Beta cell function as an assessment tool for cardiovascular risk in patients with metabolic syndrome

Hande Erman; Banu Böyük; Seher Irem Cetın; Samet Sevınc; Umit Bulut; Osman Maviş

doi:10.28982/josam.847350

Research Article

Year 2021, Volume: 5 Issue: 10, 1002 - 1006, 01.10.2021

Hande Erman Banu Böyük Seher Irem Cetın Samet Sevınc Umit Bulut Osman Maviş

https://doi.org/10.28982/josam.847350

Abstract

References

1. Grundy SM. Metabolic syndrome pandemic. Arterioscler Thromb Vasc Biol. 2008;28(4):629-36. doi: 10.1161/ATVBAHA.107.151092.
2. Sherling DH, Perumareddi P, Hennekens CH. Metabolic Syndrome. J Cardiovasc Pharmacol Ther. 2017;22(4):365-7. doi: 10.1177/1074248416686187.
3. Robberecht H, Bruyne T, Hermans N. Biomarkers of the metabolic syndrome: Influence of minerals, oligo- and trace elements. J Trace Elem Med Biol. 2017;43:23-8. doi: 10.1016/j.jtemb.2016.10.005.
4. Kim BY, Jung CH, Mok JO, Kang SK, Kim CH. Association between serum C-peptide levels and chronic microvascular complications in Korean type 2 diabetic patients. Acta Diabetol. 2012;49(1):9-15. doi: 10.1007/s00592-010-0249-6.
5. Fitzgibbons TP, Czech MP. Epicardial and perivascular adipose tissues and their influence on cardiovascular disease: basic mechanisms and clinical associations. J Am Heart Assoc. 2014;3(2):e000582. doi: 10.1161/JAHA.113.000582. PMID: 24595191; PMCID: PMC4187500.
6. Baragetti A, Pisano G, Bertelli C, Garlaschelli K, Grigore L, Fracanzani AL, et al. Subclinical atherosclerosis is associated with Epicardial Fat Thickness and hepatic steatosis in the general population. Nutr Metab Cardiovasc Dis. 2016;26(2):141-53. doi: 10.1016/j.numecd.2015.10.013. Epub 2015 Nov 2. PMID: 26777475.
7. National Cholesterol Education Program. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final report. Circulation. 2002;106:3143–421. PMID:12485966.
8. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28(7):412-9. doi: 10.1007/BF00280883. PMID: 3899825.
9. Alberti KG, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120(16):1640-5.
10. Festa A, D'Agostino R Jr, Howard G, Mykkänen L, Tracy RP, Haffner SM. Chronic subclinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS). Circulation. 2000;102(1):42-7. doi: 10.1161/01.cir.102.1.42. PMID: 10880413.
11. Lann D, LeRoith D. Insulin resistance as the underlying cause for the metabolic syndrome. Med Clin North Am. 2007;91(6):1063-77. doi:10.1016/j.mcna.2007.06.012
12. Robberecht H, Hermans N. Biomarkers of Metabolic Syndrome: Biochemical Background and Clinical Significance. Metab Syndr Relat Disord. 2016;14(2):47-93. doi: 10.1089/met.2015.0113.
13. Fuentes E, Guzmán-Jofre L, Moore-Carrasco R, Palomo I. Role of PPARs in inflammatory processes associated with metabolic syndrome (Review). Mol Med Rep. 2013;8(6):1611-6. doi: 10.3892/mmr.2013.1714. Epub 2013 Oct 7. PMID: 24100795
14. Shafqat J, Melles E, Sigmundsson K, Johansson BL, Ekberg K, Alvelius G, et al. Proinsulin C-peptide elicits disaggregation of insulin resulting in enhanced physiological insulin effects. Cell Mol Life Sci. 2006;63(15):1805-11. doi: 10.1007/s00018-006-6204-6. PMID: 16845606; PMCID: PMC2773842.
15. Marx N, Walcher D, Raichle C, Aleksic M, Bach H, Grub M et al. C-peptide colocalizes with macrophages in early arteriosclerotic lesions of diabetic subjects and induces monocyte chemotaxis in vitro. Arterioscler Thromb Vasc Biol. 2004;24(3):540-5. doi:10.1161/01.ATV.0000116027.81513.68
16. Patel N, Taveira TH, Choudhary G, Whitlatch H, Wu WC. Fasting serum C-peptide levels predict cardiovascular and overall death in nondiabetic adults. J Am Heart Assoc. 2012;1(6):e003152. doi: 10.1161/JAHA.112.003152.
