Melatonin normalizes clinical and biochemical parameters of mild inflammation in diet-induced metabolic syndrome in rats

• Autores: Cano Barquilla, Pilar; Pagano, Eleonora Samanta; Jiménez Ortega, Vanesa; Fernández Mateos, María P.; Esquifino, Ana I.; Cardinali, Daniel Pedro
• Año de publicación: 2014
• Idioma: inglés
• Tipo de recurso: artículo
• Fuente: Preprint del documento publicado en Journal of pineal research, Nº 57, 2014
• Materia: DISLIPIDEMIA; TOLERANCIA A LA GLUCOSA; DIETA; HIPERTENSION; INFLAMACION; ACIDO URICO
• Institución: Pontificia Universidad Católica Argentina

Fil: Cano Barquilla, Pilar. Universidad Complutense. Facultad de Medicina. Departamento de Bioquímica y Biología Molecular III; España
Fil: Pagano, Eleonora S. Pontifica Universidad Católica Argentina. Faculta de Ciencias Médicas. Departamento de Docencia e Investigación; Argentina
Fil: Jiménez Ortega, Vanesa. Universidad Complutense. Facultad de Medicina. Departamento de Bioquímica y Biología Molecular III; España
Fil: Fernández Mateos, Pilar. Universidad Complutense. Facultad de Medicina. Departamento de Biología Celular; España
Fil: Esquifino, Ana I. Universidad Complutense. Facultad de Medicina. Departamento de Bioquímica y Biología Molecular III; España
Fil: Cardinali, Daniel P. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Fisiología; Argentina
Abstract: The objective of the present study was to evaluate the efficacy of melatonin to affect mild inflammation in the metabolic syndrome (MS) induced by a high-fat diet in rats. Adult Wistar male rats were divided into four groups (n= 16/group): (i) control diet (3% fat); (ii) high-fat (35%) diet; (iii) high-fat diet + melatonin; (iv) melatonin. Rats had free access to high-fat or control chow and one of the following drinking solutions for 10 weeks: (a) tap water; (b) 25 μg/mL of melatonin. Plasma interleukin (IL)-1β, IL-4, IL-6, IL-10, tumor necrosis factor (TNF)-α, interferon (IFN)-γ and C-reactive protein (CRP) were measured at two time intervals, i.e. the middle of daylight period and the middle of the scotophase. In addition, a number of somatic and metabolic components employed clinically to monitor the MS were measured. Melatonin decreased the augmented circulating levels of IL-1β, IL-6, TNF-α, IFN-γ and CRP seen in obese rats and restored the depressed levels of IL-4 and IL-10. Rats fed with the high-fat diet showed significantly higher body weights and augmented systolic blood pressure from the 3rd and 4th week onwards, respectively, melatonin effectively preventing these changes. In high-fat fed rats circulating low-density lipoprotein-cholesterol, total cholesterol and triglyceride concentration augmented significantly, melatonin being effective to counteract these changes. Melatonin-treated rats showed a decreased insulin resistance, the highest values of plasma high-density lipoprotein-cholesterol and the lowest values of plasma uric acid. The results indicate that melatonin is able to normalize the altered biochemical proinflammatory profile seen in rats fed with a high-fat diet