Relation between soluble CD36 and dietary fatty acid composition in metabolic syndrome patients Relationship Between CD36 and Dietary Fatty Acids
Main Article Content
Keywords
metabolic syndrome, CD36, Lipids
Abstract
Background and aim: The CD36 fatty acid receptor, known as the scavenger receptor, is expressed in many cells and tissues. Dietary fatty acids are thought to play a role in the pathogenesis of metabolic disorders such as obesity, insulin resistance, and atherosclerosis. This study aimed to determine the relationship between soluble CD36 (sCD36) fatty acid receptors and dietary fatty acids in individuals with metabolic syndrome.
Methods: This study included 33 patients with metabolic syndrome and 32 healthy individuals aged 18-65 years. The participants' sociodemographic characteristics, biochemical parameters, anthropometric measurements, type of dietary fat, fatty acid pattern, and amount of fat consumed were recorded. The sCD36 fatty acid receptor levels in individuals were analyzed.
Results: Blood pressure and biochemical measurements (fasting glucose, HbA1c, insulin, HOMA-IR, triglyceride, total cholesterol, HDL, LDL, AST, ALT, and CRP) of individuals with metabolic syndrome were higher than those of the control group (p<0.05). However, HDL and sCD6 levels did not differ between the groups (p>0.05). Individuals with metabolic syndrome had lower olive oil, higher corn oil and tail oil consumptions (p<0.05). However, no difference was found between the groups in terms of other types of fat and dietary fatty acid patterns (p>0.05). No correlation was observed between the sCD36 receptor levels and dietary fatty acid type in individuals with metabolic syndrome (p>0.05).
Conclusions: Soluble CD36 level is not a possible biomarker for metabolic syndrome owing to its similar levels in these patients.
References
2. Li Y, Zhao L, Yu D, Wang Z, Ding G. Metabolic syndrome prevalence and its risk factors among adults in China: A nationally representative cross-sectional study. PLoS One 2018; 13 (6): e0199293. doi: 10.1371/journal.pone.0199293
3. Farmanfarma KK, Kaykhaei MA, Adineh HA, Mohammadi M, Dabiri S, Ansari-Moghaddam A. Prevalence of metabolic syndrome in Iran: A meta-analysis of 69 studies. Diabetes Metab Syndr 2019; 13 (1): 792-9. doi: 10.1016/j.dsx.2018.11.055
4. Gallardo-Alfaro L, Bibiloni MdM, Mascaró CM, et al. Leisure-Time physical activity, sedentary behaviour and diet quality are associated with metabolic syndrome severity: The PREDIMED-Plus study. Nutrients 2020; 12 (4): 1013. doi: 10.3390/nu12041013
5. Frankenberg ADv, Reis AF, Gerchman F. Relationships between adiponectin levels, the metabolic syndrome, and type 2 diabetes: a literature review. Arch Endocrinol Metab 2017; 61: 614-22. doi: 10.1590/2359-3997000000316
6. Xu H, Li X, Adams H, Kubena K, Guo S. Etiology of metabolic syndrome and dietary intervention. Int J Mol Sci 2019; 20 (1): 128. doi: 10.3390/ijms20010128
7. Shu H, Peng Y, Hang W, Nie J, Zhou N, Wang DW. The role of CD36 in cardiovascular disease. Cardiovasc Res 2022; 118 (1): 115-129. doi: 10.1093/cvr/cvaa319
8. Ulug E, Nergiz-Unal R. Dietary fatty acids and CD36-mediated cholesterol homeostasis: potential mechanisms. Nutr Res Rev 2021; 34 (1): 64-77. doi: 10.1017/S0954422420000128
9. Zhao L, Li Y, Ding Q, Li Y, Chen Y, Ruan XZ. CD36 senses dietary lipids and regulates lipids homeostasis in the intestine. Front Physiol 2021; 12: 669279. doi: 10.3389/fphys.2021.669279
10. Niot I, Besnard P. Appetite control by the tongue-gut axis and evaluation of the role of CD36/SR-B2. Biochimie 2017; 136: 27-32. doi: 10.1016/j.biochi.2017.02.011
11. Biswas S, Gao D, Altemus JB, et al. Circulating CD36 is increased in hyperlipidemic mice: Cellular sources and triggers of release. Free Radic Biol Med 2021; 168: 180-8. doi: 10.1016/j.freeradbiomed.2021.03.004
12. Ibrhium W, Nader MI, Khalaf IA. Studies in type 2 diabetic patients on CD36 gene and the levels of lipoprotein in Iraq. World Journal of Pharmaceutical Research 2016; 5(8): 277-285. doi: 10.20959/wjpr20168-6562
13. Maréchal L, Laviolette M, Rodrigue-Way A, et al. The CD36-PPARγ pathway in metabolic disorders. Int J Mol Sci 2018; 19 (5): 1529. doi: 10.3390/ijms19051529
