Arndt T, Nenoff P, Müller D, Müller F, Remke H, Mothes T
Institute of Pathological Biochemistry, Leipzig, Germany.
J Exp Anim Sci. 1993 Oct;36(1):12-8.
Glutamate-induced obesity of Wistar-rats is known to develop under normophagic and normoinsulinemic conditions, although hyperphagia and hyperinsulinemia are common to obese individuals. Rats of this obesity model show retarded growth, reduced mass of some organs, carcass and whole body as well as an extraordinary high fat content, whereas protein content is reduced. In this study, nitrogen (N) balance, urinary excretion of urea-N, ammonia-N, creatine-N and alpha-amino acid-N and plasma free fatty acid concentration of growing, glutamate-induced obese rats were determined. The main results were independent of frame of reference (mmol N/kg body mass; mmol N/kg0.75 metabolic body mass; N in % of nitrogen intake): Nitrogen intake, urinary excretion of alpha-amino acids and nitrogen excretion in faeces were equal between lean and obese rats. Nitrogen excretion in urine was elevated in obese rats, mainly resulting from increased amounts of urea and ammonia. Nitrogen balance was positive in both groups, but reduced in obese rats. These data point to normal digestion of food proteins, but an unusual high oxidative desamination rate of the absorbed amino acids in obese rats. Taking into account the various hormonal and nerval alterations in glutamate-induced obese rats, resulting e.g. in increased hepatic insulin concentration, the retained amino acid carbon should be channelled into hepatic fatty acid synthesis. Really, unfasted and overnight fasted obese rats showed elevated plasma free fatty acid concentrations. Channeling of amino acids into lipogenesis may explain the low muscle mass and striking fat accumulation--despite normophagia and peripheral normoinsulinemia--of growing, glutamate-induced obese Wistar-rats.
已知谷氨酸诱导的Wistar大鼠肥胖是在正常摄食和正常胰岛素血症条件下发生的，尽管肥胖个体通常存在摄食过多和高胰岛素血症。这种肥胖模型的大鼠生长发育迟缓，某些器官、胴体和全身质量减轻，脂肪含量异常高，而蛋白质含量降低。在本研究中，测定了生长中的、谷氨酸诱导的肥胖大鼠的氮（N）平衡、尿素氮、氨氮、肌酸氮和α-氨基酸氮的尿排泄量以及血浆游离脂肪酸浓度。主要结果与参考标准无关（mmol N/千克体重；mmol N/千克0.75代谢体重；N占氮摄入量的百分比）：瘦鼠和肥胖大鼠的氮摄入量、α-氨基酸的尿排泄量和粪便中的氮排泄量相等。肥胖大鼠的尿氮排泄量升高，主要是由于尿素和氨的量增加。两组的氮平衡均为正值，但肥胖大鼠的氮平衡降低。这些数据表明食物蛋白质消化正常，但肥胖大鼠吸收的氨基酸氧化脱氨率异常高。考虑到谷氨酸诱导的肥胖大鼠的各种激素和神经改变，例如导致肝脏胰岛素浓度升高，保留的氨基酸碳应该被引导到肝脏脂肪酸合成中。实际上，未禁食和过夜禁食的肥胖大鼠血浆游离脂肪酸浓度升高。氨基酸进入脂肪生成的过程可能解释了生长中的、谷氨酸诱导的肥胖Wistar大鼠尽管正常摄食且外周胰岛素正常，但肌肉质量低和脂肪堆积明显的现象。
