Differential Effects of ‘Vaping’ on Lipid and Glucose Profiles and Liver Metabolic Markers in Obese Versus Non-obese Mice

Tobacco smoking increases the risk of metabolic disorders due to the combination of harmful chemicals, whereas pure nicotine can improve glucose tolerance. E-cigarette vapour contains nicotine and some of the harmful chemicals found in cigarette smoke at lower levels. To investigate how e-vapour affects metabolic profiles, male Balb/c mice were exposed to a high-fat diet (HFD, 43% fat, 20kJ/g) for 16weeks, and e-vapour in the last 6weeks. HFD alone doubled fat mass and caused dyslipidaemia and glucose intolerance. E-vapour reduced fat mass in HFD-fed mice; only nicotine-containing e-vapour improved glucose tolerance. In chow-fed mice, e-vapour increased lipid content in both blood and liver. Changes in liver metabolic markers may be adaptive responses rather than causal. Future studies can investigate how e-vapour differentially affects metabolic profiles with different diets.

Ginsenoside Rb1 Ameliorates Diabetic Arterial Stiffening via AMPK Pathway

Background and Purpose: Macrovascular complication of diabetes mellitus, characterized by increased aortic stiffness, is a major cause leading to many adverse clinical outcomes. It has been reported that ginsenoside Rb1 (Rb1) can improve glucose tolerance, enhance insulin activity, and restore the impaired endothelial functions in animal models. The aim of this study was to explore whether Rb1 could alleviate the pathophysiological process of arterial stiffening in diabetes and its potential mechanisms.Experimental Approach: Diabetes was induced in male C57BL/6 mice by administration of streptozotocin. These mice were randomly selected for treatment with Rb1 (10−60 mg/kg, i. p.) once daily for 8 weeks. Aortic stiffness was assessed using ultrasound and measurement of blood pressure and relaxant responses in the aortic rings. Mechanisms of Rb1 treatment were studied in MOVAS-1 VSMCs cultured in a high-glucose medium.Key Results: Rb1 improved DM-induced arterial stiffening and the impaired aortic compliance and endothelium-dependent vasodilation. Rb1 ameliorated DM-induced aortic remodeling characterized by collagen deposition and elastic fibers disorder. MMP2, MMP9, and TGFβ1/Smad2/3 pathways were involved in this process. In addition, Rb1-mediated improvement of arterial stiffness was partly achieved via inhibiting oxidative stress in DM mice, involving regulating NADPH oxidase. Finally, Rb1 could blunt the inhibition effects of DM on AMPK phosphorylation.Conclusion and Implications: Rb1 may represent a novel prevention strategy to alleviate collagen deposition and degradation to prevent diabetic macroangiopathy and diabetes-related complications.

Intestinal-derived FGF15 protects against deleterious effects of vertical sleeve gastrectomy in mice

Bariatric surgeries such as the Vertical Sleeve Gastrectomy (VSG) are invasive but provide the most effective improvements in obesity and Type 2 diabetes. We hypothesized a potential role for the gut hormone Fibroblast-Growth Factor 15/19 which is increased after VSG and pharmacologically can improve energy homeostasis and glucose handling. We generated intestinal-specific FGF15 knockout (FGF15INT-KO) mice which were maintained on high-fat diet. FGF15INT-KO mice lost more weight after VSG as a result of increased lean tissue loss. FGF15INT-KO mice also lost more bone density and bone marrow adipose tissue after VSG. The effect of VSG to improve glucose tolerance was also absent in FGF15INT-KO. VSG resulted in increased plasma bile acid levels but were considerably higher in VSG-FGF15INT-KO mice. These data point to an important role after VSG for intestinal FGF15 to protect the organism from deleterious effects of VSG potentially by limiting the increase in circulating bile acids.

Protective Effects of Almond Oil on Streptozotocin-Induced Diabetic Rats via Regulating Nrf2/HO-1 Pathway and Gut Microbiota

Almond oil has been used as a medicine substitution for its numerous health benefits. This study aimed to evaluate the effect of almond oil on streptozotocin- (STZ-) induced diabetic rats for 4 weeks. The results showed that the administration of almond oil could significantly increase body weight, attenuate abnormally elevated blood glucose, promote insulin secretion, and improve glucose tolerance. Almond oil treatment also suppressed oxidative stress, reduced inflammation reaction, improved liver and kidney function, upregulated the expressions of Nrf2, HO-1, and NQO1, while downregulating the expression of Keap1. Furthermore, almond oil reversed the gut microbiota change by STZ and regulated the gut microbiota associated with glucose metabolism. At the phylum level, the relative abundance of Firmicutes was decreased, while Bacteroidetes was increased by almond oil treatment. More importantly, the ratio of Firmicutes/Bacteroidetes was significantly increased. At the genus level, administration of almond oil increased the abundances of Lactobacillus, Bacteroides, and Lachnospiraceae_NK4A136_group, while decreased the abundances of Ruminococcaceae_UCG-014, Clostridium_sensu_stricto_1, and Fusicatenibacter. These results provided evidence for the regulating effect of almond oil on diabetic rats via the Nrf2/HO-1 pathway and gut microbiota.

