epiglucan has been researched along with Diabetes-Mellitus--Type-1* in 7 studies
1 trial(s) available for epiglucan and Diabetes-Mellitus--Type-1
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Fungal chitin-glucan scaffold for managing diabetic xerosis of the feet in menopausal women.
Corneocyte accumulation (hyperkeratosis, xerosis) commonly occurs in the stratum corneum (SC) of the feet of diabetic patients, as well as menopausal women.. To compare the effects of a 2.5% chitin-glucan formulation with its placebo, and commercially available glycerol formulations.. This two-step controlled double-blind, randomized, intra-individual study was performed in 30 type 1 and 2 diabetic menopausal women suffering from xerosis of the feet. The formulations were applied once daily for 3 weeks. Electrometric assessments were performed on three sites of the feet at entry in the study, at weekly intervals during the treatment phase, and in a 2-week follow-up out of treatment. Positive controls consisted in two commercially available formulations enriched in glycerol.. Data revealed an unequivocal benefit provided by the 2.5% chitin-glucan formulation compared with placebo. The electrometric values were significantly higher at each evaluation time during both treatment and follow-up phases. The two glycerol-enriched formulations showed slightly different kinetics of SC moisturization. A steep increase was followed by a plateau level and a rapid decline after stopping the treatments.. The increased moisturization of the SC of the sole probably improves the desquamation process and reduces xerosis of the soles. Topics: beta-Glucans; Chitin; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Double-Blind Method; Emollients; Female; Foot Dermatoses; Galvanic Skin Response; Humans; Menopause; Middle Aged; Skin; Treatment Outcome; Water; Water Loss, Insensible | 2009 |
6 other study(ies) available for epiglucan and Diabetes-Mellitus--Type-1
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The effect of beta-glucan supplementation on glycemic control and variability in adolescents with type 1 diabetes mellitus.
This study aimed to investigate whether supplemental soluble fiber, oat β-glucan, has any effect on glycemic control and variability of adolescents with type 1 diabetes mellitus.. This study was conducted in 30 adolescents with type 1 diabetes mellitus and it consisted of three phases lasting one week. At Phase I, all subjects followed a standard diet program. For Phase II and Phase III, the subjects continued their standard diet program and added natural oat flakes containing 3 g/day and 6 g/day β-glucan, respectively. Glucose levels were monitored by continuous glucose monitoring (CGM). The maximal, minimal, mean and daytime and night blood glucose levels, percentages of glucose values in a target range and below and above a target values were calculated for each of the phases. Premeal, postmeal, peak blood glucose values and peak times of meals were evaluated for each of the phases. Glycemic variability was measured via SD, CV, MAGE, IQR, MODD, LBGI, HBGI, and CONGA parameters.. The maximal, mean and daytime and night blood glucose levels were the lowest at Phase III (p < 0.05). Minimal blood glucose levels were the highest at Phase III (p < 0.05). Phase I, II, and III showed similar durations elapsed for Level 2 and Level 1 hypoglycemia, euglycemia, Level 1 and Level 2 hyperglycemia (p > 0.05). Premeal and postmeal blood glucose levels were lowest at Phase III for breakfast, lunch, and overall (p < 0.05). The lowest peak blood glucose levels were detected at Phase III for breakfast, lunch, dinner and overall (p < 0.05). Phase III also showed delayed peaks for all time-points (p < 0.05 for each) compared to other phases. Phase III had significantly lower levels of SD, CV, LBGI, and CONGA levels than those in either Phase I or Phase II (p < 0.05 for each).. 6 g/day oat β-glucan have favorable outcomes in glycemic control and variability in adolescents with type 1 diabetes mellitus. Topics: Adolescent; Avena; beta-Glucans; Blood Glucose; Blood Glucose Self-Monitoring; Diabetes Mellitus, Type 1; Dietary Fiber; Female; Glycemic Control; Humans; Hyperglycemia; Hypoglycemia; Male; Meals; Postprandial Period | 2020 |
Effects of functional pasta ingredients on different gut microbiota as revealed by TIM-2
Diet-related modulation of gut microbiota and its metabolic activity represents an intriguing research context, particularly in the case of disorders related to imbalances in gut microbial communities. We here explored the effects of Topics: Bacillus coagulans; Bacteria; beta-Glucans; Child; Colon; Diabetes Mellitus, Type 1; Diet; Dietary Fiber; Fatty Acids; Feces; Fermentation; Gastrointestinal Microbiome; Humans; Models, Theoretical; RNA, Ribosomal, 16S; Triticum | 2019 |
Fungal β-glucan, a Dectin-1 ligand, promotes protection from type 1 diabetes by inducing regulatory innate immune response.
