Long-Term Ingestion of Monosodium L-Glutamate Did Not Induce Obesity, Dyslipidemia or Insulin Resistance: A Two-Generation Study in Mice
Long-Term Ingestion of Monosodium L-Glutamate Did Not Induce Obesity, Dyslipidemia or Insulin Resistance: A Two-Generation Study in Mice
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DOI：
10.3177/jnsv.59.129
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发表时间：
2013-04-01
影响因子：
1.6
通讯作者：
Sakai, Ryosei
中科院分区：
文献类型：
--
作者：
Nakamura, Hidehiro;Kawamata, Yasuko;Sakai, Ryosei
谷氨酸单钠(MSG)作为风味增强剂的使用已有100多年的历史，有许多研究表明普遍使用MSG是安全的。然而，最近，克里森等人。(2010)报道了一项两代人的低剂量味精研究，该研究导致小鼠腹型肥胖、胰岛素抵抗和血脂异常。出于对代谢综合征的公共卫生担忧，他们的报告值得仔细分析。本研究试图重复Colison等人的研究。调查结果。雄性或雌性C57BL/6J小鼠分别饲喂对照饲料或添加20%高果糖玉米糖浆(HFCS)。对照组给予饮用水，试验组给予0.064%味精溶液(w/v)。在整个交配过程中，以及在妊娠和哺乳期，饮食和味精的投放持续进行。为了进一步研究摄入味精的影响，在相同的剂量条件下，继续给仔鼠服用味精，直到他们达到32周龄。在整个妊娠期和出生后32wk期间，喂饲正常或HFCS饮食的小鼠服用味精不会影响生长、腰围、腹部脂肪重量或身体成分。这项研究报告称，无论饮食如何，味精不会引发胰岛素抵抗、血脂异常或肝脏脂肪变性，也不会重复上述研究的结果(Colison等人，2010年)。
The use of monosodium glutamate (MSG) as a flavor enhancer spans more than 100 y and there are many studies indicating the safety of general use of MSG. Recently, however, Collison et al. (2010) reported a two-generation study with a low dose of MSG that caused abdominal obesity, insulin resistance and dyslipidemia in mice. Due to public health concerns over metabolic syndrome, their report merits careful analysis. The present study attempted to repeat the Collison et al. findings. Groups of male or female C57BL/6J mice were fed a control diet or one supplemented with high-fructose corn syrup (HFCS) at a level of 20%. Drinking water control was provided or treatment groups were given 0.064% MSG solution (w/v). Diets and MSG administration continued throughout mating and during gestation and lactation periods. To further investigate the effects of ingestion of MSG, the offspring were continued on the same dosing conditions until they reached 32 wk of age. MSG administration in mice fed a normal or a HFCS diet throughout gestation and for 32 wk after birth, did not affect growth, girth size, abdominal fat weight or body composition. This study reports that MSG did not trigger insulin resistance, dyslipidemia or hepatic steatosis, regardless of the diet, not reproducing the results of the above-mentioned study (Collison et al., 2010).