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Clinical Studies Linking MSG and Obesity

Clinical Reference 1

   Effects of monosodium glutamate-induced obesity in spontaneously hypertensive rats vs. Wistar Kyoto rats: serum leptin and blood flow to brown adipose tissue. -- Hypertens Res. 2000 Sep;23(5):503-10.

Iwase M,   Ichikawa K,   Tashiro K,    Iino K,   Shinohara N,   Ibayashi S,    Yoshinari M,    Fujishima M.
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

We compared the effects of hypothalamic obesity induced by neonatal monosodium glutamate (MSG) treatment between spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY).

Newborn WKY and SHR were injected intraperitoneally with 4 mg/kg body weight of MSG daily for 5 days. At 6 months of age, the obesity of SHR was more advanced than that of WKY, but at 14 months of age the severity of obesity was similar between the two strains.

Hypertriglyceridemia was enhanced in MSG-treated SHR as compared with MSG-treated WKY. Systolic blood pressure measured by the tail-cuff method was consistently lower in MSG-treated SHR than in control SHR, whereas blood pressure was not affected by neonatal MSG treatment in WKY.

Food restriction reduced body weight more in control SHR than in control WKY, with the former also showing enhanced ketogenesis. Neonatal MSG treatment abolished the accelerated reduction of body weight in SHR.

Serum leptin concentration was markedly increased in MSG-treated obese rats, though no differences were seen between WKY and SHR in the control or MSG-treated groups. Serum leptin was closely correlated with both Lee obese index and mesenteric fat weight over the strain.

Blood flow in interscapular brown adipose tissue (BAT) measured by Laser Doppler flowmetry was significantly increased in response to beta3-adrenoceptor agonist BRL26830A in both the control and MSG-treated rats. However, the response of blood flow was not affected by MSG treatment or strain difference.

The present study demonstrated some strain differences in response to neonatal MSG treatment between WKY and SHR. These differences could not be explained by the difference in serum leptin level or beta3-adrenergic reactivity in BAT.

PMID: 11016806 [PubMed - indexed for MEDLINE]

Related Links:

Obesity induced by neonatal monosodium glutamate treatment in spontaneously hypertensive rats: an animal model of multiple risk factors - Hypertens Res. 1998 Mar;21(1):1-6. PMID 9582101

Effects of neonatal treatment with monosodium-glutamate in spontaneously hypertensive rats. - Brain Res. 1985 Mar;351(1):135-8 PMID 3995335

Effect of fasting and refeeding on duodenal alkaline phosphatase activity in monosodium glutamate obese rats. - Physiol Res. 2001;50(4):365-72 PMID 11551142

Visually evoked responses in the primary cortex of rats are permanently changed by early postnatal treatment with monosodium-L-glutamate. - [Brain Res. 1985] PMID 22757212275721

Opioid-mediated cardiovascular effects of clonidine in spontaneously hypertensive rats: elimination by neonatal treatment with monosodium glutamate - Endocrinology. 1986 May;118(5):1814-22. PMID 2938932

Effect of fasting and refeeding on duodenal alkaline phosphatase activity in monosodium glutamate obese rats - Physiol Res. 2001;50(4):365-72. PMID 11551142

Blood pressure development in SHR and WKY rats: effects of neonatal monosodium glutamate treatment and evidence for transient hypertension in WKY rats. - Neurosci Lett. 1987 Dec 16;83(1-2):190-4. PMID 3441296

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   Clinical Reference 2 :
Effects of monosodium glutamate-induced obesity in spontaneously hypertensive rats vs. Wistar Kyoto rats: serum leptin and blood flow to brown adipose tissue.

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