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by en 15 septiembre, 2012

 

UN ENEMIGO OCULTO EN MUCHAS COMIDAS , GLUTAMATO  MONOSÓDICO ¡ DESCUBRALO !

 Fuente:

http://www.herbalab-mexico.com/noticias/47-hay-un-enemigo-oculto-en-muchas-comidas-i-descubralo-.html

¿ Donde está ?

Está en montones de alimentos industrializados, desde las formulas para bebés hasta unas papas fritas , una lata de frijoles o un aderezo para ensaladas., está en la mayoría de los alimentos industrializados.

 

¿ Cómo se llama?

Su nombre es  GLUTAMATO MONOSODICO y , como todo enemigo, se oculta también con otros nombres que le dire más adelante.

 

Me dijeron que el glutamate es una sustancia natural muy importante que está presente en muchísimos alimentos, ¿ Es cierto?

Si,, es cierto.  Ud. está hablando del  GLUTAMATO,  aquí estamos diciendo : GLUTAMATO MONOSODICO ,  lo cual significa que es otra sustancia.  Es como hablar de personas que tienen el mismo nombre y distinto apellido.

Debe quedar bien claro que el GLUTAMATO que contienen en forma natural muchísimos alimentos de ninguna manera debe confundirse con el GLUTAMATO MONOSODICO, que siendo en su origen ácido glutámico natural  se convierte luego en laboratorio en una sustancia artificial procesada a partir de una sustancia natural.

Nuestro cuerpo produce glutamato natural  a partir de una sustancia llamada ácido glutámico y que es indispensable para el mantenimiento de la salud.

El ácido glutámico se encuentra naturalmente en muchos alimentos como tomate, zanahoria, carne de res, algas, queso parmesano, pescado especialmente sardinas , papas, pollo y muchos más. Dada su importancia está ampliamente presente en la naturaleza

Una de las funciones más importantes del glutamato en nuestro organismo es la de proporcionar energía a cerebro, músculos, sangre, hígado, riñones y otros órganos y tejidos.

La leche maternal contiene una gran cantidad de glutamato y cumple una función importantísima en el desarrollo del bebé.

La placenta, al estar en íntimo contacto con el feto posee glutamato que actúa como una sustancia energética vital.

Nuevamente repito: Debe quedar bien claro que el GLUTAMATO que contienen en forma natural muchísimos alimentos y que también está en nuestro cuerpo,   de ninguna manera debe confundirse con el GLUTAMATO MONOSODICO, que siendo en su origen ácido glutámico natural  se convierte luego en laboratorio en una sustancia artificial procesada a partir de una sustancia natural.

Entonces,  ¿ Qué es el GLUTAMATO MONOSODICO?

El Glutamato Monosódico fue una creación artificial hecha en Japón en el año  1908  por el Dr. Ikeda. El  descubrió que dicha sustancia producia un mejor sabor en los alimentos a los cuales se agregaba y que producía el deseo de seguir comiendo más.   Esto fué un atractivo enorme para los intereses económicos de la industria alimenticia, A este sabor nuevo , que no existía en la Naturaleza, lo llamaron “Umami”. Esta sustancia tenía también la ventaja de potenciar el sabor de otros alimentos especialmente los ácidos y salados sin acción sobre los dulces.

El Glutamato Monosódico atrajo también la atención de los investigadores médicos que  estaban haciendo estudios sobre la obesidad. Estos estudios hechos en ratas necesitaban por supuesto ratas obesas y esto se logró facilmente alimentándolas con  GLUTAMATO MONOSODICO.  Estas son las ratas obesas de laboratorio que son conocidas como ratas GMS,  en ingles ratas MSG La cantidad de Glutamato Monosódico que reciben tiene que ser parecida a la que se pone en los alimentos, debido a que mayor cantidad es tóxica y en grandes cantidades es mortal.

 

¿Qué daños produce consumer alimentos que tengan agregado el GLUTAMATO MONOSODICO ?

La obesidad es uno de los daños.  La cantidad de obesos tanto niños como adultdos ya es una preocupación muy grande y muy relacionada con la presencia de GLUTAMATO MONOSODICO en los alimentos industrializados.

