Czech Donald A, Kazel Melanie R, Harris John
Biopsychology Laboratory, Department of Psychology, Marquette University, SC-454, P.O. Box 1881, Milwaukee, WI 53201-1881, USA.
Physiol Behav. 2003 Oct;80(1):75-9. doi: 10.1016/s0031-9384(03)00220-8.
Possible involvement of nitric oxide (NO) in lipoprivic feeding was investigated in nondeprived male ICR mice adapted to a high-fat diet in a within-subjects design. Lipoprivation was induced by blocking fatty acid oxidation with Na-mercaptoacetate (MA), which produces a short-term increase in feeding in mice and rats. Food intake, measured at 1, 2, and 4 h following injection of 70 mg/kg of MA, was attenuated in a dose related manner with increasing pretreatment dose (1,10, 25 and 50 mg/kg sc) of the NO-synthase (NOS) inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), reaching statistical significance at 10 mg/kg of L-NAME at h1 when compared to vehicle control condition. The inactive isomer, D-NAME, was ineffective, thereby supporting stereospecific drug action and directly implicating NO. A control experiment measured general locomotor activity (grid crossings and rears) in an open arena under 10-50 mg/kg of L-NAME in the same mice; both measures were significantly different from vehicle condition only at the highest dose. These findings support involvement of NO in lipoprivic hyperphagia; they are consistent with and extend research linking NO and ingestive behaviors through use of NOS inhibitors. Possible influences of confounds were discussed.
在一项自身对照设计中，研究了一氧化氮（NO）在高脂饮食适应状态下的非剥夺雄性ICR小鼠脂肪缺乏性摄食中的可能作用。通过用巯基乙酸钠（MA）阻断脂肪酸氧化来诱导脂肪缺乏，MA可使小鼠和大鼠的摄食短期内增加。在注射70 mg/kg MA后的1、2和4小时测量食物摄入量，随着一氧化氮合酶（NOS）抑制剂N（G）-硝基-L-精氨酸甲酯（L-NAME）预处理剂量（1、10、25和50 mg/kg皮下注射）的增加，食物摄入量呈剂量相关方式减少，与溶剂对照条件相比，在1小时时L-NAME剂量为10 mg/kg时达到统计学显著差异。无活性异构体D-NAME无效，从而支持了药物的立体特异性作用并直接表明是NO起作用。一项对照实验在同一批小鼠中测量了10 - 50 mg/kg L-NAME作用下在开放场地中的一般运动活动（穿越格数和直立次数）；仅在最高剂量时这两项测量结果才与溶剂条件有显著差异。这些发现支持了NO参与脂肪缺乏性贪食；它们与通过使用NOS抑制剂将NO与摄食行为联系起来的研究一致并扩展了该研究。文中讨论了混杂因素的可能影响。
