title: Effects of monosodium glutamate-induced obesity in spontaneously hypertensive rats vs. Wistar Kyoto rats: serum leptin and blood flow to brown adipose tissue.
abstract: 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.
authors.affiliation: Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Iwase
authors.forename: K
authors.initials: K
authors.lastname: Ichikawa
authors.forename: K
authors.initials: K
authors.lastname: Tashiro
authors.forename: K
authors.initials: K
authors.lastname: Iino
authors.forename: N
authors.initials: N
authors.lastname: Shinohara
authors.forename: S
authors.initials: S
authors.lastname: Ibayashi
authors.forename: M
authors.initials: M
authors.lastname: Yoshinari
authors.forename: M
authors.initials: M
authors.lastname: Fujishima
mesh_terms: D002001:Adipose Tissue, Brown / Q000098:blood supply* / Q000378:metabolism; D058667:Adrenergic beta-3 Receptor Agonists; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure; D004195:Disease Models, Animal; D002149:Energy Intake; D004983:Ethanolamines / Q000494:pharmacology; D005260:Female; D005503:Food Additives / Q000494:pharmacology*; D006973:Hypertension / Q000097:blood*; D020738:Leptin / Q000097:blood*; D008297:Male; D009765:Obesity / Q000097:blood* / Q000139:chemically induced; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012970:Sodium Glutamate / Q000494:pharmacology*; D015431:Weight Loss
chemical_list: D058667:Adrenergic beta-3 Receptor Agonists; D000318:Adrenergic beta-Agonists; D004983:Ethanolamines; D005503:Food Additives; D020738:Leptin; C039248:BRL 26830A; D012970:Sodium Glutamate