Glucose-lowering effects of a synbiotic combination containing Pediococcus acidilactici in C. elegans and mice
Keywords: 
Diabetes
Microbiota
Obesity
Probiotics
Synbiotic
The metabolic syndrome
Issue Date: 
2023
Publisher: 
Springer
Project: 
info:eu-repo/grantAgreement/MINECO/Centros de Investigación Biomédica en Red (CIBER)/CB12/03/30002/[ES]/INCORPORACION GRUPOS CIBER FISIOPATOLOGIA DE LA OBESIDAD Y NUTRICION (CIBER OBN)
ISSN: 
1432-0428
Note: 
This article is licensed under a Creative Commons Attribution 4.0 International License
Citation: 
Yavorov-Dayliev, D. (Deyan); Milagro-Yoldi, F.I. (Fermín Ignacio); Ayo, J. (Josune); et al. "Glucose-lowering effects of a synbiotic combination containing Pediococcus acidilactici in C. elegans and mice". Diabetologia. 66, 2023, 2117 - 2138
Abstract
Aims/hypothesis Modulation of gut microbiota has emerged as a promising strategy to treat or prevent the development of diferent metabolic diseases, including type 2 diabetes and obesity. Previous data from our group suggest that the strain Pediococcus acidilactici CECT9879 (pA1c) could be an efective probiotic for regulating glucose metabolism. Hence, the objectives of this study were to verify the efectiveness of pA1c on glycaemic regulation in diet-induced obese mice and to evaluate whether the combination of pA1c with other normoglycaemic ingredients, such as chromium picolinate (PC) and oat β-glucans (BGC), could increase the efcacy of this probiotic on the regulation of glucose and lipid metabolism. Methods Caenorhabditis elegans was used as a screening model to describe the potential synbiotic activities, together with the underlying mechanisms of action. In addition, 4-week-old male C57BL/6J mice were fed with a high-fat/high-sucrose diet (HFS) for 6 weeks to induce hyperglycaemia and obesity. Mice were then divided into eight groups (n=12 mice/group) according to dietary supplementation: control-diet group; HFS group; pA1c group (1010 colony-forming units/day); PC; BGC; pA1c+PC+BGC; pA1c+PC; and pA1c+BGC. Supplementations were maintained for 10 weeks. Fasting blood glucose was determined and an IPGTT was performed prior to euthanasia. Fat depots, liver and other organs were weighed, and serum biochemical variables were analysed. Gene expression analyses were conducted by real-time quantitative PCR. Sequencing of the V3–V4 region of the 16S rRNA gene from faecal samples of each group was performed, and diferential abundance for family, genera and species was analysed by ALDEx2R package. Results Supplementation with the synbiotic (pA1c+PC+BGC) counteracted the efect of the high glucose by modulating the insulin–IGF-1 signalling pathway in C. elegans, through the reversal of the glucose nuclear localisation of daf-16. In diet-induced obese mice, all groups supplemented with the probiotic signifcantly ameliorated glucose tolerance after an IPGTT, demonstrating the glycaemia-regulating efect of pA1c. Further, mice supplemented with pA1c+PC+BGC exhibited lower fasting blood glucose, a reduced proportion of visceral adiposity and a higher proportion of muscle tissue, together with an improvement in the brown adipose tissue in comparison with the HFS group. Besides, the efect of the HFS diet on steatosis and liver damage was normalised by the synbiotic. Gene expression analyses demonstrated that the synbiotic activity was mediated not only by modulation of the insulin–IGF-1 signalling pathway, through the overexpression of GLUT-1 and GLUT-4 mediators, but also by a decreased expression of proinfammatory cytokines such as monocyte chemotactic protein-1. 16S metagenomics demonstrated that the synbiotic combinations allowed an increase in the concentration of P. acidilactici, together with improvements in the intestinal microbiota such as a reduction in Prevotella and an increase in Akkermansia muciniphila. Conclusions/interpretation Our data suggest that the combination of pA1c with PC and BGC could be a potential synbiotic for blood glucose regulation and may help to fght insulin resistance, diabetes and obesity.

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