Hay daños  que se producen en una zona  del cerebro que regula todo el sistema glandular interno o sea altera la producción de hormonas.

Las pruebas en animales muestran que los que son alimentados con comida que contiene Glutamato Monosódico, aumentan su apetito en un 40%. Esto explica por que cuando comemos  papas fritas , comida chatarra,  salchichas,  sopas de sobre, y de lata etc. tengamos la sensación de querer seguir comiendo más.

Los daños cerebrales producidos por el Glutamato Monosódico son más importantes cuanto más temprano se consumen en la vida o sea que la peligrosidad de su consumo es mayor cuanto más pequeño es el niño que lo consume.

Canadá demuestra, luego de serios estudios, que sin ninguna duda, las fórmulas para alimentación de bebés contienen Glutamato Monosódico y Aspartame y que ambos son toxinas que  dañan el cerebro  y son particularmente peligrosas en el lactante pues ellos aún no tienen madura la barrera  que impide la entrada de muchas toxinas al cerebro.  Las formulas  para bebés más peligrosas son las llamadas hipoalergénicas.

La Federación de Sociedades Americanas de Biología Experimental  (Federation of American Societies Experimental Biology for) dice que: …Es prudente evitar el uso de L-ácido glutámico en embarazadas, lactantes , niños, mujeres en edad fertil y personas con desórdenes afectivos. Hacen notar también que el Glutamato Monosódico, aparece como “ácido glutámico” en la lista de ingredientes de los suplementos alimenticios.

El Glutamato Monosódico esta clasificado como “neurotoxina” y es considerado responsible de muchas enfermedades cerebrales como la de desencadenar ataques de epilepsia, en las personas predispuestas.

Es interesante notar la existencia de un trabajo científico realizado en Mèxico y en el cual se demiuestra que el Glutamato Monosódico, administrado durante la etapa fetal, daña el cerebro de ratas y ratones, Este es un trabajo de Tesis realizado en el Laboratorio de Toxicología del Departamento de Farmacología,Facultad de Medicina de la U.N.A.M. y Laboratorio de Formación Reticular, Unidad de Investigaciones cerebrales, Instituto Nacional de Neurología y Neurocirugía , “Dr. Manuel Velasco Suárez” Secretaría de Salud. México D.F.  Puede leerse este trabajo en  http://148.206.53.231/UAM3282.PDF

Los trabajos científicos sobre Glutamato Monosódico y epilepsia, fueron también presentados por Coyle en 1976, Greenqmyre en 1986 y Zeevalk en 1990

La Comisión europea con fecha Mayo 27-1999 y en relación con la autorización de la vacuna del  Rota virus, establece que esta vacuna no debe darse a niños que presenten sensibilidad al latex y /o al Glutamato Monosódico.

¿Cuales son los nombres con los cuales se disfraza  el GLUTAMATO MONOSODICO?

Algunos de los nombres con los que se disfraza son

Ácido glutámico –

Ajinomoto = Vetsin –

Carragenano –

Caseinato de Calcio –

Caseinato de sodio –

Extracto de levadura –

Extracto de levadura autolizada  –

Extracto de proteina vegetal –

Gelatina hidrolizada –

Glutamato monopotásico – (reemplazante de la sal común)

Levadura hidrolizada –

MSG –

o con el número E620, E621, E622, E623, E624, E625, E627, E631, o E635.

Proteina de soya aislada –

Proteína hidrolizada –

Proteina hidrolizada de plantas (PHP) –

Proteina texturizada –

Proteina Vegetal  Hidrolizada (PVH) –

Realzador del sabor –

Saborizante natural –

Sazonador natural

Senomyx –

¿ Qué podemos hacer  para evitar comer alimentos que contengan Glutamato Monosódico ?

