The influence of obesity by a diet high in saturated fats and carbohydrates balance in the manifestation of systemic complications and comorbidities

Nutrire - Tập 42 Số 1 - 2017
Caroline Soares Adorni1, Camila Renata Corrêa2, Danielle Fernandes Vileigas1, Dijon Henrique Salomé de Campos1, Carlos Roberto Padovani3, Igor Otávio Minatel4, Antônio Carlos Cicogna1
1Department of Internal Medicine, Botucatu Medical School, São Paulo State University, Botucatu, Brazil
2Department of Pathology, Botucatu School of Medicine, São Paulo State University–UNESP, Distrito de Rubião Jr s/n, Botucatu, SP, Brazil
3Department of Biostatistics, Botucatu Biosciences Institute, São Paulo State University, Botucatu, Brazil
4Department of Biochemistry, Botucatu Biosciences Institute, São Paulo State University, Botucatu, Brazil

Tóm tắt

Abstract Background The aim of this study is to test the hypothesis that obesity induced by a diet rich in saturated fats and balanced in carbohydrates is associated with the development of systemic complications and comorbidities. Methods Thirty-seven 60-day-old male Wistar rats were randomized into two groups: control (C, n = 18, standard diet) and obese (OB, n = 19, high-saturated fat diet), for 33 weeks. Nutritional profile: food and caloric intake, feed efficiency, body weight, and adiposity index. Complications: in plasma were analyzed dyslipidemia, insulin resistance (HOMA-IR), glucose intolerance, hyperleptinemia, hyperinsulinemia, plasmatic C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α); in the myocardial and epididymal adipose tissue were assessed IL-6 and TNF-α. Comorbidities: diabetes mellitus and systemic blood pressure (SBP). Student’s t test, ANOVA, and Bonferroni P < 0.05. Results The final body weight, feed efficiency, and adiposity index were higher in OB group than in control; although food intake was lower in OB group, caloric intake was similar in both groups. Specific parameters, such as LDL, cholesterol, triglycerides, HOMA-IR, CRP, TNF-α in epididymal adipose tissue, and IL-6 in the myocardium, were higher in obese rats than in controls. SBP, baseline glucose, and glucose after 2 h of overload were significantly increased in OB group; however, the severity was not enough to classify the animals as diabetic and hypertensive. Conclusion Obesity induced by a diet high in saturated fatty acids with balanced carbohydrates for 33 weeks in Wistar rats was effective in triggering complications but unable to develop comorbidities.

Từ khóa


Tài liệu tham khảo

World OH. World Health Organisation obesity and overweight fact sheet. Who. 2016;1(1):2016.

Cotillard A, Poitou C, Torcivia A, Bouillot J, Dietrich A, Klöting N, et al. Adipocyte size threshold matters: link with risk of type 2 diabetes and improved insulin resistance after gastric bypass. J Clin Endocrinol Metab. 2014;99(8):1466–70.

Skurk T, Alberti-huber C, Herder C, Hauner H. Relationship between adipocyte size and adipokine expression and secretion. J Clin Endocrinol Metab. 2016;92(3):1023–33.

Friedman J. Obesity: causes and control of excess body fat. Nature. 2009;342(May):340–2.

Lopaschuk GD, Folmes CDL, Stanley WC. Cardiac energy metabolism in obesity. Circ Res. 2007;101:335–47.

Junio A, Ferron T, Jacobsen BB, Grippa P, Ana S. Cardiac dysfunction induced by obesity is not related to β-adrenergic system impairment at the receptor-signalling pathway. PLoS One. 2015;10:1–18

Dupuy AM, Jaussent I, Lacroux A, Durant R, Cristol JP, Delcourt C. Waist circumference adds to the variance in plasma C-reactive protein levels in elderly patients with metabolic syndrome. Gerontology. 2007;53(6):329–39.

