabolites regulate the intestinal microbiota composition. High Fat Diet induce gut microbiota dysbiosis that contributes to obesity-associated chronic metabolic diseases. In this regard, natural polysaccharides reverse High Fat Diet-induced metabolic diseases by regulating gut microbiota.

Polysaccharides, prevent Metabolic syndrome in High Fat Diet-fed mice by increasing SCFAs contents and the beneficial bacteria, Akkermansia, Bifidobacterium, and decreasing the obesity-associated intestinal bacteria, Oscillospira and Odoribacteraceae.

Metabolic syndrome remains the most common non-communicable disease that is characterized by central obesity, insulin resistance, hyperlipidaemia, and hypertension. Metabolic syndrome increases the risk of developing several chronic diseases, including T2DM, NAFLD, cardiovascular diseases, and cancer.  The contributors of Metabolic Syndrome include genetic factors, and lifestyle, such as dietary over-consumption of High Fat Diet.

Increasing studies show that the gut plays an important role in Metabolic Syndrome, and the gut-centric theory in Metabolic Syndrome emerged since 2007.

Strong evidence for the important role of gut in Metabolic Syndrome is the potent efficacy of weight-loss in gastrointestinal surgery.

Currently, intestinal microbiota is highly associated with Metabolic Syndrome, and the gut microbiota dysbiosis results in obesity, and consequently Metabolic Syndrome.

Therefore, intervention of gut microbiota composition is an effective option for treating Metabolic Syndrome patients.