  1. Hacer una lista con los nombres ocultos de Glutamato Monosódico y llevarla siempre con nosotros. Leer las etiquetas de todos los alimentos que compramos , para saber cuales debemos rechazar.
  2. Comer alimentos no procesados industrialmente como  por ejemplo frutas y verduras frescas.
  3. Tener en cuenta que muchos medicos y nutriologos,  no estudian y aun siendo buenas personas,  no lo son como profesionales pues no se actualizan con investigaciones realizadas por científicos independientes o sea no atados a ningún interés comercial.  Estos  medicos y nutriólogos  que no siguen estudiando son seres humanos con errores como cualquier persona.  Simplemente no hay que juzgarlos y hay que borrarlos de nuestra lista de personas capacitadas para cuidar nuestra salud

Resumen y traducción del inglés, Dra. Nélida Barreiro Trelles

A continuación hay algunas referencias científicas serias sobre los daños que produce el consumo de GLUTAMATO MONOSODICO, se refieren especialmente a los daños cerebrales y obesidad.

Referencias:

Hermanussen M, García AP, Sunder M, Voigt M, Salazar V, Tresguerres JA. Obesity, voracity, and short stature: the impact of glutamate on the regulation of appetite. Eur J Clin Nutr. 2006 Jan;60(1):25-31.

Fernandez-Tresguerres Hernández JA. [Effect of monosodium glutamate given orally on appetite control (a new theory for the obesity epidemic)]  [Article in Spanish]  An R Acad Nac Med (Madr). 2005;122(2):341-55; discussion 355-60.

1:  Nakayama D, Magami Y, Azuma T, Inokuchi H, Furukawa M, Ohyashiki J, Yoshimoto T, Mizuguchi J, Moriyasu F, Kawai K, Hattori T. Turnover of acinar and islet cells in the pancreas of monosodium glutamate-treated obese mice. ?Obes Res. 2003 Jan;11(1):87-94. ?PMID: 12529490 [PubMed – in process]

2:  Guimaraes RB, Telles MM, Coelho VB, Mori RC, Nascimento CM, Ribeiro EB. Adrenalectomy abolishes the food-induced hypothalamic serotonin release in both normal and monosodium glutamate-obese rats. ?Brain Res Bull. 2002 Aug 15;58(4):363-9. ?PMID: 12183012 [PubMed – indexed for MEDLINE]

3:  Hahm S, Fekete C, Mizuno TM, Windsor J, Yan H, Boozer CN, Lee C, Elmquist JK, Lechan RM, Mobbs CV, Salton SR. VGF is required for obesity induced by diet, gold thioglucose treatment, and agouti and is differentially regulated in pro-opiomelanocortin- and neuropeptide Y-containing arcuate neurons in response to fasting. ?J Neurosci. 2002 Aug 15;22(16):6929-38. ?PMID: 12177191 [PubMed – indexed for MEDLINE]

4:  de Carvalho Papa P, Vargas AM, da Silva JL, Nunes MT, Machado UF. GLUT4 protein is differently modulated during development of obesity in monosodium glutamate-treated mice. ?Life Sci. 2002 Sep 6;71(16):1917-28. ?PMID: 12175706 [PubMed – indexed for MEDLINE]

5:  Schoelch C, Hubschle T, Schmidt I, Nuesslein-Hildesheim B. MSG lesions decrease body mass of suckling-age rats by attenuating circadian decreases of energy expenditure. ?Am J Physiol Endocrinol Metab. 2002 Sep;283(3):E604-11. ?PMID: 12169455 [PubMed – indexed for MEDLINE]

6:  Kaufhold A, Nigam PK, Dhir RN, Shapiro BH. Prevention of latently expressed CYP2C11, CYP3A2, and growth hormone defects in neonatally monosodium glutamate-treated male rats by the N-methyl-D-aspartate receptor antagonist dizocilpine maleate. ?J Pharmacol Exp Ther. 2002 Aug;302(2):490-6. ?PMID: 12130706 [PubMed – indexed for MEDLINE]

7:  Balbo SL, Mathias PC, Bonfleur ML, Alves HF, Siroti FJ, Monteiro OG, Ribeiro FB, Souza AC. Vagotomy reduces obesity in MSG-treated rats. ?Res Commun Mol Pathol Pharmacol. 2000 Nov-Dec;108(5-6):291-6. ?PMID: 11958282 [PubMed – indexed for MEDLINE]

8:  de Mello MA, de Souza CT, Braga LR, dos Santos JW, Ribeiro IA, Gobatto CA. Glucose tolerance and insulin action in monosodium glutamate (MSG) obese exercise-trained rats. ?Physiol Chem Phys Med NMR. 2001;33(1):63-71. ?PMID: 11758736 [PubMed – indexed for MEDLINE]

