Fruktoz tüketimi karotis arter hastalığı ile ilişkili olabilir

Öz

Amaç: Yüksek fruktoz tüketiminin kardiyovasküler hastalıklar ile ilişkili olduğu bilinmektedir, fakat çalışmalar sınırlıdır. Bu çalışmanın amacı, karotis arter darlığı (KAD) ile yüksek früktoz tüketimi arasındaki ilişkiyi değerlendirmektir. Gereç ve Yöntemler: Hastalar, KAD>60% olan (60 hasta), KAD <60% olan (60 hasta) ve karotis aterosklereotik hastalığı bulunmayan (60 hasta) olarak üç gruba ayrılmıştır. Hastaların geriye dönük 3 günlük besin tüketim kayıtlar alınmıştır. Veriler gruplar arasında karşılaştırılmıştır. Bulgular: Fruktoz tüketimi, KAD<%60 olan hastalara göre normal bireylerde daha düşük bulunmuştur (p<0.001). Ayrıca, KAD>60% olanlara göre KAD<60% olanlarda frukotz tüketimi daha düşüktür. Çok değişkenli regresyon analizinde yüksek früktoz tüketimi 60% üzeri karotis stenozu için bağımsız risk faktörü olarak saptanmıştır (p<0.001). Sonuç: Çalışmamızda KAD olan bireylerde früktoz tüketimi yüksek saptanmıştır. Çalışmamız artmış Fruktoz tüketiminin KAD’a etkisi olabileceğini gösteren literatürde ki ilk çalışmadır.

Anahtar Kelimeler

• Karotis arter hastalığı
• fruktoz
• ateroskleroz

High fructose intake may be related to carotid artery stenosis

Öz

Aim: It is known that high fructose intake is related to cardiovascular diseases but there is a limited number of researches in this era. The objective of this research is to evaluate the relation between Carotid Artery Stenosis (CAS) and high fructose intake. Material And Methods: The patients are categorized into three groups: Patients with CAS≥60% (60 patients), patients with CAS<60% (60 patients) and patients with no carotid atherosclerosis (60 patients). Nutrient intake level of patients is observed and recorded by 24-Hour Dietary Recall Forms and the intake frequency of high-fructose dietary is enquired. Physical activity levels are also evaluated. All the collected data is compared among the groups. Results: Fructose intake among ordinary people is found to be lower than the patients with CAS<60% (p<0.001). Besides, fructose intake of patients with CAS<60% is lower than fructose intake of patients with CAS≥60%. Multivariate regression analysis showed that high fructose intake is an independent risk factor for carotid stenosis over 60% (p<0.001). Fructose intake levels were higher in the calcific plaque group than in the non-calcific plaque group (p<0.001). Conclusions: We determined a high fructose intake in patients with CAS. In light of our research data, we consider high fructose intake to have a potential role in the pathophysiology of CAS.

Anahtar Kelimeler

• Carotid artery stenosis
• fructose
• atherosclerosis

Kaynakça

1. 1. Touboul PJ, Hernández-Hernández R, Küçükoğlu S, Woo KS, Vicaut E, Labreuche J, et al. Carotid artery intima media thickness, plaque and Framingham cardiovascular score in Asia, Africa/Middle East and Latin America: the PARC-AALA study. The international journal of cardiovascular imaging 2007; 23: 557-67.
2. 2. Köz C. Carotid intima-media thickness in type 1 diabetes mellitus. The Anatolian journal of cardiology 2010; 10: 59-60.
3. 3. Güleç S. Global risk and objectives in cardiovascular disease. Archives of the Turkish Society of Cardiology 2009; 37: 1-10.
4. 4. Ratchford EV, Evans NS. Carotid artery disease. Vascular medicine. 2014; 19: 512-5.
5. 5. Franceschini N, Giambartolomei C, de Vries PS et al. GWAS and colocalization analyses implicate carotid intima-media thickness and carotid plaque loci in cardiovascular outcomes. Nature communications 2018; 9: 5141.
6. 6. Jaffe R. Diabetes as an immune dysfunction syndrome. 1st ed Bioactive Food as Dietary Interventions for Diabetes 2013.
7. 7. Tappy L, Lê KA, Tran C, Paquot N. Fructose and metabolic diseases: new findings, new questions. Nutrition (Burbank, Los Angeles County, Calif) 2010; 26: 1044-9.
8. 8. Elitok A, Emet S, Bayramov F et al. Effect of bariatric surgery on flow-mediated dilation and carotid intima-media thickness in patients with morbid obesity: 1-year follow-up study. The Anatolian journal of cardiology 2020; 23: 218-22.

