Probiotics modulate gut microbiota and improve insulin sensitivity in DIO mice
Open accessAbstract
Obesity and type 2 diabetes are characterized by subclinical inflammatory process. Changes in composition or modulation of the gut microbiota may play an important role in the obesity-associated inflammatory process. In the current study, we evaluated the effects of probiotics (Lactobacillus rhamnosus, L. acidophilus and Bifidobacterium bifidumi) on gut microbiota, changes in permeability, and insulin sensitivity and signaling in high-fat diet and control animals. More importantly, we investigated the effects of these gut modulations on hypothalamic control of food intake, and insulin and leptin signaling. Swiss mice were submitted to a high-fat diet (HFD) with probiotics or pair-feeding for 5 weeks. Metagenome analyses were performed on DNA samples from mouse feces. Blood was drawn to determine levels of glucose, insulin, LPS, cytokines and GLP-1. Liver, muscle, ileum and hypothalamus tissue proteins were analyzed by Western blotting and real-time polymerase chain reaction. In addition, liver and adipose tissues were analyzed using histology and immunohistochemistry. The HFD induced huge alterations in gut microbiota accompanied by increased intestinal permeability, LPS translocation and systemic low-grade inflammation, resulting in decreased glucose tolerance and hyperphagic behavior. All these obesity-related features were reversed by changes in the gut microbiota profile induced by probiotics. Probiotics also induced an improvement in hypothalamic insulin and leptin resistance. Our data demonstrate that the intestinal microbiome is a key modulator of inflammatory and metabolic pathways in both peripheral and central tissues. These findings shed light on probiotics as an important tool to prevent and treat patients with obesity and insulin resistance.
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Treatment with probiotics can reverse intestinal flora dysbiosis and treat inflammatory responses in mice.
“Treatment with probiotics can reverse intestinal flora dysbiosis and treat inflammatory responses in mice.”
From Probiotics Regulate Gut Microbiota: An Effective Method to Improve Immunity (2021) · cites this paper as [16]
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- Authors
- Bagarolli, R. A., Tobar, N., Oliveira, A. G., Araújo, T. G., Carvalho, B. M., Rocha, G. Z., Vecina, J. F., Calisto, K., Guadagnini, D., Prada, P. O., Santos, A., Saad, S. T. O., & Saad, M. J. A.
- Affiliations
- Universidade Estadual de Campinas (UNICAMP) (BR)
- Universidade Estadual Paulista (Unesp) (BR)
- Universidade Federal de Pernambuco (BR)
- ORCID
- Venue
- The Journal of Nutritional Biochemistry
- Publisher
- Elsevier BV
- Published
- 2017-12
- Volume
- 50
- Pages
- 16-25
- ISSN
- 0955-2863 (ISSN-L)
- OpenAlex
- W2746430677
- Cited by
- 266
- References
- 68
- Citations by year
- 2026: 12 · 2025: 30 · 2024: 25 · 2023: 32 · 2022: 38 · 2021: 44 · 2020: 46 · 2019: 23 · 2018: 16
- FWCI
- 9.50
- Type
- journal article
- Language
- en
- Open access
- green
- americanae.aecid.es
- Licence
- Locations
- The Journal of Nutritional Biochemistry (publishedVersion)
- PubMed (publishedVersion)
- Americanae (AECID Library) (submittedVersion, other-oa)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- Funders
- State University of Campinas (FAEPEX)
- CEPID (201307607-8)
- OCRC (Centro de Pesquisa em Obesidade e Comorbidades)
- INCT (Instituto Nacional de Ciência e Tecnologia de Obesidade e Diabetes) (573856/2008-7)
- FAPESP (Fundação de Amparo à Pesquisa do Estado de São Paulo) (2012/15009-0, 2016/07122-2)
- CAPES/CNPq (Conselho Nacional de Desenvolvimento Científico e Tecnológico)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- probiotics, gut microbiota, insulin sensitivity, insulin resistance, type 2 diabetes, obesity, high-fat diet, Lactobacillus rhamnosus, Lactobacillus acidophilus, Bifidobacterium bifidum, intestinal permeability, lipopolysaccharide translocation, low-grade inflammation, leptin signaling, food intake regulation, glucose tolerance, glucagon-like peptide-1, pair feeding
- MeSH terms
- Gastrointestinal Microbiome, Bifidobacterium bifidum, Animals, Appetite Regulation, Cell Membrane Permeability, Diabetes Mellitus, Type 2, Feces, Insulin Resistance, Intestinal Mucosa, Lactobacillus acidophilus, Liver, Male, Obesity, Random Allocation, Glucose Clamp Technique, Probiotics, Mice, Lacticaseibacillus rhamnosus, Adipose Tissue, White, Molecular Typing, Diet, High-Fat, Dysbiosis
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