9:  Pinterova L, Zelezna B, Fickova M, Macho L, Krizanova O, Jezova D, Zorad S. Elevated AT1 receptor protein but lower angiotensin II-binding in adipose tissue of rats with monosodium glutamate-induced obesity. ?Horm Metab Res. 2001 Dec;33(12):708-12. ?PMID: 11753755 [PubMed – indexed for MEDLINE]

10:  Larsen PJ, Fledelius C, Knudsen LB, Tang-Christensen M. Systemic administration of the long-acting GLP-1 derivative NN2211 induces lasting and reversible weight loss in both normal and obese rats. ?Diabetes. 2001 Nov;50(11):2530-9. ?PMID: 11679431 [PubMed – indexed for MEDLINE]

11:  Racek L, Lenhardt L, Mozes S. Effect of fasting and refeeding on duodenal alkaline phosphatase activity in monosodium glutamate obese rats. ?Physiol Res. 2001;50(4):365-72. ?PMID: 11551142 [PubMed – indexed for MEDLINE]

12:  Lucinei Balbo S, Gravena C, Bonfleur ML, de Freitas Mathias PC. Insulin secretion and acetylcholinesterase activity in monosodium l-glutamate-induced obese mice. ?Horm Res. 2000;54(4):186-91. ?PMID: 11416236 [PubMed – indexed for MEDLINE]

13:  Dolnikoff M, Martin-Hidalgo A, Machado UF, Lima FB, Herrera E. Decreased lipolysis and enhanced glycerol and glucose utilization by adipose tissue prior to development of obesity in monosodium glutamate (MSG) treated-rats. ?Int J Obes Relat Metab Disord. 2001 Mar;25(3):426-33. ?PMID: 11319642 [PubMed – indexed for MEDLINE]

14:  Imai T, Jiang M, Chambon P, Metzger D. Impaired adipogenesis and lipolysis in the mouse upon selective ablation of the retinoid X receptor alpha mediated by a tamoxifen-inducible chimeric Cre recombinase (Cre-ERT2) in adipocytes. ?Proc Natl Acad Sci U S A. 2001 Jan 2;98(1):224-8. ?PMID: 11134524 [PubMed – indexed for MEDLINE]

15:  Nakagawa T, Ukai K, Ohyama T, Gomita Y, Okamura H. Effects of chronic administration of sibutramine on body weight, food intake and motor activity in neonatally monosodium glutamate-treated obese female rats: relationship of antiobesity effect with monoamines. ?Exp Anim. 2000 Oct;49(4):239-49. ?PMID: 11109549 [PubMed – indexed for MEDLINE]

16:  Martinkova A, Lenhardt L, Mozes S.  Effect of neonatal MSG treatment on day-night alkaline phosphatase activity in the rat duodenum. ?Physiol Res. 2000;49(3):339-45. ?PMID: 11043921 [PubMed – indexed for MEDLINE]

17:  Iwase M, Ichikawa K, Tashiro K, Iino K, Shinohara N, Ibayashi S, Yoshinari M, Fujishima M.  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. ?PMID: 11016806 [PubMed – indexed for MEDLINE]

18:  Mozes S, Lenhardt L, Martinkova A. Alkaline phosphatase activity of duodenal enterocytes after neonatal administration of monosodium glutamate to rats. ?Physiol Res. 2000;49(2):269-77. ?PMID: 10984094 [PubMed – indexed for MEDLINE]

19:  Macho L, Fickova M, Jezova, Zorad S.  Late effects of postnatal administration of monosodium glutamate on insulin action in adult rats. ?Physiol Res. 2000;49 Suppl 1:S79-85. ?PMID: 10984075 [PubMed – indexed for MEDLINE]20:  Miskowiak B, Kesa B, Limanowski A, Partyka M, Filipiak B.Long-term effect of neonatal monosodium glutamate (MSG) treatment on reproductive system of the female rat. Folia Morphol (Warsz). 1999;58(2):105-13. ?PMID: 10598403 [PubMed – indexed for MEDLINE]

