Barbosa Amanda Marreiro, Francisco Priscila de Cássia, Motta Katia, Chagas Thayz Rodrigues, Dos Santos Cristiane, Rafacho Alex, Nunes Everson Araújo
a Laboratory of Investigation in Chronic Diseases, Department of Physiological Sciences, Center of Biological Sciences, Federal University of Santa Catarina (UFSC), Florianópolis, Brazil.
b Multicenter Graduate Program in Physiological Sciences, Graduate Program in Nutrition, Center of Health Sciences, UFSC, Florianópolis, Brazil.
Appl Physiol Nutr Metab. 2016 Apr;41(4):382-90. doi: 10.1139/apnm-2015-0487. Epub 2015 Dec 1.
Dexamethasone is an anti-inflammatory glucocorticoid that may alter glucose and lipid homeostasis when administered in high doses or for long periods of time. Omega-3 fatty acids, present in fish oil (FO), can be used as potential modulators of intermediary glucose and lipid metabolism. Herein, we evaluate the effects of FO supplementation (1 g·kg(-1) body weight (BW)) on glucose and lipid metabolism in rats treated with dexamethasone (0.5 mg·kg(-1) BW) for 15 days. Adult male Wistar rats were distributed among 4 groups: control (saline, 1 mL·kg(-1) BW and mineral oil, 1 g·kg(-1) BW), DEX (dexamethasone and mineral oil), FO (fish oil and saline), and DFO (fish oil and dexamethasone). Dexamethasone and saline were administered intraperitoneally, and fish oil and mineral oil were administered by gavage. We evaluated functional and molecular parameters of lipid and glycemic profiles at 8 days and at the end of treatment. FO supplementation increased hepatic docosahexaenoic acid (DEX: 5.6% ± 0.7%; DFO: 10.5% ± 0.8%) and eicosapentaenoic acid (DEX: 0.3% ± 0.0%; DFO: 1.3% ± 0.1%) contents and attenuated the increase of plasma triacylglycerol, total cholesterol, and non-high-density lipoprotein cholesterol concentrations in DFO rats compared with DEX rats. These effects seem not to depend on hepatic expression of insulin receptor substrate 1, protein kinase B, peroxisome proliferator-activated receptor γ coactivator 1-α, and peroxisome proliferator-activated receptor γ. There was no effect of supplementation on body weight loss, fasting glycemia, and glucose tolerance in rats treated with dexamethasone. In conclusion, we show that FO supplementation for 15 days attenuates the dyslipidemia induced by dexamethasone treatment.
地塞米松是一种抗炎糖皮质激素，大剂量或长期使用时可能会改变葡萄糖和脂质稳态。鱼油（FO）中含有的ω-3脂肪酸可作为葡萄糖和脂质中间代谢的潜在调节剂。在此，我们评估补充鱼油（1 g·kg⁻¹体重（BW））对接受地塞米松（0.5 mg·kg⁻¹ BW）治疗15天的大鼠葡萄糖和脂质代谢的影响。成年雄性Wistar大鼠分为4组：对照组（生理盐水，1 mL·kg⁻¹ BW和矿物油，1 g·kg⁻¹ BW）、DEX组（地塞米松和矿物油）、FO组（鱼油和生理盐水）和DFO组（鱼油和地塞米松）。地塞米松和生理盐水经腹腔注射给药，鱼油和矿物油经灌胃给药。我们在治疗8天和治疗结束时评估了脂质和血糖谱的功能及分子参数。补充鱼油增加了肝脏二十二碳六烯酸（DEX组：5.6%±0.7%；DFO组：10.5%±0.8%）和二十碳五烯酸（DEX组：0.3%±0.0%；DFO组：1.3%±0.1%）的含量，并减轻了DFO组大鼠与DEX组大鼠相比血浆三酰甘油、总胆固醇和非高密度脂蛋白胆固醇浓度的升高。这些作用似乎不依赖于胰岛素受体底物1、蛋白激酶B、过氧化物酶体增殖物激活受体γ辅激活因子1-α和过氧化物酶体增殖物激活受体γ的肝脏表达。补充鱼油对接受地塞米松治疗的大鼠体重减轻、空腹血糖和葡萄糖耐量没有影响。总之，我们表明补充鱼油15天可减轻地塞米松治疗诱导的血脂异常。
