Cafeteria diet intake for fourteen weeks can cause obesity and insulin resistance in Wistar rats

Autores/as

  • Danilo Antônio Corrêa PINTO JÚNIOR Universidade Estadual Paulista Júlio de Mesquita Filho
  • Patricia Monteiro SERAPHIM Universidade Estadual Paulista Júlio de Mesquita Filho

Palabras clave:

Cafeteria diet, High-fat food, Insulin resistance, Obesity

Resumen

Objective
Obesity is a strong predictor of some kinds of diseases. High intake of high-fat foods contributes significantly to the growth of the obese population globally. The aim of this study was to verify if consumption of a cafeteria diet for fourteen weeks could increase white fat mass, body weight and skeletal muscle mass and promote insulin resistance in male Wistar rats.

Methods
Twenty animals were divided into two groups: control and obese. Both were fed standard chow and water ad libitum. Additionally, a cafeteria diet consisting of bacon, bologna sausage, sandwich cookies and soft drink was given to the obese group.

Results
The obese group was significantly heavier (p<0.0001) than controls from the second week until the end of the cafeteria-diet intervention. Absolute and relative fat mass, liver weight and Lee Index increased significantly (p<0.05) in the obese group. Furthermore, the obese group had lower (p<0.05) insulin sensitivity than the control group.

Conclusion
In conclusion, fourteen weeks of cafeteria diet promoted a progressive increase of fat mass and insulin resistance. Therefore, this is a great and inexpensive diet-induced insulin resistance model. 

Citas

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.

Publicado

2023-08-17

Cómo citar

Corrêa PINTO JÚNIOR, D. A., & Monteiro SERAPHIM, P. . (2023). Cafeteria diet intake for fourteen weeks can cause obesity and insulin resistance in Wistar rats. Revista De Nutrição, 25(3). Recuperado a partir de https://puccampinas.emnuvens.com.br/nutricao/article/view/9247

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ARTIGOS ORIGINAIS