Dieta de cafeteria por quatorze semanas pode causar obesidade e resistência insulínica em ratos Wistar
Palavras-chave:
Dieta de cafeteria, Alimento hipercalórico, Resistência à insulina, ObesidadeResumo
Objetivo
A obesidade é um forte preditor de alguns tipos de doenças. A grande oferta de comida e a predominância de ácidos graxos presentes na maioria dos alimentos contribuem diretamente para o aumento da população obesa no mundo. O objetivo do estudo foi verificar se uma dieta de cafeteria durante um período de catorze semanas pode causar aumento dos pesos de tecido adiposo branco, corporal e muscular e provocar um quadro de resistência insulínica em ratos machos Wistar.
Métodos
Vinte ratos machos Wistar foram divididos em dois grupos: controle e obeso. Os dois grupos foram alimentados com ração padrão e água ad libitum. Ao grupo obeso foi ofertada dieta ocidental, composta por salsicha, mortadela, bolacha recheada, bacon e refrigerante.
Resultados
Os animais do grupo obeso estavam significantemente mais pesados a partir da segunda semana de tratamento e essa diferença permaneceu até o final do estudo (p<0,0001). O peso absoluto e relativo do tecido adiposo branco e do fígado, e o Índice de Lee foram maiores no grupo obeso (p<0,05), que apresentou uma menor sensibilidade à insulina no final do estudo quando comparado ao grupo controle (p<0,05). Podemos observar que a dieta cafeteria promoveu um aumento progressivo e significativo da massa de gordura corporal associada à disfunção da ação da insulina.
Conclusão
Conclui-se que uma dieta de cafeteria por um período de catorze semanas é capaz de promover aumento progressivo da massa adiposa associada à disfunção da insulina, sendo ótimo e fácil modelo de para induzir resistência à insulina.
Referências
World Healthy Organization. Obesity and overweight. Geneva: WHO; 2012.
Damaso A, Guerra RLF, Botero JP, Prado WL. Etiologia da obesidade. In: Damaso A. Obesidade. Rio de Janeiro: Medsi; 2003.
Pan A, Sun Q, Bernstein AM, Schulze MB, Manson JE, Willett WC, et al. Red meat consumption and risk of type 2 diabetes: 3 cohorts of US adults and an updated metaanalysis. Am J Clin Nutr. 2011; 94:1-9.
Machado UF, Schaan BD, Seraphim PM. Glucose transporters in the metabolic syndrome. Arq Bras Endocrinol Metab. 2006; 50(2):177-89.
Rizvi AA. Hypertension, obesity and inflammation: the complex designs of a deadly trio. Metab Syndr Relat Disord. 2010; 8(4):287-94.
Blundell JE, Gillet A. Control of food intake in the obese. Obes Res. 2001; 9(4):263S-70S.
De Souza CT, Araújo EP, Bordin S, Ashimine R, Zollner R, Boschero AC, et al. Consumption of a fat: rich diet activates a proinflammatory response and induces insulin resistance in the hypothalamus. Endocrinology. 2005; 146(10):4192-9.
Bertrand RL, Senadheera S, Markus I, Liu L, Howitt L, Chen H, et al. A Western diet increases serotonin availability in rat small intestine. Endocrinology. 2011; 152(1):36-47.
Ghitza UE, Nair SG, Golden SA, Gray SM, Uejima JL, Bossert JM, et al. Peptide YY3-36 decrases reinstatement of high-fat-food seeking during dieting in a rat relapse model. J Neurosci. 2007; 27(43):11522-32.
Scoaris CR, Rizo GV, Roldi LP, De Moraes SMF, De Proença ARG, Peralta RM, et al. Effects of cafeteria diet on the jejunum in sedentary and physically trained rats. Nutrition. 2010; 26(3):312-20.
Brunetti L, Leone S, Orlando G, Recinella L, Ferrante C, Chiavaroli A, et al. Effects of obestatin on feeding and body weight after standard or cafeteria diet in the rat. Peptides. 2009; 30(7):1323-7.
Lamas O, Martinez JA, Marti A. Energy restriction restores the the impaired immune response in overweight (cafeteria) rats. J Nutr Biochem. 2004; 15(7):418-25.
Ribot J, Rodríguez AM, Rodríguez E, Palou A. Adiponectin and resistin response in the onset of obesity in male and female rats. Obesity. 2008; 16(4):723-30.
Padua MF, Padua TF, Pauli JR, Souza CT, Silva ASR, Ropelle ECC, et al. Physical exercise decreases fasting hyperglycemia in diabetic mice through AMPK activation. Rev Bras Med Esporte. 2009; 15(3):179-84.