14. Zhang D, Zhang R, Liu Y, et al. CD36 gene variants is associated with type 2 diabetes mellitus through the interaction of obesity in rural Chinese adults. Gene 2018; 659: 155-9. doi: 10.1016/j.gene.2018.03.060
15. Kanoke A, Nishijima Y, Hsieh CL, Liu J. Abstract WP292: Insulin Resistance is Associated with a Reduction of Leukocyte Surface CD36 Expression and an Increase of Soluble CD36. Stroke 2017; 48 (suppl_1): AWP292-AWP. doi: 10.1161/str.48.suppl_1.wp292
16. Ekici M, Kisa U, Durmaz SA, Ugur E, Nergiz-Unal R. Fatty acid transport receptor soluble CD36 and dietary fatty acid pattern in type 2 diabetic patients: a comparative study. Br J Nutr 2018; 119 (2): 153-62. doi: 10.1017/S0007114517003269
17. Castelblanco E, Sanjurjo L, Falguera M, et al. Circulating soluble CD36 is similar in type 1 and type 2 diabetes mellitus versus non-diabetic subjects. J Clin Med 2019; 8 (5): 710. doi: 10.3390/jcm8050710
18. Lopez-Carmona M, Plaza-Seron M, Vargas-Candela A, Tinahones F, Gomez-Huelgas R, Bernal-Lopez M. CD36 overexpression: A possible etiopathogenic mechanism of atherosclerosis in patients with prediabetes and diabetes. Diabetol Metab Syndr 2017; 9 (1): 1-10. doi: 10.1186/s13098-017-0253-x
19. Madrigal-Ruíz P-M, Navarro-Hernández R-E, Ruíz-Quezada S-L, et al. Low CD36 and LOX-1 Levels and CD36 Gene Subexpression Are Associated with Metabolic Dysregulation in Older Individuals with Abdominal Obesity. J Diabetes Res 2016; 2016: 5678946. doi: 10.1155/2016/5678946
20. Lu Z, Li Y, Brinson CW, Kirkwood KL, Lopes‐Virella MF, Huang Y. CD36 is upregulated in mice with periodontitis and metabolic syndrome and involved in macrophage gene upregulation by palmitate. Oral Dis 2017; 23 (2): 210-8. doi: 10.1111/odi.12596
21. Li G, Robles S, Lu Z, et al. Upregulation of free fatty acid receptors in periodontal tissues of patients with metabolic syndrome and periodontitis. J Periodontal Res 2019; 54 (4): 356-63. doi: 10.1111/jre.12636
22. Lee R, Nieman D. Nutritional assessment: McGraw-Hill Education; 2012.
23. Perona JS, Schmidt-RioValle J, Rueda-Medina B, Correa-Rodríguez M, González-Jiménez E. Waist circumference shows the highest predictive value for metabolic syndrome, and waist-to-hip ratio for its components, in Spanish adolescents. Nutr Res 2017; 45: 38-45. doi: 10.1016/j.nutres.2017.06.007
24. Yang H, Xin Z, Feng J-P, Yang J-K. Waist-to-height ratio is better than body mass index and waist circumference as a screening criterion for metabolic syndrome in Han Chinese adults. Medicine 2017; 96 (39): e8192. doi: 10.1097/MD.0000000000008192
25. McCrory MA, Harbaugh AG, Appeadu S, Roberts SB. Fast-food offerings in the United States in 1986, 1991, and 2016 show large increases in food variety, portion size, dietary energy, and selected micronutrients. J Acad Nutr Diet 2019; 119 (6): 923-33. doi: 10.1016/j.jand.2018.12.004
26. Alkhatatbeh MJ, Ayoub NM, Mhaidat NM, Saadeh NA, Lincz LF. Soluble cluster of differentiation 36 concentrations are not associated with cardiovascular risk factors in middle‑aged subjects. Biomed Rep 2016; 4 (5): 642-8. doi: 10.3892/br.2016.622
27. Ekici M, Kisa U, Durmaz SA, Ugur E, Nergiz-Unal R. Fatty acid transport receptor soluble CD36 and dietary fatty acid pattern in type 2 diabetic patients: a comparative study. Br J Nutr 2018; 119 (2): 153. doi: 10.1017/S0007114517003269
28. Zafar U, Khaliq S, Ahmad HU, Manzoor S, Lone KP. Metabolic syndrome: an update on diagnostic criteria, pathogenesis, and genetic links. Hormones 2018; 17 (3): 299-313. doi: 10.1007/s42000-018-0051-3
29. Perona JS. Membrane lipid alterations in the metabolic syndrome and the role of dietary oils. Biochim Biophys Acta Biomembr 2017; 1859 (9 Pt B): 1690-1703. doi: 10.1016/j.bbamem.2017.04.015
30. Lama A, Pirozzi C, Mollica MP, et al. Polyphenol‐rich virgin olive oil reduces insulin resistance and liver inflammation and improves mitochondrial dysfunction in high‐fat diet fed rats. Mol Nutr Food Res 2017; 61 (3): 1600418. doi: 10.1002/mnfr.201600418
31. Jurado-Ruiz E, Álvarez-Amor L, Varela LM, et al. Extra virgin olive oil diet intervention improves insulin resistance and islet performance in diet-induced diabetes in mice. Sci Rep 2019; 9 (1): 1-13. doi: 10.1038/s41598-019-47904-z
