Coarse cereals rich in polyphenols, dietary fiber, and other functional components exert multiple health benefits. We investigated the effects of cooked oats, tartary buckwheat, and foxtail millet on lipid profile, oxido-inflammatory responses, gut microbiota, and colonic short-chain fatty acids composition in high-fat diet (HFD) fed rats. Rats were fed with a basal diet, HFD, oats diet (22% oat in HFD), tartary buckwheat diet (22% tartary buckwheat in HFD), and foxtail millet diet (22% foxtail millet in HFD) for 12 weeks. Results demonstrated that oats and tartary buckwheat attenuated oxidative stress and inflammatory responses in serum, and significantly increased the relative abundance of Lactobacillus and Romboutsia in colonic digesta. Spearman’s correlation analysis revealed that the changed bacteria were strongly correlated with oxidative stress and inflammation-related parameters. The concentration of the butyrate level was elevated by 2.16-fold after oats supplementation. In addition, oats and tartary buckwheat significantly downregulated the expression of sterol regulatory element-binding protein 2 and peroxisome proliferator-activated receptors γ in liver tissue. In summary, our results suggested that oats and tartary buckwheat could modulate gut microbiota composition, improve lipid metabolism, and decrease oxidative stress and inflammatory responses in HFD fed rats. The present work could provide scientific evidence for developing coarse cereals-based functional food for preventing hyperlipidemia.

Type 2 diabetes (T2D) is a chronic disease prevalent in the world, accompanied by a variety of diseases, endangering human health and safety. Bile acids (BAs) play an important role in the regulation of host glucose and lipid metabolism homeostasis, and are strictly regulated by gut microbiota. However, the relationship between key BAs, BAs transporters and signaling, as well as gut microbiota, and host metabolism in T2D remains elusive. In this study, 9-week-old db/db mice were used as diabetes model (db/db group, n = 10), and their wild-type (wt) littermates of same age were used as the healthy control (CON group, n = 10). After 8 weeks of feeding, the BA profiles and microbial composition in the colon, and gene expression level of BA regulatory factors were analyzed in the db/db and CON groups to explore the underlying mechanisms of T2D. Compared with healthy mice, the body weight, blood glucose and lipid levels of db/db mice were significantly increased. The concentrations of total BAs, primary BAs, conjugated BAs and non-12α–hydroxylated BAs (non-12–OH BAs) were significantly decreased, while Deoxycholic acid (DCA) in secondary BAs was increased in db/db group. Compared with wt mice, the synthesis of BAs in the liver was transformed from the alternative pathway to the classical pathway, and hepatic BAs transporters (NTCP, BSEP, MRP2, OATP–1 and OSTβ) and receptors (FXR and TGR5) were significantly down-regulated in the db/db mice. In the colon, the mRNA level of FXR was up-regulated, while TGR5 was down-regulated. The diabetic (db/db) mice presented a changed gut microbiota composition, including an increased abundance of secondary BAs-producing bacteria, Escherichia–Shigella, and a decreased the abundance of Akkermansia, which are involved in the synthesis of non-12–OH BAs. We further found that the reduced BA types in db/db mice were negatively correlated with metabolic-disorder-related indicators, while an increased DCA level had the opposite correlation. Our results shed light into how the imbalance of BAs’ metabolism mediated by intestinal flora may be potential mechanisms of T2D.

WDF, ODF, and WODF improved T2DM symptoms in db / db diabetic mice through the IRS-1/PI3K/AKT pathway and gut microbiota-BAs-TGR5/FXR axis.

Background: Low birth weight (LBW) is correlated with gut microbiota dysbiosis and intestinal barrier function disruption, increasing susceptibility to enteric diseases. These alterations underscore the critical need to identify key regulators of gut homeostasis, among which bile acids are increasingly recognized as pivotal for barrier integrity, microbial ecology, and host metabolism. Methods: Eight pairs of LBW (the initial BW was 0.850 ± 0.053 kg) and normal-birth-weight (NBW; 1.488 ± 0.083 kg) piglets were compared to evaluate cecal morphology and bile acid profiles. Subsequently, sixteen LBW piglets and eight NBW piglets were allocated into three groups: NBW (1.563 ± 0.052 kg), LBW control (LBW-CON; 0.950 ± 0.120 kg), and LBW with bile acid supplementation (LBW-bile powder; 0.925 ± 0.116 kg). Piglets in the LBW-bile powder group received 25 mg/kg BW of bile powder (hyodeoxycholic acid-enriched) by daily oral gavage for 14 days. Results: LBW piglets exhibited retarded cecal development and lower abundance of hyocholic acid species (p = 0.006). Importantly, bile powder supplementation significantly improved cecal length (p = 0.009) and mucosal thickness (p = 0.020) compared with LBW-CON piglets. Microbial analysis showed that the microbial dysbiosis index was restored to near-normal levels. Transcriptomic analysis revealed impaired extracellular matrix structure and mucus secretion in LBW piglets. Notably, bile powder supplementation markedly upregulated the protein expression of WNT8B (p < 0.001) and the bile acid receptors (i.e., GPBAR1 and FXR), alongside enhanced tight junctions and the goblet cell marker mucin-2 expression (p < 0.05). Conclusions: These findings suggest that specific bile acid supplementation improves gut barrier function and partially supports cecal development in LBW piglets.