β-Glucans are naturally occurring polysaccharides in cereal grains, mushrooms, algae, or microbes, including bacteria, fungi, and yeast. Immune cells recognize these β-glucans through a cell surface pathogen recognition receptor called Dectin-1. Studies using β-glucans and other Dectin-1 binding components have demonstrated the potential of these agents in activating the immune cells for cancer treatment and controlling infections. In this study, we show that the β-glucan from Saccharomyces cerevisiae induces the expression of immune regulatory cytokines (IL-10, TGF-β1, and IL-2) and a tolerogenic enzyme (IDO) in bone marrow-derived dendritic cells as well as spleen cells. These properties can be exploited to modulate autoimmunity in the NOD mouse model of type 1 diabetes (T1D). Treatment of prediabetic NOD mice with low-dose β-glucan resulted in a profound delay in hyperglycemia, and this protection was associated with increase in the frequencies of Foxp3(+), LAP(+), and GARP(+) T cells. Upon Ag presentation, β-glucan-exposed dendritic cells induced a significant increase in Foxp3(+) and LAP(+) T cells in in vitro cultures. Furthermore, systemic coadministration of β-glucan plus pancreatic β cell Ag resulted in an enhanced protection of NOD mice from T1D as compared with treatment with β-glucan alone. These observations demonstrate that the innate immune response induced by low-dose β-glucan is regulatory in nature and can be exploited to modulate T cell response to β cell Ag for inducing an effective protection from T1D. Topics: Animals; beta-Glucans; Cytokines; Dendritic Cells; Diabetes Mellitus, Type 1; Dose-Response Relationship, Immunologic; Fungal Polysaccharides; Immunity, Innate; Insulin-Secreting Cells; Lectins, C-Type; Mice; Mice, Inbred NOD; Mice, SCID; Mice, Transgenic; Saccharomyces cerevisiae; T-Lymphocytes | 2014 |
Control of T Cell-mediated autoimmunity by metabolite flux to N-glycan biosynthesis.
Autoimmunity is a complex trait disease where the environment influences susceptibility to disease by unclear mechanisms. T cell receptor clustering and signaling at the immune synapse, T cell proliferation, CTLA-4 endocytosis, T(H)1 differentiation, and autoimmunity are negatively regulated by beta1,6GlcNAc-branched N-glycans attached to cell surface glycoproteins. Beta1,6GlcNAc-branched N-glycan expression in T cells is dependent on metabolite supply to UDP-GlcNAc biosynthesis (hexosamine pathway) and in turn to Golgi N-acetylglucosaminyltransferases Mgat1, -2, -4, and -5. In Jurkat T cells, beta1,6GlcNAc-branching in N-glycans is stimulated by metabolites supplying the hexosamine pathway including glucose, GlcNAc, acetoacetate, glutamine, ammonia, or uridine but not by control metabolites mannosamine, galactose, mannose, succinate, or pyruvate. Hexosamine supplementation in vitro and in vivo also increases beta1,6GlcNAc-branched N-glycans in naïve mouse T cells and suppresses T cell receptor signaling, T cell proliferation, CTLA-4 endocytosis, T(H)1 differentiation, experimental autoimmune encephalomyelitis, and autoimmune diabetes in non-obese diabetic mice. Our results indicate that metabolite flux through the hexosamine and N-glycan pathways conditionally regulates autoimmunity by modulating multiple T cell functionalities downstream of beta1,6GlcNAc-branched N-glycans. This suggests metabolic therapy as a potential treatment for autoimmune disease. Topics: Animals; Antigens, CD; Antigens, Differentiation; Autoimmunity; beta-Glucans; Cell Differentiation; CTLA-4 Antigen; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Encephalomyelitis, Autoimmune, Experimental; Endocytosis; Golgi Apparatus; Humans; Jurkat Cells; Mice; Mice, Knockout; N-Acetylglucosaminyltransferases; Receptors, Antigen, T-Cell; Signal Transduction; Th1 Cells; Uridine Diphosphate N-Acetylglucosamine | 2007 |
Controversies on the prevention of insulin-dependent diabetes mellitus by immunomodulation: lessons from NOD mice treated with beta-1,6;1,3-D-glucan and rhIGF-I.
Topics: Adjuvants, Immunologic; Amino Acid Sequence; Animals; Blood Glucose; Diabetes Mellitus, Type 1; Disease Models, Animal; Female; Glucans; Insulin; Insulin-Like Growth Factor I; Mice; Mice, Inbred NOD; Molecular Sequence Data; Peptide Fragments; Random Allocation; Recombinant Proteins; Spleen; Statistics as Topic; T-Lymphocytes | 1998 |
An immunopotentiator of beta-1,6;1,3 D-glucan prevents diabetes and insulitis in BB rats.
The preventive effect of an immunopotentiator, beta-1,6;1,3 D-glucan, on the development of diabetes and insulitis was studied in BB rats. The intravenous administration of 1 mg kg-1 week-1 of beta-1,6;1,3 D-glucan from the age of 4 weeks decreased the cumulative incidence of diabetes from 43.3% (13/30) to 6.7% (2/30) (P less than 0.005) and also the incidence of insulitis from 82.4% (14/17) to 26.3% (5/19) at the age of 20 weeks (P less than 0.002). Eight of nine rats were free from diabetes for 5 weeks after stopping beta-1,6;1,3 D-glucan at the age of 20 weeks. The total numbers of leukocytes in the peripheral blood and spleen of the rats were increased by beta-1,6;1,3 D-glucan treatment (P less than 0.05), whereas their T lymphocytes subsets were not changed. These data indicate that immunopotentiators could modulate the autoimmune mechanisms directed to pancreatic islets and inhibit the development of diabetes in BB rats. Topics: Adjuvants, Immunologic; Animals; Autoimmunity; Diabetes Mellitus, Type 1; Female; Glucans; Hyperinsulinism; Incidence; Injections, Intravenous; Leukocyte Count; Rats; Rats, Inbred BB; Rats, Wistar; T-Lymphocytes | 1992 |