Non-caloric artificial sweeteners (NASs) provide sweet tastes to food without adding calories or glucose. NASs can be used as alternative sweeteners for controlling blood glucose levels and weight gain. Although the consumption of NASs has increased over the past decade in Japan and other countries, whether these sweeteners affect the composition of the gut microbiome is unclear. In the present study, we examined the effects of sucralose or acesulfame-K ingestion (at most the maximum acceptable daily intake (ADI) levels, 15 mg/kg body weight) on the gut microbiome in mice. Consumption of sucralose, but not acesulfame-K, for 8 weeks reduced the relative amount of Clostridium cluster XIVa in feces. Meanwhile, sucralose and acesulfame-K did not increase food intake, body weight gain or liver weight, or fat in the epididymis or cecum. Only sucralose intake increased the concentration of hepatic cholesterol and cholic acid. Moreover, the relative concentration of butyrate and the ratio of secondary/primary bile acids in luminal metabolites increased with sucralose consumption in a dose-dependent manner. These results suggest that daily intake of maximum ADI levels of sucralose, but not acesulfame-K, affected the relative amount of the Clostridium cluster XIVa in fecal microbiome and cholesterol bile acid metabolism in mice.
The gut microbiota produce hundreds of bioactive compounds, including B‐vitamins, which play significant physiological roles in hosts by supporting the fitness of symbiotic species and suppressing the growth of competitive species. B‐vitamins are also essential to the host and certain gut bacterium. Although dietary B‐vitamins are mainly absorbed from the small intestine, excess B‐vitamins unable to be absorbed in the small intestine are supplied to the distal gut. In addition, B‐vitamins are supplied from biosynthesis by distal gut microbiota. B‐vitamins in the distal colon may perform many important functions in the body. They act as 1) nutrients for a host and their microbiota, 2) regulators of immune cell activity, 3) mediators of drug efficacy, 4) supporters of survival, or the fitness of certain bacterium, 5) suppressors of colonization by pathogenic bacteria, and 6) modulators of colitis. Insights into basic biophysical principles, including the bioavailability of B‐vitamins and their derivatives in the distal gut are still not fully elucidated. Here, the function of single B‐vitamin in the distal gut including their roles in relation to bacteria are briefly reviewed. The prospect of extending analytical methods to better understand the role of B‐vitamins in the gut is also explored.
OBJECTIVE-c-Cbl plays an important role in whole-body fuel homeostasis by regulating insulin action. In the present study, we examined the role of Cbl-b, another member of the Cbl family, in insulin action. RESEARCH DESIGN AND METHODS-C57BL/6(Cbl-b ϩ/ϩ ) or Cbl-b-deficient (Cbl-b Ϫ/Ϫ ) mice were subjected to insulin and glucose tolerance tests and a hyperinsulinemic-euglycemic clamp test. Infiltration of macrophages into white adipose tissue (WAT) was assessed by immunohistochemistry and flow cytometry. We examined macrophage activation using co-cultures of 3T3-L1 adipocytes and peritoneal macrophages. RESULTS-ElderlyCbl-b Ϫ/Ϫ mice developed glucose intolerance and peripheral insulin resistance; serum insulin concentrations after a glucose challenge were always higher in elderly Cbl-b Ϫ/Ϫ mice than age-matched Cbl-b ϩ/ϩ mice. Deficiency of the Cbl-b gene significantly decreased the uptake of 2-deoxyglucose into WAT and glucose infusion rate, whereas fatty liver was apparent in elderly Cbl-b Ϫ/Ϫ mice. Cbl-b deficiency was associated with infiltration of macrophages into the WAT and expression of cytokines, such as tumor necrosis factor-␣, interleukin-6, and monocyte chemoattractant protein (MCP)-1. Co-culture of Cbl-b Ϫ/Ϫ macrophages with 3T3-L1 adipocytes induced leptin expression and dephosphorylation of insulin receptor substrate 1, leading to impaired glucose uptake in adipocytes. Furthermore, Vav1, a key factor in macrophage activation, was highly phosphorylated in peritoneal Cbl-b Ϫ/Ϫ macrophages compared with Cbl-b ϩ/ϩ macrophages. Treatment with a neutralizing anti-MCP-1 antibody improved peripheral insulin resistance and macrophage infiltration into WAT in elderly Cbl-b Ϫ/Ϫ mice. O besity is a major cause of insulin resistance (1) and is considered a chronic low-grade inflammatory disease (2). Substantial evidence has accumulated in recent years that chronic infiltration and activation of macrophages in white adipose tissue (WAT) underlie the obesity-related component of these insulin-resistant states (3-5). Infiltrating macrophages secrete proinflammatory cytokines and stimulate the secretion of adipokines from adipocytes (4,5). Tumor necrosis factor (TNF)-␣ and interleukin (IL)-6 are key factors that induce insulin resistance (6,7). Leptin and adiponectin are also suggested to act as hormones that regulate insulin resistance; hyperleptinemia in obese subjects is associated with insulin resistance in tissues such as liver, WAT, and skeletal muscle (8), whereas adiponectin increases insulin sensitivity of these tissues (9). However, the molecular mechanism of macrophage activation in WAT is still unknown. CONCLUSIONS-Cbl-b is a unique ubiquitin ligase that is associated with maturation and activation of macrophages and T-cells (10,11). Expression of Cbl-b is upregulated by macrophage/monocyte differentiation of HL60 and U937 cell lines (10). Cbl-b influences CD28-dependent T-cell activation by selectively restraining T-cell receptor-mediated Vav1 activation (12)(13)(14). A recent study reported that the ...