The Influence of Diet Change and Oral Metformin on Blood Glucose Regulation and the Fecal Microbiota of Healthy Horses

Common treatments for Equine Metabolic Syndrome (EMS) and associated conditions include removal from pasture and adoption of an all-hay diet. Pharmacological treatments for EMS include metformin, a biguanide antihyperglycemic agent also administered to people to help improve glucose tolerance and insulin sensitivity. Both treatments may work, at least partially, through the gut microbiota, yet little is known regarding these effects in the equine host. To determine the influence on the fecal microbiota of this diet change and administration of metformin, six healthy horses were removed from pasture and switched to an all-hay diet, with four of those horses also receiving oral metformin for seven days. Control horses (n = 24) remaining on pasture and receiving no metformin were sampled at the beginning and end of one week. All samples were subjected to 16S rRNA sequencing, and horses undergoing the diet change were subjected to an oral sugar test twice, one week apart. Characteristic changes in the microbiota following diet change included the significant expansion of the phylum Kiritimatiellaeota. As Kiritimatiellaeota are related to Verrucomicrobia, found to expand in the microbiota of mice and humans in response to metformin, this taxon may represent the cognate microbes in equine hosts.

Glucose-lowering activity of dark tea protein extract by modulating spleen-brain axis of diabetic mice

The present study was to explore the glucose-lowering effects of the previously characterized dark tea (Camellia sinensis L) protein extract (DTPE) from Heimaojian on spleen-brain axis of diabetic mice. DTPE was orally administrated (50-100 mg/kg) to alloxan-induced mice for 21 days, biochemical assay and transcriptome profiling (RNA-Seq) were performed. The results showed that DTPE can improve glucose tolerance. Compared with model group, at day 21, the fasting blood glucose values were significantly (p<0.05) decreased by 44.9% (13.8 vs 7.6 mmol/L) and 51.4% (13.8 vs 6.7 mmol/L) for high dose of DTPE (100 mg/kg) and drug metformin (125 mg/kg) groups, respectively. Subsequently, transcriptome profiling (RNA-Seq) was performed on the spleen and brain of diabetic mice. Totally, 52 spleen-derived and 47 brain-derived differentially expressed genes related to the synthesis, transport and metabolism of glucose were identified. The regulatory network analysis indicated that DTPE may exert glucose-lowering effects through a 37-gene sub-network related to metabolism, Parkinson’s disease, oxidative phosphorylation and immunity. In summary, for the first time, the present data revealed that dark tea-derived DTPE could exert a potential anti-hyperglycemic effect by modulating spleen-brain axis.

MicroRNA, Diabetes Mellitus and Colorectal Cancer

Diabetes mellitus (DM) is an endocrinological disorder that is due to either the pancreas not producing enough insulin, or the body does not respond appropriately to insulin. There are many complications of DM such as retinopathy, nephropathy, and peripheral neuropathy. In addition to these complications, DM was reported to be associated with different cancers. In this review, we discuss the association between DM and colorectal cancer (CRC). CRC is the third most commonly diagnosed cancer worldwide that mostly affects older people, however, its incidence and mortality are rising among young people. We discuss the relationship between DM and CRC based on their common microRNA (miRNA) biomarkers. miRNAs are non-coding RNAs playing important functions in cell differentiation, development, regulation of cell cycle, and apoptosis. miRNAs can inhibit cell proliferation and induce apoptosis in CRC cells. miRNAs also can improve glucose tolerance and insulin sensitivity. Therefore, investigating the common miRNA biomarkers of both DM and CRC can shed a light on how these two diseases are correlated and more understanding of the link between these two diseases can help the prevention of both DM and CRC.

Characterization of the Gut Microbiota of Individuals at Different T2D Stages Reveals a Complex Relationship with the Host

In this work, we studied 217 Mexican subjects divided into six groups with different stages of glucose intolerance: 76 Controls (CO), 54 prediabetes (PRE), 14 T2D no medication (T2D−No−M), 14 T2D with Metformin (T2D−M), 22 T2D with polypharmacy (T2D−P), and 37 T2D with polypharmacy and insulin (T2D−P+I). We aimed to determine differences in the gut microbiota diversity for each condition. At the phylum level, we found that Firmicutes and Bacteroidetes outline major changes in the gut microbiota. The gut bacterial richness and diversity of individuals in the T2D−No−M group were lesser than other groups. Interestingly, we found a significant difference in the beta diversity of the gut microbiota among all groups. Higher abundance was found for Comamonadaceae in PRE, and Sutterella spp. in T2D−No−M. In addition, we found associations of specific microbial taxa with clinical parameters. Finally, we report predicted metabolic pathways of gut microbiota linked to T2D−M and PRE conditions. Collectively, these results indicate that each group has specific predicted metabolic characteristics and gut bacteria populations for each phenotype. The results of this study could be used to define strategies to modulate gut microbiota through noninvasive treatments, such as dietary intervention, probiotics or prebiotics, and to improve glucose tolerance of individuals with prediabetes or T2D.