Early Developmental Exposure to High Fructose Intake in Rats with NaCl Stimulation Causes Cardiac Damage

Overview

Journal Eur J Nutr

Specialty Nutritional Sciences

Date 2015 Jan 8

PMID 25564432

Citations 4

Authors

I C Araujo

R P Andrade

F Santos

E S Soares

R Yokota

C Mostarda

P Fiorino

K De Angelis

M C Irigoyen

M Morris

V Farah

Affiliations

Soon will be listed here.

Abstract

Purpose: Metabolic syndrome (MS) increases the risk of type 2 diabetes and cardiovascular disease. High consumption of fructose is a proposed cause of increased MS, manifested through hypertension, obesity, insulin resistance, and dyslipidemia. High NaCl also increases the risk of CD. The purpose of this study is to evaluate the influence of fructose and sodium on autonomic dysfunction and its relation with CD in MS. Fructose overload was started at weaning and continued through adulthood.

Methods: Male Wistar rats (21 days) were divided into four groups: Control (C), fructose consumption (10%, F), NaCl consumption (salt 1% for the 10 last days, S), and fructose and NaCl (FS), and monitored for 8 weeks. Metabolic evaluations consisted of Lee index, glycemia, insulin and glucose tolerance tests, triglycerides, and total cholesterol measurements. Cardiovascular parameters measured were arterial pressure (AP) and cardiac function performed by echocardiography. They also measured the influence of renin angiotensin (RAS) and autonomic nervous systems by drug blockage with losartan, atropine, and atenolol.

Results: Energy analysis showed no change between groups. Fructose overload induced a MS state, confirmed by insulin resistance, glucose intolerance, and dyslipidemia. Fasting glucose was increased in F and FS rat groups compared with C and S groups. AP was higher in F, S, and FS groups in comparison with the C group. The hypotensive response after sympathetic blockade was increased in F, S, and FS versus C. The cardiac vagal tonus was reduced in F and FS animal groups. The intrinsic heart rate was decreased in the FS group (372 ± 9 bpm) compared with the C group (410 ± 13 bpm). The morphometric measurements evaluated through left ventricular diameter during diastole and the left ventricular diameter during systole decreased in the FS group (16 and 26%, respectively). Diastolic function was reduced in F and FS. The depressor response induced by losartan was increased in the F group in comparison with other groups. However, there was a uniform increase in plasma ACE activity in all treated groups compared with the C group.

Conclusions: Data suggest that early exposure to high fructose intake produced marked alterations in metabolic and cardiovascular function. When stimulated by NaCl, the fructose-fed subjects showed further impairment in cardiac function.

Citing Articles

Intra-Renal Angiotensin Levels Are Increased in High-Fructose Fed Rats in the Extracorporeal Renal Perfusion Model.

Yokota R, Ronchi F, Fernandes F, Jara Z, Rosa R, Leite A Front Physiol. 2018; 9:1433.

PMID: 30364140 PMC: 6191567. DOI: 10.3389/fphys.2018.01433.

Early Effects of a Low Fat, Fructose-Rich Diet on Liver Metabolism, Insulin Signaling, and Oxidative Stress in Young and Adult Rats.

Crescenzo R, Cigliano L, Mazzoli A, Cancelliere R, Carotenuto R, Tussellino M Front Physiol. 2018; 9:411.

PMID: 29755364 PMC: 5932594. DOI: 10.3389/fphys.2018.00411.

Exercise Training Prevents Cardiovascular Derangements Induced by Fructose Overload in Developing Rats.

Farah D, Nunes J, Sartori M, Dias D, Sirvente R, Silva M PLoS One. 2016; 11(12):e0167291.

PMID: 27930685 PMC: 5145255. DOI: 10.1371/journal.pone.0167291.

Fructose Containing Sugars at Normal Levels of Consumption Do Not Effect Adversely Components of the Metabolic Syndrome and Risk Factors for Cardiovascular Disease.

Angelopoulos T, Lowndes J, Sinnett S, Rippe J Nutrients. 2016; 8(4):179.

PMID: 27023594 PMC: 4848648. DOI: 10.3390/nu8040179.

References

Stanhope K, Havel P . Endocrine and metabolic effects of consuming beverages sweetened with fructose, glucose, sucrose, or high-fructose corn syrup. Am J Clin Nutr. 2008; 88(6):1733S-1737S. PMC: 3037017. DOI: 10.3945/ajcn.2008.25825D. View

Rocchini A, Yang J, Smith M, Supiano M . Serial changes in norepinephrine kinetics associated with feeding dogs a high-fat diet. J Clin Hypertens (Greenwich). 2010; 12(2):117-24. PMC: 8673245. DOI: 10.1111/j.1751-7176.2009.00230.x. View

Gavras I, Gavras H . 'Volume-expanded' hypertension: the effect of fluid overload and the role of the sympathetic nervous system in salt-dependent hypertension. J Hypertens. 2012; 30(4):655-9. DOI: 10.1097/HJH.0b013e32834f6de1. View

