Efecto neuroprotector de nicotinamida vía sistema colinérgico en un modelo de obesidad en rata

Abstract

Excessive intake of saturated fats and simple sugars is associated with learning and memory impairment. This type of diet can produce different physiological changes, such as low-grade systemic inflammation and oxidative stress. The high production of pro-inflammatory cytokines and reactive oxygen species can enter the central nervous system and affect neural homeostasis. In this context, acetylcholine, the main parasympathetic neurotransmitter and inflammation regulator could be affected.Acetylcholine concentrations in organs and tissues depends on its hydrolysis through the activities of acetylcholinesterase and butyrylcholinesterase (AChE and BChE, respectively). Changes in the diet increase their cholinesterases activity by hydrolyzing ACh, contributing to the inflammation process and affecting the synapse, which favors cognitive impairment. The use of vitamins as adjuvants to treat inflammatory diseases is frequent nowadays. Nicotinamide (NAM) is a vitamin that exerts antioxidant and antiinflammatory effects. In this study we evaluated cholinergic activity associated with the antioxidant and anti-inflammatory effect of NAM in a model of diet-induced cognitive deficit. Thirty male Sprague Dawley rats were distributed in 5 groups and subjected to the following treatments: 1) CON (Control); 2) Hypercaloric diet (HC, 18% fat and 40% sucrose); 3) HC-NAM 5 mM; 4) HC-NAM 10 mM; 5) HC-NAM 15 mM for 13 weeks with ad libitum food and water. AChE and BuChE activities, GSH concentrations, thiobarbituric acid reactive substances (TBARS) and pro-inflammatory cytokines were evaluated; as well as memory and spatial learning. The results showed that the hypercaloric diet increased plasma triacylglycerols, interleukin (IL) -6, TBARS and decreased IL-10 levels, it also increased liver and hippocampal TBARS levels, and