Anders LC, Yeo H, Kaelin BR, Lang AL, Bushau AM, Douglas AN, et al. Role of dietary fatty acids in liver injury caused by vinyl chloride metabolites in mice. Toxicol Appl Pharmacol. 2016;(in press).

Erdei N, Tóth A, Pásztor E, Papp Z, Edes I, Koller A, et al. High-fat diet-induced reduction in nitric oxide-dependent arteriolar dilation in rats: role of xanthine oxidase-derived superoxide anion. Am J Physiol Heart Circ Physiol. 2006;291:H2107–15.

Panchal SK, Poudyal H, Waanders J, Brown L. Coffee extract attenuates changes in cardiovascular and hepatic structure and function without decreasing obesity in high-carbohydrate, high-fat diet-fed male rats. J Nutr. 2012;142(4):690–7.

Johnson AR, Wilkerson MD, Sampey BP, Troester MA, Hayes DN, Makowski L. Cafeteria diet-induced obesity causes oxidative damage in white adipose. Biochem Biophys Res Commun. 2016;473(2):545–50.

Li H, Lelliott C, Håkansson P, Ploj K, Tuneld A, Verolin-johansson M, et al. Intestinal, adipose, and liver inflammation in diet-induced obese mice. Metabolism [Internet]. 2008;57(12):1704–10. Available from: http://dx.doi.org/10.1016/j.metabol.2008.07.029.

Gomez-smith M, Karthikeyan S, Jeffers MS, Thomason LA, Stefanovic B, Corbett D. A physiological characterization of the cafeteria diet model of metabolic syndrome in the rat. Physiol Behav [Internet]. 2016;16: Available from: http://dx.doi.org/10.1016/j.physbeh.2016.09.029

Ruiz-núñez B, Dijck-brouwer DAJ, Muskiet FAJ. ScienceDirect. The relation of saturated fatty acids with low-grade inflammation and cardiovascular disease. J Nutr Biochem [Internet]. 2016;36:1–20. Available from: http://dx.doi.org/10.1016/j.jnutbio.2015.12.007

Lee J, Lee J, Cho W, Yim N, Kim H, Yun B, et al. KBH-1, an herbal composition, improves hepatic steatosis and leptin resistance in high-fat diet-induced obese rats. BMC Complement Altern Med [Internet]. 2016;16:1–12.

Kelly KB, Kennelly JP, Ordonez M, Nelson R, Leonard K, Stabler S, et al. Weight gain, and adipose tissue inflammation in high fat diet-fed rats. Nutrients. 2016;8:2–13.

Lima-leopoldo AP, Leopoldo AS, Silva DCT, Nascimento AF, De Campos DHS, Luvizotto RAM, et al. Long-term obesity promotes alterations in diastolic function induced by reduction of phospholamban phosphorylation at serine-16 without affecting calcium handling. J Appl Physiol. 2014;117(6):669–78.

Nascimento AF, Sugizaki MM, Leopoldo AS, Lima-Leopoldo AP, Luvizotto RAM, Nogueira CR, et al. A hypercaloric pellet-diet cycle induces obesity and co-morbidities in wistar rats. Arq Bras Endocrinol Metabol. 2008;52(6):968–74.

Zock PL, Blom WAM, Nettleton JA, Hornstra G. Progressing insights into the role of dietary fats in the prevention of cardiovascular disease. Curr Cardiol Rep. 2016;18(11):111.

Mayor S. Eating more unsaturated fats and less carbohydrate reduces blood glucose, study finds. BMJ. 2016;4053(July):i4053.

Johns DJ, Lindroos A-K, Jebb SA, Sjöström L, Carlsson LMS, Ambrosini GL. Dietary patterns, cardiometabolic risk factors, and the incidence of cardiovascular disease in severe obesity. Obesity. 2015;23(0):1063–70.