21:  Kim YW, Kim JY, Lee SK.Surgical removal of visceral fat decreases plasma free fatty acid and increases insulin sensitivity on liver and peripheral tissue in monosodium glutamate (MSG)-obese rats. ?J Korean Med Sci. 1999 Oct;14(5):539-45. ?PMID: 10576150 [PubMed – indexed for MEDLINE]

22:  Mori RC, Guimaraes RB, Nascimento CM, Ribeiro EB.Lateral hypothalamic serotonergic responsiveness to food intake in rat obesity as measured by microdialysis. ?Can J Physiol Pharmacol. 1999 Apr;77(4):286-92. ?PMID: 10535677 [PubMed – indexed for MEDLINE]

23:  Liu YF, Cai DF, Chen XH.[Effect of zuogui wan on the contents of hypothalamic monoaminic transmitters and body weight in rats treated with monosodium glutamate neonatally] ?Zhongguo Zhong Xi Yi Jie He Za Zhi. 1997 Nov;17(11):673-5. Chinese. ?PMID: 10322848 [PubMed – indexed for MEDLINE]

24:Morris MJ, Tortelli CF, Filippis A, Proietto J.Reduced BAT function as a mechanism for obesity in the hypophagic, neuropeptide Y deficient monosodium glutamate-treated rat. ?Regul Pept. 1998 Sep 25;75-76:441-7. ?PMID: 9802441 [PubMed – indexed for MEDLINE]

25:  Bergen HT, Mizuno TM, Taylor J, Mobbs CV. Hyperphagia and weight gain after gold-thioglucose: relation to hypothalamic neuropeptide Y and proopiomelanocortin. ?Endocrinology. 1998 Nov;139(11):4483-8. ?PMID: 9794456 [PubMed – indexed for MEDLINE]

26:  Palmiter RD, Erickson JC, Hollopeter G, Baraban SC, Schwartz MW.Life without neuropeptide Y. ?Recent Prog Horm Res. 1998;53:163-99. Review. ?PMID: 9769708 [PubMed – indexed for MEDLINE]

27:  Tsukahara F, Uchida Y, Ohba K, Ogawa A, Yoshioka T, Muraki T. The effect of acute cold exposure and norepinephrine on uncoupling protein gene expression in brown adipose tissue of monosodium glutamate-obese mice. ?Jpn J Pharmacol. 1998 Jul;77(3):247-9. ?PMID: 9717772 [PubMed – indexed for MEDLINE]

28:  Hollopeter G, Erickson JC, Palmiter RD.Role of neuropeptide Y in diet-, chemical- and genetic-induced obesity of mice. ?Int J Obes Relat Metab Disord. 1998 Jun;22(6):506-12. ?PMID: 9665670 [PubMed – indexed for MEDLINE]

29:  Hriscu M, Saulea G, Vidrascu N, Baciu I.Effects of monosodium glutamate on blood neutrophils phagocytic activity and phagocytic response in mice. ?Rom J Physiol. 1997 Jan-Dec;34(1-4):95-101. ?PMID: 9653813 [PubMed – indexed for MEDLINE]

30:  Iwase M, Yamamoto M, Iino K, Ichikawa K, Shinohara N, Yoshinari M, Fujishima M. 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 [PubMed – indexed for MEDLINE]

31:  Yoshida T, Umekawa T, Kumamoto K, Sakane N, Kogure A, Kondo M, Wakabayashi Y, Kawada T, Nagase I, Saito M. beta 3-Adrenergic agonist induces a functionally active uncoupling protein in fat and slow-twitch muscle fibers. ?Am J Physiol. 1998 Mar;274(3 Pt 1):E469-75. ?PMID: 9530130 [PubMed – indexed for MEDLINE]

32:  Papa PC, Seraphim PM, Machado UF. Loss of weight restores GLUT 4 content in insulin-sensitive tissues of monosodium glutamate-treated obese mice. ?Int J Obes Relat Metab Disord. 1997 Nov;21(11):1065-70. ?PMID: 9368832 [PubMed – indexed for MEDLINE]

33:  Zorad S, Macho L, Jezova D, Fickova M.Partial characterization of insulin resistance in adipose tissue of monosodium glutamate-induced obese rats. ?Ann N Y Acad Sci. 1997 Sep 20;827:541-5. No abstract available. ?PMID: 9329787 [PubMed – indexed for MEDLINE]