9. 9. Akhavan-Khaleghi N, Hosseinsabet A. Evaluation of the longitudinal deformation of the left ventricular myocardium in subjects with impaired fasting glucose with and without increased glycated hemoglobin. The Anatolian journal of cardiology 2018; 19: 160-7.
10. 10. Cirillo P, Pellegrino G, Conte S et al. Fructose induces prothrombotic phenotype in human endothelial cells : A new role for "added sugar" in cardio-metabolic risk. Journal of thrombosis and thrombolysis 2015; 40: 444-51.
11. 11. Conti FF, Brito Jde O, Bernardes N et al. Cardiovascular autonomic dysfunction and oxidative stress induced by fructose overload in an experimental model of hypertension and menopause. BMC cardiovascular disorders 2014; 14: 185.
12. 12. Jaiswal N, Maurya CK, Arha D et al. Fructose induces mitochondrial dysfunction and triggers apoptosis in skeletal muscle cells by provoking oxidative stress. Apoptosis : an international journal on programmed cell death 2015; 20: 930-47.
13. 13. Celik A, Koç F, Kadi H, Ceyhan K, Erkorkmaz U. Inflammation is related to unbalanced cardiac autonomic functions in hypertension: an observational study. The Anatolian journal of cardiology 2012; 12: 233-40.
14. 14. Tokgözoğlu L. Atherosclerosis and the role of inflammation. Archives of the Turkish Society of Cardiology 2009; 37: 1-6.
15. 15. Piepoli MF, Hoes AW, Agewall S et al. 2016 European Guidelines on cardiovascular disease prevention in clinical practice: The Sixth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (EACPR). European heart journal 2016; 37: 2315-81.
16. 16. Ferguson GG, Eliasziw M, Barr HW et al. The North American Symptomatic Carotid Endarterectomy Trial : surgical results in 1415 patients. Stroke 1999; 30: 1751-8
17. 17. Cheng X, Qiu L, Wang F. 18α-Glycyrrhetinic acid (GA) ameliorates fructose-induced nephropathy in mice by suppressing oxidative stress, dyslipidemia and inflammation. Biomedicine & pharmacotherapy 2020; 125: 109702.
18. 18. Zhao C, Zhang Y, Liu H, Li P, Zhang H, Cheng G. Fortunellin protects against high fructose-induced diabetic heart injury in mice by suppressing inflammation and oxidative stress via AMPK/Nrf-2 pathway regulation. Biochemical and biophysical research communications 2017; 490: 552-9.
19. 19. Breda J, Jewell J, Keller A. The Importance of the World Health Organization Sugar Guidelines for Dental Health and Obesity Prevention. Caries research 2019; 53: 149-52.
20. 20. Livesey G, Taylor R. Fructose consumption and consequences for glycation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. The American journal of clinical nutrition 2008; 88: 1419-37.
21. 21. Turan T, Menteşe Ü, Ağaç MT et al. The relation between intensity and complexity of coronary artery lesion and oxidative stress in patients with acute coronary syndrome. The Anatolian journal of cardiology 2015; 15: 795-800.
22. 22. Gökdemir MT, Kaya H, Söğüt O, Kaya Z, Albayrak L, Taşkın A. The role of oxidative stress and inflammation in the early evaluation of acute non-ST-elevation myocardial infarction: an observational study. The Anatolian journal of cardiology 2013; 13: 131-6.
23. 23. Lucas ML, Carraro CC, Belló-Klein A, Kalil AN, Aerts N. Oxidative stress in carotid arteries of patients submitted to carotid endarterectomy. The role of aging process. Acta cirurgica brasileira 2016; 31: 564-8.
24. 24. Oktay V, Baydar O, Sinan Ü Y et al. The effect of oxidative stress related with ischemia-reperfusion damage on the pathogenesis of atrial fibrillation developing after coronary artery bypass graft surgery. Archives of the Turkish Society of Cardiology 2014; 42: 419-25.
25. 25. Marchegiani F. Further evidence to support a role of oxidative stress and inflammation in myocardial infarction. The Anatolian journal of cardiology 2013; 13: 137-8.
26. 26. Delbosc S, Paizanis E, Magous R et al. Involvement of oxidative stress and NADPH oxidase activation in the development of cardiovascular complications in a model of insulin resistance, the fructose-fed rat. Atherosclerosis 2005; 179: 43-9.
27. 27. Ziyrek M, Tayyareci Y, Yurdakul S, Sahin ST, Yıldırımtürk O, Aytekin S. Association of mitral annular calcification with endothelial dysfunction, carotid intima-media thickness and serum fetuin-A: an observational study. The Anatolian journal of cardiology 2013; 13: 752-8.
28. 28. Cigliano L, Spagnuolo MS, Crescenzo R et al. Short-Term Fructose Feeding Induces Inflammation and Oxidative Stress in the Hippocampus of Young and Adult Rats. Molecular neurobiology 2018; 55: 2869-83.
29. 29. Veličković N, Djordjevic A, Vasiljević A, Bursać B, Milutinović DV, Matić G. Tissue-specific regulation of inflammation by macrophage migration inhibitory factor and glucocorticoids in fructose-fed Wistar rats. The British journal of nutrition 2013; 110: 456-65.
30. 30. Li JM, Ge CX, Xu MX, Wang W, Yu R, Fan CY, et al. Betaine recovers hypothalamic neural injury by inhibiting astrogliosis and inflammation in fructose-fed rats. Molecular nutrition & food research 2015; 59: 189-202.