2+ or pertussis toxin. The FliC-induced increase in hBD-2 promoter activity via nuclear factor U UB (NF-U UB) was also inhibited by chelation of intracellular Ca 2+ or by U73122. We conclude that FliC increased [Ca 2+ ] in via inositol 1,4,5-trisphosphate, which was followed by up-regulating hBD-2 mRNA expression via an NF-U UB-dependent pathway. ß
Growing evidence suggests that intake of flavonoid-containing foods may exert cardiovascular benefits in human subjects. We have investigated the effects of a 10-week blueberry (BB) supplementation on blood pressure (BP) and vascular reactivity in rats fed a highfat/high-cholesterol diet, known to induce endothelial dysfunction. Rats were randomly assigned to follow a control chow diet, a chow diet supplemented with 2 % (w/w) BB, a high-fat diet (10 % lard; 0·5 % cholesterol) or the high fat plus BB for 10 weeks. Rats supplemented with BB showed significant reductions in systolic BP (SBP) of 11 and 14 %, at weeks 8 and 10, respectively, relative to rats fed the control chow diet (week 8 SBP: 107·5 (SEM 4·7) v. 122·2 (SEM 2·1) mmHg, P¼0·018; week 10 SBP: 115·0 (SEM 3·1) v. 132·7 (SEM 1·5) mmHg, P, 0·0001). Furthermore, SBP was reduced by 14 % in rats fed with the high fat plus 2 % BB diet at week 10, compared to those on the high-fat diet only (SBP: 118·2 (SEM 3·6) v. 139·5 (SEM 4·5) mmHg, P,0·0001). Aortas harvested from BB-fed animals exhibited significantly reduced contractile responses (to L-phenylephrine) compared to those fed the control chow or high-fat diets. Furthermore, in rats fed with high fat supplemented with BB, aorta relaxation was significantly greater in response to acetylcholine compared to animals fed with the fat diet. These data suggest that BB consumption can lower BP and improve endothelial dysfunction induced by a high fat, high cholesterol containing diet.
The sugar alcohol xylitol inhibits the growth of some bacterial species including Streptococcus mutans. It is used as a food additive to prevent caries. We previously showed that 1.5–4.0 g/kg body weight/day xylitol as part of a high-fat diet (HFD) improved lipid metabolism in rats. However, the effects of lower daily doses of dietary xylitol on gut microbiota and lipid metabolism are unclear. We examined the effect of 40 and 200 mg/kg body weight/day xylitol intake on gut microbiota and lipid metabolism in mice. Bacterial compositions were characterized by denaturing gradient gel electrophoresis and targeted real-time PCR. Luminal metabolites were determined by capillary electrophoresis electrospray ionization time-of-flight mass spectrometry. Plasma lipid parameters and glucose tolerance were examined. Dietary supplementation with low- or medium-dose xylitol (40 or 194 mg/kg body weight/day, respectively) significantly altered the fecal microbiota composition in mice. Relative to mice not fed xylitol, the addition of medium-dose xylitol to a regular and HFD in experimental mice reduced the abundance of fecal Bacteroidetes phylum and the genus Barnesiella, whereas the abundance of Firmicutes phylum and the genus Prevotella was increased in mice fed an HFD with medium-dose dietary xylitol. Body composition, hepatic and serum lipid parameters, oral glucose tolerance, and luminal metabolites were unaffected by xylitol consumption. In mice, 40 and 194 mg/kg body weight/day xylitol in the diet induced gradual changes in gut microbiota but not in lipid metabolism.
HARADA, NAGAKATSU, CHIKA NINOMIYA, YOSHIE OSAKO, MASAKI MORISHIMA, KAZUAKI MAWATARI, AKIRA TAKAHASHI, AND YUTAKA NAKAYA. Taurine alters respiratory gas exchange and nutrient metabolism in type 2 diabetic rats. Obes Res. 2004; 12:1077-1084. Objective: To assess the effect of taurine supplementation on respiratory gas exchange, which might reflect the improved metabolism of glucose and/or lipid in the type 2 diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats. Research Methods and Procedures:Male OLETF rats (16 weeks of age) were randomly divided into two groups: unsupplemented group and taurine-supplemented (3% in drinking water) group. After 9 weeks of treatment, indirect calorimetry and insulin tolerance tests were conducted. The amounts of visceral fat pads, tissue glycogen, the blood concentrations of glucose, triacylglycerol, taurine, and electrolytes, and the level of hematocrit were compared between groups. A nondiabetic rat strain (Long-Evans Tokushima Otsuka) was used as the age-matched normal control. Results: The indirect calorimetry showed that the treatment of OLETF rats with taurine could reduce a part of postprandial glucose oxidation possibly responsible for the increase of triacylglycerol synthesis in the body. Taurine supplementation also improved hyperglycemia and insulin resistance and increased muscle glycogen content in the OLETF rats. Supplementation with taurine increased the blood concentration of taurine and electrolyte and fluid volume, all of which were considered to be related to the improvement of metabolic disturbance in OLETF rats. Discussion: Taurine supplementation may be an effective treatment for glucose intolerance and fat/lipid accumulation observed in type 2 diabetes associated with obesity. These metabolic changes might be ascribed, in part, to the alteration of circulating blood profiles, where the improved hyperglycemia and/or the blood accumulation of taurine itself would play roles.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.