34:  Ribeiro EB, do Nascimento CM, Andrade IS, Hirata AE, Dolnikoff MS. Hormonal and metabolic adaptations to fasting in monosodium glutamate-obese rats. ?J Comp Physiol [B]. 1997 Aug;167(6):430-7. ?PMID: 9286091 [PubMed – indexed for MEDLINE]

35:  Dawson R, Pelleymounter MA, Millard WJ, Liu S, Eppler B.Attenuation of leptin-mediated effects by monosodium glutamate-induced arcuate nucleus damage. ?Am J Physiol. 1997 Jul;273(1 Pt 1):E202-6. ?PMID: 9252497 [PubMed – indexed for MEDLINE]

36:  Hirata AE, Andrade IS, Vaskevicius P, Dolnikoff MS. Monosodium glutamate (MSG)-obese rats develop glucose intolerance and insulin resistance to peripheral glucose uptake. ?Braz J Med Biol Res. 1997 May;30(5):671-4. ?PMID: 9283637 [PubMed – indexed for MEDLINE]

37:  Popova IuP, Kondrashov SIu, Malikova NA, Aleshko-Ozhevskii, Sheviakova LV, Makhova NN, Mazo VK, Galkin AA, Shirina LI.[Lipid peroxidation and various parameters of mineral metabolism in patients with alimentary obesity during therapy with monosodium glutamate] ?Vopr Pitan. 1997;(3):8-10. Russian. ?PMID: 9289922 [PubMed – indexed for MEDLINE]

38:  Spurlock ME, Hahn KJ, Miner JL.Regulation of adipsin and body composition in the monosodium glutamate (MSG)-treated mouse. ?Physiol Behav. 1996 Nov;60(5):1217-21. ?PMID: 8916174 [PubMed – indexed for MEDLINE]

39:  Otoya RE, Seltzer AM, Donoso AO.Decrease of (+)-3-[125I]MK-801 binding to NMDA brain receptors revealed at puberty in rats treated neonatally with monosodium glutamate. ?Brain Res Dev Brain Res. 1996 Sep 2;95(2):149-56. ?PMID: 8874889 [PubMed – indexed for MEDLINE]

40:  Caputo FA, Ali SF, Wolff GL, Scallet AC. Neonatal MSG reduces hypothalamic DA, beta-endorphin, and delays weight gain in genetically obese (A viable yellow/alpha) mice. ?Pharmacol Biochem Behav. 1996 Feb;53(2):425-32. ?PMID: 8808153 [PubMed – indexed for MEDLINE]

41:  Frederich RC, Hamann A, Anderson S, Lollmann B, Lowell BB, Flier JS.Leptin levels reflect body lipid content in mice: evidence for diet-induced resistance to leptin action. ?Nat Med. 1995 Dec;1(12):1311-4. ?PMID: 7489415 [PubMed – indexed for MEDLINE]

42:  Yoshida T, Sakane N, Wakabayashi Y, Umekawa T, Kondo M.Thermogenic, anti-obesity effects of bofu-tsusho-san in MSG-obese  mice. ?Int J Obes Relat Metab Disord. 1995 Oct;19(10):717-22. ?PMID: 8589765 [PubMed – indexed for MEDLINE]

43:  Frederich RC, Lollmann B, Hamann A, Napolitano-Rosen A, Kahn BB, Lowell BB, Flier JS  Expression of ob mRNA and its encoded protein in rodents. Impact of nutrition and obesity. ?J Clin Invest. 1995 Sep;96(3):1658-63. ?PMID: 7657836 [PubMed – indexed for MEDLINE]

44:  Fabres-Machado U, Saito M. The effect of adipose cell size on the measurement of GLUT 4 in white adipose tissue of obese mice. ?Braz J Med Biol Res. 1995 Mar;28(3):369-76. ?PMID: 8520534 [PubMed – indexed for MEDLINE]

45:  Guengerich FP. Influence of nutrients and other dietary materials on cytochrome P-450 enzymes. ?Am J Clin Nutr. 1995 Mar;61(3 Suppl):651S-658S. Review. ?PMID: 7879733 [PubMed – indexed for MEDLINE]

