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

Low-Dose Coconut Oil Supplementation Induces Hypothalamic Inflammation, Behavioral Dysfunction, and Metabolic Damage in Healthy Mice

Full text
Show less -
Veras, Alana Carolina Costa [1] ; dos Santos, Tamires [1] ; Martins, Isis de Cassia Alves [1] ; de Souza, Camilla Mendes [1] ; Amaral, Camila Libardi [1] ; Franco, Beatriz da Silva [2] ; Holanda, Alessandro Spencer de Souza [2] ; Esteves, Andrea Maculano [2] ; Milanski, Marciane [3, 1] ; Torsoni, Adriana Souza [3, 1] ; Ignacio-Souza, Leticia Martins [3, 1] ; Torsoni, Marcio Alberto [3, 1]
Total Authors: 12
[1] Univ Estadual Campinas, Lab Metab Disorders, Sch Appl Sci, Limeira - Brazil
[2] Univ Estadual Campinas, Sch Appl Sci, Lab Sleep & Exercise, Limeira - Brazil
[3] Univ Estadual Campinas, Obes & Comorbid Res Ctr, Campinas - Brazil
Total Affiliations: 3
Document type: Journal article
Web of Science Citations: 0

Scope Coconut oil (CO) diets remain controversial due to the possible association with metabolic disorder and obesity. This study investigates the metabolic effects of a low amount of CO supplementation. Methods and Results Swiss male mice are assigned to be supplemented orally during 8 weeks with 300 mu L of water for the control group (CV), 100 or 300 mu L of CO (CO100 and CO300) and 100 or 300 mu L of soybean oil (SO; SO100 and SO300). CO led to anxious behavior, increase in body weight gain, and adiposity. In the hypothalamus, CO and SO increase cytokines expression and pJNK, pNFKB, and TLR4 levels. Nevertheless, the adipose tissue presented increases macrophage infiltration, TNF-alpha and IL-6 after CO and SO consumption. IL-1B and CCL2 expression, pJNK and pNFKB levels increase only in CO300. In the hepatic tissue, CO increases TNF-alpha and chemokines expression. Neuronal cell line (mHypoA-2/29) exposed to serum from CO and SO mice shows increased NFKB migration to the nucleus, TNF-alpha, and NFKBia expression, but are prevented by inhibitor of TLR4 (TAK-242). Conclusions These results show that a low-dose CO changes the behavioral pattern, induces inflammatory pathway activation, TLR4 expression in healthy mice, and stimulates the pro-inflammatory response through a TLR4-mediated mechanism. (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