Please use this identifier to cite or link to this item: http://repositorio.ufla.br/jspui/handle/1/57802
Title: Dose-response effect of prebiotic ingestion (β-glucans isolated from Saccharomyces cerevisiae) in diabetic rats with periodontal disease
Keywords: Periodontitis
Diabetes mellitus
Bone loss
Inflammatory status
β-glucans
Periodontite
Perda óssea
Status inflamatório
β-glucanos
Prebióticos
Issue Date: Oct-2021
Publisher: Springer Nature
Citation: AZZI, D. V. et al. Dose-response effect of prebiotic ingestion (β-glucans isolated from Saccharomyces cerevisiae) in diabetic rats with periodontal disease. Diabetology & Metabolic Syndrome, [S. I.], v. 13, 2021. DOI: https://doi.org/10.1186/s13098-021-00729-1.
Abstract: Background: Periodontal disease is one of the most frequent comorbidities in diabetic patients and can contribute to poor blood glucose control. Objective: To evaluate the efects of ingesting diferent doses of beta-glucans (BG) isolated from Saccharomyces cer‑ evisiae on alveolar bone loss (ABL) and infammatory/metabolic parameters in normal and diabetic rats with ligatureinduced periodontal disease (PD). Design: Sixty male rats were assigned into two groups: non-diabetic or diabetic (i.p. 70 mg/kg streptozotocin) with PD. Then, groups were subdivided into fve subgroups according BG doses: 0 mg/Kg; 10 mg/Kg; 20 mg/Kg; 40 mg/Kg or 80 mg/Kg. Animals received BG for 28 days and ligatures were placed on lower frst molars during the last 14 days. Results: ABL of diabetic and non-diabetic animals receiving BG 40 mg/kg (1.33 ± 0.03 mm and 0.77 ± 0.07 mm, respectively) and 80 mg/kg (1.26 ± 0.07 mm and 0.78 ± 0.05 mm, respectively) doses was lower (p < 0.05) in com‑ parison to respective controls (1.59 ± 0.11 mm and 0.90 mm ±0.08). COX-2 (Control: 1.66 ± 0.12; 40 mg/kg: 1.13 ± 0.07; 80 mg/kg: 0.92 ± 0.18) and RANKL expressions (Control: 1.74 ± 0.34; 40 mg/kg: 1.03 ± 0.29 ;80 mg/kg: 0.75 ± 0.21), together with the RANKL/OPG ratio (Control: 1.17 ± 0.08; 40 mg/kg: 0.67 ± 0.09; 80 mg/kg: 0.63 ± 0.28) were attenuated above the same dose (p < 0.05). BG did not infuence (p > 0.05) metabolic parameters in non-diabetic rats. In diabetic animals, doses above 40 mg/kg reduced IL-1β (Control: 387 ± 66; 40 mg/kg: 309 ± 27; 80 mg/kg: 300 ± 14) and TNF-α (Control: 229 ± 19; 40 mg/kg: 128 ± 53; 80 mg/kg: 71 ± 25), blood glucose levels (Control: 402 ± 49; 40 mg/kg: 334 ± 32; 80 mg/kg: 287 ± 56), total cholesterol (Control: 124 ± 8; 40 mg/kg: 120 ± 10; 80 mg/kg: 108 ± 9), LDL-c + VLDL-c (Control: 106 ± 8; 40 mg/kg: 103 ± 10; 80 mg/kg: 87 ± 10) and triacylglycerols (Control: 508 ± 90; 40 mg/kg: 301 ± 40; 80 mg/kg: 208 ± 61), whereas increased HDL-c (Control: 18 ± 0.5; 40 mg/kg: 19 ± 1; 80 mg/kg: 21 ± 1) (p < 0.05). Optimal dose needed to reduce ABL was higher in diabetic animals with PD.
URI: http://repositorio.ufla.br/jspui/handle/1/57802
Appears in Collections:DMV - Artigos publicados em periódicos

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