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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Omega-3 Supplementation Prevents Short-Term High-Fat Diet Effects on the alpha 7 Nicotinic Cholinergic Receptor Expression and Inflammatory Response

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Martins, I. C. A. [1] ; Contieri, L. S. [1] ; Amaral, C. L. [1] ; Costa, S. O. [1] ; Souza, A. C. P. [1] ; Ignacio-Souza, L. M. [2, 1] ; Milanski, M. [2, 1] ; Torsoni, A. S. [2, 1] ; Torsoni, M. A. [2, 1]
Total Authors: 9
[1] Univ Estadual Campinas, Sch Appl Sci, Lab Metab Disorders, Campinas, SP - Brazil
[2] Univ Estadual Campinas, Obes & Comorbid Res Ctr, Campinas, SP - Brazil
Total Affiliations: 2
Document type: Journal article
Source: Mediators of Inflammation; v. 2021, AUG 10 2021.
Web of Science Citations: 0

The study is aimed at investigating if PUFA supplementation could prevent the effects of a short-term HFD on alpha 7nAChR expression and on the severity of sepsis. Swiss mice were used for the in vivo experiments. For the in vitro experiments, we used a microglia cell line (BV-2) and a hepatoma cell line (Hepa-1c1c7) derived from mice. The animals were either fed standard chow, fed a short-term HFD (60%), or given supplementation with omega-3 fatty acid (2 g/kg or 4 g/kg bw) for 17 days, followed by a short-term HFD. Endotoxemia was induced with an intraperitoneal (i.p.) lipopolysaccharide injection (LPS, 5 or 12 mg/kg), and sepsis was induced by subjecting the animals to cecal ligation and puncture (CLP). BV-2 and Hepa-1c1c7 cells were treated with LPS (100 and 500 ng/mL, respectively) for 3 hours. RT-PCR or Western blotting was used to evaluate alpha 7nAChR expression, inflammatory markers, DNMT1, and overall ubiquitination. LPS and HFD reduced the expression of alpha 7nAChR and increased the expression of inflammatory markers. Omega-3 partially prevented the damage caused by the HFD to the expression of alpha 7nAChR in the bone marrow and hypothalamus, decreased the inflammatory markers, and reduced susceptibility to sepsis-induced death. Exposing the BV-2 cells to LPS increased the protein content of DNMT1 and the overall ubiquitination and reduced the expression of alpha 7nAChR. The inflammation induced by LPS in the BV-2 cell decreased alpha 7nAChR expression and concomitantly increased DNMT1 expression and the ubiquitinated protein levels, indicating the participation of pre- and posttranscriptional mechanisms. (AU)

FAPESP's process: 16/23484-1 - Participation of alpha7 nicotinic acetylcholine receptor (alpha7nAChR) in the development of insulin resistance prevention
Grantee:Marcio Alberto Torsoni
Support type: Regular Research Grants
FAPESP's process: 18/01863-6 - Role of hypothalamic cholinergic receptor alpha7 (alpha7nAChR) in control of energy homeostasis and association with leptin signaling in mice
Grantee:Camilla Mendes de Souza
Support type: Scholarships in Brazil - Master
FAPESP's process: 13/07607-8 - OCRC - Obesity and Comorbidities Research Center
Grantee:Licio Augusto Velloso
Support type: Research Grants - Research, Innovation and Dissemination Centers - RIDC
FAPESP's process: 19/07615-7 - Role of nicotinic acetylcholine receptors alpha7 (±7nAChR) in the hypothalamic control of energy homeostasis and association with central signaling of leptin in mice
Grantee:Marcio Alberto Torsoni
Support type: Regular Research Grants