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

Diabetology & Metabolic Syndrome

Gabriel Lasmar Reis¹  Antonio Chalfun-Júnior¹  Raphael Ricon de Oliveira¹  Andressa Ribeiro Veiga Lima²  Robson Sfaciotti Barducci³  Márcio Gilberto Zangeronimo⁴  Renata de Carvalho Foureaux⁴  Viviam de Oliveira Silva⁴  Adriana Silva Albuquerque⁴  Diana Vilela Azzi⁴  Luciano José Pereira⁴  Andressa Naira de Jesus Pereira⁴  Eric Francelino Andrade⁵ 

[1] Department of Biology, Universidade Federal de Lavras (UFLA);Department of Health Sciences, Universidade Federal de Lavras (UFLA);Department of Research and Development, Biorigin Company;Department of Veterinary Medicine, Universidade Federal de Lavras (UFLA);Institute of Agrarian Sciences, Universidade Federal dos Vales do Jequitinhonha e Mucuri (UFVJM);

关键词: Periodontitis;    Diabetes mellitus;    Bone loss;    Inflammatory status;    β-glucans;   

DOI  :  10.1186/s13098-021-00729-1

来源: DOAJ

【 摘 要 】

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 effects of ingesting different doses of beta-glucans (BG) isolated from Saccharomyces cerevisiae on alveolar bone loss (ABL) and inflammatory/metabolic parameters in normal and diabetic rats with ligature-induced 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 five 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 first 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 comparison 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 influence (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. Conclusions BG ingestion reduced ABL and improved inflammatory profile in a dose-dependent manner. Best effects were achieved with doses above 40 mg/kg.

【 授权许可】

Unknown