Bernardis LL, Patterson BD. Correlation between “Lee Index” and carcass fat content in weanling and adult female rats with hypothalamic lesions. J Endocrinol. 1968; 40(4):527-8.
Araújo GG, Araújo MB, Dangelo RA, ManchadoGobatto FB, Mota CSA, Ribeiro C, et al. Maximal Lactate stead state in obese rats of both genders. Rev Bras Med Esporte. 2009; 15(1):46-9.
De Carvalho MHC, Colaço AL, Fortes ZB. Citokines, endothelial dysfunction and insulin resistance. Arq Bras Endocrinol Metab. 2006; 50(2):304-12.
Hotamisligil GS, Peraldi P, Budavari A, Ellis R, White MF, Spiegelman BM. IRS - 1 mediated inhibition of insulin receptor tyrosine kinase activity in TNF - alpha and obesity - induced insulin resistance. Science. 1996; 271(5249):665-8.
Prada PO, Zecchin HG, Gasparetti AL, Torsoni MA, Ueno M, Hirata AE, et al. Western Diet modulates insulin signaling, c - Jun N - Terminal Kinase activity, and Insulin Receptor Substrate - 1ser307 Phosphorylation in a Tissue - Specific Fashion. Endocrinology. 2005; 146(3):1576-87.
Sabio G, Davis R. cJUN NH2 - terminal kinase 1 (JNK1): roles in metabolic regulation of insulin resistance. Trends Biochem Sci. 2010; 35:490-6.
Kaneto H, Nakatani Y, Kawamori D, Miyatsuka T, Matsuoka TA, Matsuhisa M, et al. Role of oxidative stress, endoplasmic reticulum stress, and c - Jun N Terminal kinase in pancreatic E - cell dysfunction and insulin resistance. Int J Biochem Cell Biol. 2006; 38(5-6):782-93.
Nakatani Y, Kaneto H, Kawatomi Y, Hatazaki M, Matsuoka T, Ozawa K, et al. Involvement of endoplasmic reticulum stress in insulin resistance and diabetes. J Biol Chem. 2005; 280(1):847-51.
Ozawa K, Mayuki M, Munehide M, Katsura T, Yoshihisa N, Masahiro H, et al. The endoplasmic reticulum chaperone improves insulin resistance in type 2 diabetes. Diabetes. 2005; 54(3):657-63.
Hotamisligil GS. Role of endoplasmic reticulum stress and c - Jun NH2 - terminal kinase pathways in inflammation and origin of obesity and diabetes. Diabetes. 2005; 54(2):S73-S78.
Tanti JF, Jager J. Cellular mechanisms of insulin resistance: role of stress - regulated serine kinase and insulin receptor substrates (IRS) serine phosphorylation. Curr Opin Pharmacol. 2009; 9(6): 753-62.
Shoelson SE, Lee J, Goldfine AB. Inflammation and insulin resistance. J Clin Invest. 2006; 116(7): 1793-801.
Ray M, Yu S, Sharda DR, Wilson CB, liu Q, Kaushal N, et al. Inhibition of TLR4: Induced by INB kinase activity by the RON receptor tyrosine kinase and its ligand, macrophage - stimulating protein. J Immun. 2010; 185(12):7309-16.
Lee JY, Sohn KH, Rhee SH, Hwang D. Saturated fatty acids, but not unsaturated fatty acids, induce the expression of cyclooxygenase: 2 mediated through Toll - like receptor 4. J Biol Chem. 2001; 276(20):16683-9.
Kim F, Pham M, Luttrell I, Bannerman DD, Tupper J, Thaler J, et al. Toll: like receptor - 4 mediates vascular inflammation and insulin resistance in diet - induced obesity. Circ Res. 2007; 100(11): 1589-96.
Sampey BP, Vanhoose AM, Winfield HM, Freemerman AJ, Muehlbauer MJ, Fueger PT, et al. Cafeteria diet is a robust model of human metabolic syndrome with liver and adipose inflammation: comparison to high: fat feed. Obesity. 2011; 19(6): 1109-17.
Costa ACP, Pinto Jr DAC, Brandão BB, Moreira RJ, Machado UF, Seraphim PM. Resistive training reduces inflammation in skeletal muscle and improves the peripheral insulin sensitivity in obese rats induced by hyperlipidic diet. Arq Bras Endocrinol Metab. 2011; 55(2):155-63.
Miyake K, Ogawa W, Matsumoto M, Nakamura T, Sakaue H, Kasuga M. Hyperinsulinemia, glucose intolerance, and dyslipidemia induced by acute inhibition of phosphoinositide 3: kinase signaling in the liver. J Clin Invest. 2002; 110(10):1483-91.
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Copyright (c) 2023 Danilo Antônio Corrêa PINTO JÚNIOR, Patricia Monteiro SERAPHIM
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