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Dietary polyphenols protect against metabolic syndrome, despite limited absorption and digestion, raising questions about their mechanism of action. We hypothesized that one mechanism may involve the gut microbiota. To test this hypothesis, C57BL/6J mice were fed a high-fat diet (HFD) containing 1% Concord grape polyphenols (GP). Relative to vehicle controls, GP attenuated several effects of HFD feeding, including weight gain, adiposity, serum inflammatory markers (tumor necrosis factor [TNF]α, interleukin [IL]-6, and lipopolysaccharide), and glucose intolerance. GP lowered intestinal expression of inflammatory markers (TNFα, IL-6, inducible nitric oxide synthase) and a gene for glucose absorption (Glut2). GP increased intestinal expression of genes involved in barrier function (occludin) and limiting triglyceride storage (fasting-induced adipocyte factor). GP also increased intestinal gene expression of proglucagon, a precursor of proteins that promote insulin production and gut barrier integrity. 16S rRNA gene sequencing and quantitative PCR of cecal and fecal samples demonstrated that GP dramatically increased the growth of Akkermansia muciniphila and decreased the proportion of Firmicutes to Bacteroidetes, consistent with prior reports that similar changes in microbial community structure can protect from diet-induced obesity and metabolic disease. These data suggest that GP act in the intestine to modify gut microbial community structure, resulting in lower intestinal and systemic inflammation and improved metabolic outcomes. The gut microbiota may thus provide the missing link in the mechanism of action of poorly absorbed dietary polyphenols.

Quinoa (Chenopodium quinoa Willd., Amaranthaceae) is a grain-like, stress-tolerant food crop that has provided subsistence, nutrition, and medicine for Andean indigenous cultures for thousands of years. Quinoa contains a high content of health-beneficial phytochemicals, including amino acids, fiber, polyunsaturated fatty acids, vitamins, minerals, saponins, phytosterols, phytoecdysteroids, phenolics, betalains, and glycine betaine. Over the past 2 decades, numerous food and nutraceutical products and processes have been developed from quinoa. Furthermore, 4 clinical studies have demonstrated that quinoa supplementation exerts significant, positive effects on metabolic, cardiovascular, and gastrointestinal health in humans. However, vast challenges and opportunities remain within the scientific, agricultural, and development sectors to optimize quinoa's role in the promotion of global human health and nutrition.

Moringa (Moringa oleifera Lam.) is an edible plant used as food and medicine throughout the tropics. A moringa concentrate (MC) made by extracting fresh leaves with water utilized naturally occurring myrosinase to convert four moringa glucosinolates (1–4) into moringa isothiocyanates (5–8). Optimum conditions maximizing MC yield, compound 5 (4-[(α-L-rhamnosyloxy)benzyl]isothiocyanate), and compound 8 (4-[(4’-O-acetyl-α-L-rhamnosyloxy)benzyl]isothiocyanate) content were established (1:5 fresh leaf weight to water ratio at room temperature). The optimized MC contained 1.66% isothiocyanates and 3.82% total polyphenols. Compound 8 exhibited 80% stability at 37 °C for 30 days. MC, 5, and 8 significantly decreased gene expression and production of inflammatory markers in RAW macrophages. Specifically, 5 and 8 attenuated expression of iNOS and IL-1β and production of nitric oxide and TNFβ at 1 and 5 µM. Our results suggest a potential for stable and concentrated moringa isothiocyanates (5–8), delivered in MC as a food-grade product, to alleviate low-grade inflammation associated with chronic diseases.

We used a murine model of type II diabetes, which reproduces the major features of the human disease, and a number of cellular models to study the antidiabetic effect of ANC, a standardised anthocyanin-rich formulation from maqui berry (Aristotelia chilensis). We also isolated delphinidin 3-sambubioside-5-glucoside (D3S5G), a characteristic anthocyanin from maqui berry, and studied its antidiabetic properties. We observed that oral administration of ANC improved fasting blood glucose levels and glucose tolerance in hyperglycaemic obese C57BL/6J mice fed a high fat diet. In H4IIE rat liver cells, ANC decreased glucose production and enhanced the insulin-stimulated down regulation of the gluconeogenic enzyme, glucose-6-phosphatase. In L6 myotubes ANC treatment increased both insulin and non-insulin mediated glucose uptake. As with the ACN, oral administration of pure D3S5G dose-dependently decreased fasting blood glucose levels in obese C57BL/6J mice, and decreased glucose production in rat liver cells. D3S5G also increased glucose uptake in L6 myotubes and is at least partially responsible for ANC’s anti-diabetic properties.