Dose-response effect of prebiotic ingestion (β-glucans isolated from Saccharomyces cerevisiae) in diabetic rats with periodontal disease

• Autor(a) principal: Azzi, Diana Vilela
• Data de Publicação: 2021
• Outros Autores: Pereira, Andressa Naira de Jesus, Silva, Viviam de Oliveira, Foureaux, Renata de Carvalho, Lima, Andressa Ribeiro Veiga, Barducci, Robson Sfaciotti, Albuquerque, Adriana Silva, Reis, Gabriel Lasmar, Oliveira, Raphael Ricon de, Andrade, Eric Francelino, Zangeronimo, Márcio Gilberto, Chalfun Júnior, Antonio, Pereira, Luciano José
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFLA
• Texto Completo: http://repositorio.ufla.br/jspui/handle/1/48992
• topic: Periodontitis; Diabetes mellitus; Bone loss; Inflammatory status; β-glucans; Periodontite; Perda óssea; Status inflamatório; β-glucanos; Prebióticos

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.