Fermented Maillard Reaction Products by Lactobacillus gasseri 4M13 Alters the Intestinal Microbiota and Improves Dysfunction in Type 2 Diabetic Mice with Colitis

Abstract

Inflammatory bowel disease is a chronic relapsing disease. Multiple factors can cause inflammatory bowel disease (IBD), including diet, imbalance of the immune system, and impaired intestinal barrier function. Type 2 diabetes mellitus is a complex and chronic metabolic disease caused by a combination of insulin resistance and an ineffective insulin secretory response. The co-occurrence of these two diseases, demonstrating interrelated effects within the gut microbiota, has been frequently reported. This study evaluated the effects of a fermented glycated conjugate of whey protein and galactose with Lactobacillus gasseri 4M13 (FMRP) to prevent type 2 diabetes mellitus with inflammatory bowel disease. C57BLKS/J- db/db mice were orally administered FMRP for 14 consecutive days and 2% dextran sulfate sodium (DSS) in water ad libitum for 5 days to induce colitis. FMRP-fed mice showed improved insulin secretion and symptoms of colitis. Compared to the DSS group, the FMRP group showed a decreased abundance of six bacterial genera and increased abundance of Alistipes and Hungateiclostridium. In cecal contents, the levels of short-chain fatty acids increased in the FMRP group compared to those in the DSS group. Continuous administration of FMRP thus may improve the homeostasis of not only insulin secretion and inflammation, but also the intestinal environment in inflammatory bowel disease and type 2 diabetes mellitus.

Amelioration of Type 2 Diabetes Using Four Strains of Lactobacillus Probiotics: Effects on Gut Microbiota Reconstitution-Mediated Regulation of Glucose Homeostasis, Inflammation, and Oxidative Stress in Mice

“…plantarum, and L. gasseri, amplify the activity of these antioxidant enzymes in T2D mice, thereby minimizing liver damage and oxidative stressthis aligns with our findings. − MDA, a marker product of lipid peroxidation, is elevated in T2D patients . CKCC1, CKCC3, and CKCC4 also reduced serum MDA levels in T2D mice (Figure D).…”

“…Specifically, IL-6 may hinder glucose-responsive insulin production in islets. TNF-α can deactivate the insulin receptor by phosphorylating its serine residue substrate . Elevated levels of IL-6 and TNF-α exacerbate T2D by promoting insulin resistance, impairing β-cell function, and triggering cell apoptosis.…”

Dynamic Changes in Intestinal Gene Expression and Microbiota across Chicken Egg-Laying Stages

“…Conjoint analysis of differential genes and microbes found that the abundance of Muricomes was significantly correlated with the expression of NFKBIZ , LYG2 , and IRG1L . The level of Muricomes was abundant in mice with colonitis [ 40 ], and it was associated with liver LDL-cholesterol, which increased in mice fed high-fat food [ 41 ]. The product encoded by NFKBIZ is one of the nuclear I kappa B proteins and an activator of IL-6 production.…”

Surrogate fostering of mice prevents prenatal estradiol-induced insulin resistance via modulation of the microbiota-gut-brain axis

“…According to published studies, a drop in Alloprevotella ( Wang J. et al, 2020 ; Wu et al, 2021 ; Zhang et al, 2021 ; Zhao et al, 2021 ; Hao et al, 2022 ; Liu et al, 2022 ) and an increase in Blautia ( Zhao et al, 2021 ; Bao et al, 2022 ) and Tyzzerella ( Li et al, 2022 ) are found in animal models of in insulin resistance or glucose intolerance. On the other hand, antidiabetic medications and bioactive compounds modulate the gut microbial community of diabetic mouse model, characterized by increased Alistipes ( Hu et al, 2019 ; Jeong et al, 2021 ; Li et al, 2021 ; Wu R. et al, 2022 ) and decreased Anaerotruncus ( Yong et al, 2022 ), Oscillibacter ( Lin et al, 2022 ; Wang et al, 2022 ), Allobaculum ( Jia et al, 2017 ; Shen et al, 2021 ; Xu et al, 2021 ; Ma et al, 2022 ), Acetatifactor ( Wu Y. et al, 2022 ) and Turicibacter ( Zhao et al, 2021 ). These findings coincide with the correlation between microbiota and metabolic phenotypes in our study.…”