32. Santangelo C, Vari R, Scazzocchio B, et al. Anti-inflammatory activity of extra virgin olive oil polyphenols: which role in the prevention and treatment of immune-mediated inflammatory diseases? Endocr Metab Immune Disord Drug Targets 2018; 18 (1): 36-50. doi: 10.2174/1871530317666171114114321
33. Saibandith B, Spencer JP, Rowland IR, Commane DM. Olive polyphenols and the metabolic syndrome. Molecules 2017; 22 (7): 1082. doi: 10.3390/molecules22071082
34. Yubero-Serrano EM, Lopez-Moreno J, Gomez-Delgado F, Lopez-Miranda J. Extra virgin olive oil: More than a healthy fat. Eur J Clin Nutr 2019; 72 (1): 8-17. doi: 10.1038/s41430-018-0304-x
35. DiNicolantonio JJ, O’Keefe JH. Effects of dietary fats on blood lipids: a review of direct comparison trials. Open Heart 2018; 5(2): e000871. doi: 10.1136/openhrt-2018-000871
36. Martín-Peláez S, Castañer O, Konstantinidou V, et al. Effect of olive oil phenolic compounds on the expression of blood pressure-related genes in healthy individuals. Eur J Nutr 2017; 56(2): 663-70. doi: 10.1007/s00394-015-1110-z
37. Zamora-Zamora F, Martínez-Galiano J, Gaforio JJ, Delgado-Rodríguez M. Effects of olive oil on blood pressure: A systematic review and meta-analysis. Rev Esp Salud Publica 2018; 92: e201811083. doi: 10.3989/gya.0105181
38. Miller M, Sorkin JD, Mastella L, et al. Poly is more effective than monounsaturated fat for dietary management in the metabolic syndrome: The muffin study. J Clin Lipidol 2016; 10 (4): 996-1003. doi: 10.1016/j.jacl.2016.04.011
39. Więckowska-Gacek A, Mietelska-Porowska A, Wydrych M, Wojda U. Western diet as a trigger of Alzheimer’s disease: From metabolic syndrome and systemic inflammation to neuroinflammation and neurodegeneration. Ageing Res Rev 2021; 70: 101397. doi: 10.1016/j.arr.2021.101397
40. Puchałowicz K, Rać ME. The Multifunctionality of CD36 in Diabetes Mellitus and Its Complications—Update in Pathogenesis, Treatment and Monitoring. Cells 2020; 9 (8): 1877. doi: 10.3390/cells9081877
41. Liu J, Yang P, Zuo G, et al. Long-chain fatty acid activates hepatocytes through CD36 mediated oxidative stress. Lipids Health Dis 2018; 17 (1): 1-9. doi: 10.1186/s12944-018-0790-9
42. Jabs M, Rose AJ, Lehmann LH, et al. Inhibition of endothelial notch signaling impairs fatty acid transport and leads to metabolic and vascular remodeling of the adult heart. Circulation 2018; 137 (24): 2592-608. doi: 10.1161/CIRCULATIONAHA.117.029733
43. Mallick R, Basak S, Duttaroy AK. Fatty acids and evolving roles of their proteins in neurological, cardiovascular disorders and cancers. Prog lipid res 2021; 83: 101116. doi: 10.1016/j.plipres.2021.101116
44. Pahlavani M, Ramalho T, Koboziev I, et al. Adipose tissue inflammation in insulin resistance: review of mechanisms mediating anti-inflammatory effects of omega-3 polyunsaturated fatty acids. J Investig Med 2017; 65 (7): 1021-7. doi: 10.1136/jim-2017-000535
45. Sundborn G, Thornley S, Merriman TR, et al. Are liquid sugars different from solid sugar in their ability to cause metabolic syndrome? Obesity 2019; 27 (6): 879-87. doi: 10.1002/oby.22472
46. Fabiani R, Naldini G, Chiavarini M. Dietary patterns and metabolic syndrome in adult subjects: a systematic review and meta-analysis. Nutrients 2019; 11 (9): 2056. doi: 10.3390/nu11092056
47. Topouchian J, Labat C, Gautier S, et al. Effects of metabolic syndrome on arterial function in different age groups: the Advanced Approach to Arterial Stiffness study. J Hypertens 2018; 36 (4): 824. doi: 10.1097/HJH.0000000000001631
48. Ranasinghe P, Cooray DN, Jayawardena R, Katulanda P. The influence of family history of hypertension on disease prevalence and associated metabolic risk factors among Sri Lankan adults. BMC Public Health 2015; 15 (1): 576. doi: 10.1186/s12889-015-1927-7
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Özlem Özdemir, Ordu University, Faculty of Medicine
Ordu University, Faculty of Medicine
Department of Internal Medicine, MD
Mehmet Fisunoğlu, Hacettepe University, Faculty of Health Science
Hacettepe University, Faculty of Health Science
Department of Nutrition and Dietetics, PhD
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