46:  Yoshida T, Yoshioka K, Sakane N, Umekawa T, Kondo M. Probucol prevents the progression of fatty liver in MSG obese mice. ?Exp Clin Endocrinol Diabetes. 1995;103(2):119-22. ?PMID: 7553075 [PubMed – indexed for MEDLINE]

47:  Platt KA, Claffey KP, Wilkison WO, Spiegelman BM, Ross SR. Independent regulation of adipose tissue-specificity and obesity response of the adipsin promoter in transgenic mice. ?J Biol Chem. 1994 Nov 18;269(46):28558-62. ?PMID: 7961801 [PubMed – indexed for MEDLINE]

48:  Kubota A, Nakagawa Y, Igarashi Y.Studies of gene expression in liver of insulin-like growth factor (IGF)-I, IGF binding protein-3 and growth hormone  GH) receptor/GH binding protein in rats treated neonatally with monosodium glutamate. ?Horm Metab Res. 1994 Nov;26(11):497-503. ?PMID: 7533119 [PubMed – indexed for MEDLINE]

49:  Yoshida T, Sakane N, Wakabayashi Y, Umekawa T, Kondo M. Anti-obesity effect of CL 316,243, a highly specific beta 3-adrenoceptor agonist, in mice with monosodium-L-glutamate-induced obesity. ?Eur J Endocrinol. 1994 Jul;131(1):97-102. ?PMID: 7913651 [PubMed – indexed for MEDLINE]

50:  Pampori NA, Shapiro BH. Subnormal concentrations in the feminine profile of circulating growth hormone enhance expression of female-specific CYP2C12. ?Biochem Pharmacol. 1994 Jun 1;47(11):1999-2004. ?PMID: 8010984 [PubMed – indexed for MEDLINE]

51:  Marmo MR, Dolnikoff MS, Kettelhut IC, Matsushita DM, Hell NS, Lima FB. Neonatal monosodium glutamate treatment increases epididymal adipose tissue sensitivity to insulin in three-month old rats. ?Braz J Med Biol Res. 1994 May;27(5):1249-53. ?PMID: 8000347 [PubMed – indexed for MEDLINE]

52:  Yoshida T, Sakane N, Wakabayashi Y, Yoshioka K, Umekawa T, Kondo M. The alpha/beta-adrenergic receptor blocker arotinolol activates the thermogenesis of brown adipose tissue in monosodium-L-glutamate-induced obese mice. ?Int J Obes Relat Metab Disord. 1994 May;18(5):339-43. ?PMID: 7520314 [PubMed – indexed for MEDLINE]

53:  Machado UF, Shimizu I, Saito M. Reduced content and preserved translocation of glucose transporter (GLUT 4) in white adipose tissue of obese mice. ?Physiol Behav. 1994 Apr;55(4):621-5. ?PMID: 8190786 [PubMed – indexed for MEDLINE]

54:  Pampori NA, Shapiro BH. Effects of neonatally administered monosodium glutamate on the sexually dimorphic profiles of circulating growth hormone regulating murine hepatic monooxygenases. ?Biochem Pharmacol. 1994 Mar 29;47(7):1221-9. ?PMID: 8161351 [PubMed – indexed for MEDLINE]

55:  Zhang WM, Kuchar S, Mozes S. Body fat and RNA content of the VMH cells in rats neonatally treated with monosodium glutamate. ?Brain Res Bull. 1994;35(4):383-5. ?PMID: 7531599 [PubMed – indexed for MEDLINE]

56:  Miskowiak B, Partyka M. Effects of neonatal treatment with MSG (monosodium glutamate) on hypothalamo-pituitary-thyroid axis in adult male rats. ?Histol Histopathol. 1993 Oct;8(4):731-4. ?PMID: 8305823 [PubMed – indexed for MEDLINE]

57:  Machado UF, Shimizu Y, Saito M. ?Decreased glucose transporter (GLUT 4) content in insulin-sensitive tissues of obese aurothioglucose- and monosodium glutamate-treated mice. ?Horm Metab Res. 1993 Sep;25(9):462-5. ?PMID: 8225198 [PubMed – indexed for MEDLINE]

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