Mostarda C, Rodrigues B, Vane M, Moreira E, Rosa K, Moraes-Silva I . Autonomic impairment after myocardial infarction: role in cardiac remodelling and mortality. Clin Exp Pharmacol Physiol. 2009; 37(4):447-52. DOI: 10.1111/j.1440-1681.2009.05327.x. View

Sharma N, Okere I, Barrows B, Lei B, Duda M, Yuan C . High-sugar diets increase cardiac dysfunction and mortality in hypertension compared to low-carbohydrate or high-starch diets. J Hypertens. 2008; 26(7):1402-10. PMC: 3103886. DOI: 10.1097/HJH.0b013e3283007dda. View

Hwang I, Ho H, Hoffman B, Reaven G . Fructose-induced insulin resistance and hypertension in rats. Hypertension. 1987; 10(5):512-6. DOI: 10.1161/01.hyp.10.5.512. View

Xing S, Bi X, Tan H, Zhang Y, Xing Q, Zhang W . Overexpression of interleukin-18 aggravates cardiac fibrosis and diastolic dysfunction in fructose-fed rats. Mol Med. 2010; 16(11-12):465-70. PMC: 2972394. DOI: 10.2119/molmed.2010.00028. View

De Angelis K, Irigoyen M, Morris M . Diabetes and cardiovascular autonomic dysfunction: application of animal models. Auton Neurosci. 2008; 145(1-2):3-10. PMC: 2659465. DOI: 10.1016/j.autneu.2008.10.013. View

Hallfrisch J, Ellwood K, Michaelis 4th O, Reiser S, ODorisio T, PRATHER E . Effects of dietary fructose on plasma glucose and hormone responses in normal and hyperinsulinemic men. J Nutr. 1983; 113(9):1819-26. DOI: 10.1093/jn/113.9.1819. View

10.

Tiwari S, Riazi S, Ecelbarger C . Insulin's impact on renal sodium transport and blood pressure in health, obesity, and diabetes. Am J Physiol Renal Physiol. 2007; 293(4):F974-84. DOI: 10.1152/ajprenal.00149.2007. View

11.

Cunha T, Farah V, Paulini J, Pazzine M, Elased K, Marcondes F . Relationship between renal and cardiovascular changes in a murine model of glucose intolerance. Regul Pept. 2007; 139(1-3):1-4. DOI: 10.1016/j.regpep.2006.11.023. View

12.

Whelton P, Appel L, Sacco R, Anderson C, Antman E, Campbell N . Sodium, blood pressure, and cardiovascular disease: further evidence supporting the American Heart Association sodium reduction recommendations. Circulation. 2012; 126(24):2880-9. DOI: 10.1161/CIR.0b013e318279acbf. View

13.

Farah V, Elased K, Chen Y, Key M, Cunha T, Irigoyen M . Nocturnal hypertension in mice consuming a high fructose diet. Auton Neurosci. 2006; 130(1-2):41-50. DOI: 10.1016/j.autneu.2006.05.006. View

14.

Appel L, Frohlich E, Hall J, Pearson T, Sacco R, Seals D . The importance of population-wide sodium reduction as a means to prevent cardiovascular disease and stroke: a call to action from the American Heart Association. Circulation. 2011; 123(10):1138-43. DOI: 10.1161/CIR.0b013e31820d0793. View

15.

Schweda F, Kurtz A . Regulation of renin release by local and systemic factors. Rev Physiol Biochem Pharmacol. 2011; 161:1-44. DOI: 10.1007/112_2008_1. View

16.

Moraes-Silva I, Mostarda C, Moreira E, Silva K, Dos Santos F, De Angelis K . Preventive role of exercise training in autonomic, hemodynamic, and metabolic parameters in rats under high risk of metabolic syndrome development. J Appl Physiol (1985). 2013; 114(6):786-91. DOI: 10.1152/japplphysiol.00586.2012. View

17.

Jalal D, Smits G, Johnson R, Chonchol M . Increased fructose associates with elevated blood pressure. J Am Soc Nephrol. 2010; 21(9):1543-9. PMC: 3013529. DOI: 10.1681/ASN.2009111111. View

18.

Soleimani M, Alborzi P . The role of salt in the pathogenesis of fructose-induced hypertension. Int J Nephrol. 2011; 2011:392708. PMC: 3140039. DOI: 10.4061/2011/392708. View

19.

Mostarda C, Moraes-Silva I, Salemi V, Machi J, Rodrigues B, De Angelis K . Exercise training prevents diastolic dysfunction induced by metabolic syndrome in rats. Clinics (Sao Paulo). 2012; 67(7):815-20. PMC: 3400174. DOI: 10.6061/clinics/2012(07)18. View

20.

Kobayashi R, Nagano M, Nakamura F, Higaki J, Fujioka Y, Ikegami H . Role of angiotensin II in high fructose-induced left ventricular hypertrophy in rats. Hypertension. 1993; 21(6 Pt 2):1051-5. DOI: 10.1161/01.hyp.21.6.1051. View