Novelli Ethel Lourenzi Barbosa, Santos Priscila Portugal, Assalin Heloisa Balan, Souza Gisele, Rocha Katiucha, Ebaid Geovana Xavier, Seiva Fábio Rodrigues Ferreira, Mani Fernanda, Fernandes Ana Angélica
Department of Chemistry and Biochemistry, Institute of Biological Sciences, São Paulo State University, UNESP, Botucatu, São Paulo, Brazil.
Pharmacol Res. 2009 Jan;59(1):74-9. doi: 10.1016/j.phrs.2008.10.004. Epub 2008 Oct 17.
To study the effects of N-acetylcysteine (NAC, C(5)H(9)-NO(3)S) on high-sucrose diet-induced obesity and its effects on energy metabolism and cardiac oxidative stress, male Wistar 24 rats were divided into four groups (n=6): (C) given standard chow and water; (N) receiving standard chow and 2g/l N-acetylcysteine in its drinking water; (HS) given standard chow and 30% sucrose in its drinking water, and (HS-N) receiving standard chow, 30% sucrose and N-acetylcysteine in its drinking water. After 30 days of the treatment, obesity was evidenced in HS rats from enhanced body weight, respiratory quotient, hypertriglyceridemia. As well depressed resting metabolic rate, and oxygen consumption per surface area. HS rats had triacylglycerol accumulation, oxidative stress and metabolic shifting in cardiac tissue. NAC enhanced fat oxidation and energy expenditure, normalizing these adverse effects, comparing HS-N and HS rats. The beta-hydroxyacyl coenzymne-A dehydrogenase activity was higher in HS-N animals, indicating higher heart fatty acid degradation than in HS. NAC normalized myocardial glycogen and lactate dehydrogenase activity, comparing HS-N and HS rats, but had no effects on calorimetric and biochemical parameters in standard-fed rats, comparing N and C groups. In conclusion, N-acetylcysteine offers promising therapeutic value in prevention of high-sucrose induced-obesity and its effect on cardiac tissue. N-acetylcysteine reduced the oxidative stress and prevented the metabolic shifting in cardiac tissue, enhancing fatty acid oxidation and reducing anaerobic metabolism in high-sucrose-fed conditions. The application of this agent in food system via exogenous addition may be feasible and beneficial for antioxidant protection and energy metabolism in cardiac tissue.
为研究N-乙酰半胱氨酸（NAC，C(5)H(9)-NO(3)S）对高糖饮食诱导的肥胖的影响及其对能量代谢和心脏氧化应激的作用，将24只雄性Wistar大鼠分为四组（n = 6）：（C）组给予标准饲料和水；（N）组饮用含2g/L N-乙酰半胱氨酸的标准饲料和水；（HS）组饮用含30%蔗糖的标准饲料和水，（HS-N）组饮用含标准饲料、30%蔗糖和N-乙酰半胱氨酸的水。治疗30天后，HS组大鼠体重增加、呼吸商升高、甘油三酯血症，静息代谢率降低，单位表面积耗氧量增加，出现肥胖。HS组大鼠心脏组织有三酰甘油蓄积、氧化应激和代谢改变。与HS组大鼠相比，HS-N组大鼠NAC增强了脂肪氧化和能量消耗，使这些不良反应恢复正常。HS-N组动物的β-羟酰基辅酶A脱氢酶活性较高，表明心脏脂肪酸降解高于HS组。与HS组大鼠相比，HS-N组大鼠NAC使心肌糖原和乳酸脱氢酶活性恢复正常，但与N组和C组相比，对标准喂养大鼠的热量和生化参数无影响。总之，N-乙酰半胱氨酸在预防高糖诱导的肥胖及其对心脏组织的影响方面具有有前景的治疗价值。N-乙酰半胱氨酸降低了氧化应激，防止了心脏组织的代谢改变，在高糖喂养条件下增强了脂肪酸氧化并减少了无氧代谢。通过外源添加将该试剂应用于食品系统可能对心脏组织的抗氧化保护和能量代谢是可行且有益的。