Cabello-Saavedra E, Bes-Rastrollo M, Martinez JA, Diez-Espino J, Buil-Cosiales P, Serrano-Martinez M, et al. Macronutrient intake and metabolic syndrome in subjects at high cardiovascular risk. Ann Nutr Metab. 2010;56(2):152–9.

Sawin EA, Stroup BM, Murali SG, O’Neill LM, Ntambi JM ND. Differential effects of dietary fat content and protein source on bone phenotype and fatty acid oxidation in female C57Bl/6 mice. 2016. p.:e0163234.

Gakidou E, Mallinger L, Abbott-klafter J, Guerrero R, Villalpando S. Murray. Management of diabetes and associated cardiovascular risk factors in seven countries: a comparison of data from national health examination. 2011;89(3):172–83. http://www.who.int/bulletin/volumes/89/3/10-080820/en/.

Wang Z, Yang Y, Xiang X, Zhu Y, Men J HM. Estimation of the normal range of blood glucose in rats. Vol. 133, Wei Sheng Yan Jiu. 2010. p. 2010.

Després J-P. Abdominal obesity and cardiovascular disease: is inflammation the missing link? Can J Cardiol. 2012;28(6):642–52.

Henrique D, De Campos S, Leopoldo AS, Lima-leopoldo AP, Ferreira A, De Oliveira-junior SA, et al. Obesity preserves myocardial function during blockade of the glycolytic pathway. Arq Bras Cardiol. 2014;103:330–7.

Relling DP, Esberg LB, Fang CX, Johnson WT, Murphy EJ, Carlson EC, et al. High-fat diet-induced juvenile obesity leads to cardiomyocyte dysfunction and upregulation of Foxo3a transcription factor independent of lipotoxicity and apoptosis. J Hypertens. 2006;24(3):549–61.

Mazidi M, Heidari-Bakavoli A, Khayyatzadeh SS, Azarpazhooh MR, Nematy M, Safarian M, et al. Serum hs-CRP varies with dietary cholesterol, but not dietary fatty acid intake in individuals free of any history of cardiovascular disease. Eur J Clin Nutr. 2015;2016:1–4.

Stark AH, Timar B, Madar Z. Adaptation of Sprague Dawley rats to long-term feeding of high fat or high fructose diets. Eur J Nutr. 2000;39(5):229–34.

Meshkani R, Vakili S. Clinica Chimica Acta. Tissue resident macrophages: key players in the pathogenesis of type 2 diabetes and its complications. Clin Chim Acta [Internet]. 2016;462:77–89.

Dispirito JR, Mathis D. Seminars in Immunology. Immunological contributions to adipose tissue homeostasis. Semin Immunol [Internet]. 2015;27(5):315–21.

Panchal SK, Poudyal H, Iyer A, Nazer R, Alam MA, Diwan V, et al. High-carbohydrate, high-fat diet-induced metabolic syndrome and cardiovascular remodeling in rats. J Cardiovasc Pharmacol. 2011;57(5):611–24.

Panchal SK, Brown L. Rodent models for metabolic syndrome research. J Biomed Biotechnol. 2011;2011(351982):14.

Vileigas DF, de Deus AF, da Silva DCT, de Tomasi LC, de Campos DHS, Adorni CS, et al. Saturated high‐fat diet‐induced obesity increases adenylate cyclase of myocardial β ‐adrenergic system and does not compromise cardiac function. Physiol Rep. 2016;4(17):e12914.

Silvares RR, Pereira ENGDS, Flores EEI, Estato V, Reis PA, Silva IJD, et al. Combined therapy with metformin and insulin attenuates systemic and hepatic alterations in a model of high-fat diet-/streptozotocin-induced diabetes. Int J Exp Pathol. 2016;97(3):266–77.

Poudyal H, Panchal SK, Ward LC, Waanders J, Brown L. Chronic high-carbohydrate, high-fat feeding in rats induces reversible metabolic, cardiovascular, and liver changes. Am J Physiol Endocrinol Metab. 2012;312:1472–82.