17. Li Y, Zhao D, Li Y, Meng L, Enwer G. Serum C-peptide as a key contributor to lipid-related residual cardiovascular risk in the elderly. Arch Gerontol Geriatr. 2017;73:263-268. doi: 10.1016/j.archger.2017.05.018.
18. Henrichot E, Juge-Aubry CE, Pernin A, Pache JC, Velebit V, Dayer JM, et al. Production of chemokines by perivascular adipose tissue: a role in the pathogenesis of atherosclerosis?. Arterioscler Thromb Vasc Biol. 2005;25(12):2594–2599. doi:10.1161/01.ATV.0000188508.40052.35
19. Fitzgibbons TP, Czech MP. Epicardial and perivascular adipose tissues and their influence on cardiovascular disease: basic mechanisms and clinical associations. J Am Heart Assoc. 2014;3(2):e000582. doi:10.1161/JAHA.113.000582
20. Ansaldo AM, Montecucco F, Sahebkar A, Dallegri F, Carbone F. Epicardial adipose tissue and cardiovascular diseases. Int J Cardiol. 2019;278:254-260. doi: 10.1016/j.ijcard.2018.09.089. Epub 2018 Oct 1. PMID: 30297191
21. Versteylen MO, Takx RA, Joosen IA, Nelemans PJ, Das M,Crijns HJ, et al. Epicardial adipose tissue volume as a predictor for coronary artery disease in diabetic, impaired fasting glucose, and non-diabetic patients presenting with chest pain. Eur Heart J Cardiovasc Imaging. 2012;13(6):517–523. doi:10.1093/ehjci/jes024.
22. Bachar GN, Dicker D, Kornowski R, Atar E. Epicardial adipose tissue as a predictor of coronary artery disease in asymptomatic subjects. Am J Cardiol. 2012;110(4):534–538. doi:10.1016/j.amjcard.2012.04.024
23. Iacobellis G, Singh N, Wharton S, Sharma AM. Substantial changes in epicardial fat thickness after weight loss in severely obese subjects. Obesity (Silver Spring). 2008;16(7):1693-7. doi: 10.1038/oby.2008.251. Epub 2008 May 1. PMID: 18451775.
24. González N, Moreno-Villegas Z, González-Bris A, Egido J, Lorenzo Ó. Regulation of visceral and epicardial adipose tissue for preventing cardiovascular injuries associated to obesity and diabetes. Cardiovasc Diabetol. 2017;16(1):44. doi: 10.1186/s12933-017-0528-4. PMID: 28376896; PMCID: PMC5379721.
25. Akyol B, Boyraz M, Aysoy C. Relationship of epicardial adipose tissue thickness with early indicators of atherosclerosis and cardiac functional changes in obese adolescents with metabolic syndrome. J Clin Res Pediatr Endocrinol 2013;5:156-163.
26. Wahren J, Larsson C. C-peptide: new findings and therapeutic possibilities. Diabetes Res Clin Pract. 2015;107(3):309-19. doi: 10.1016/j.diabres.2015.01.016

Beta cell function as an assessment tool for cardiovascular risk in patients with metabolic syndrome

Year 2021, Volume: 5 Issue: 10, 1002 - 1006, 01.10.2021

Hande Erman Banu Böyük Seher Irem Cetın Samet Sevınc Umit Bulut Osman Maviş

https://doi.org/10.28982/josam.847350

Abstract

Background/Aim: Epicardial fat tissue (EFT) is considered a cardiovascular risk factor independent from visceral adiposity, obesity, hypertension, and diabetes. Fasting serum C-peptide is a known marker of endogenous insulin secretion and beta cell function. Our aim was to evaluate C- peptide levels in patients with metabolic syndrome (MetS) in relation to the EFT thickness.
Methods: Forty-five subjects with MetS without a history of coronary artery disease and 25 healthy volunteers were enrolled this prospective case-control study. We examined the laboratory values, including C peptide, insulin, and HOMA-IR after 8 hours of fasting. EFT thickness was measured by two-dimensional transthoracic echocardiography.
Results: The serum C peptide levels were significantly higher in patients with metabolic syndrome compared to the healthy controls [3.41(1.98) ng/ml vs 2.07 (1.39), P<0.001]. C peptide levels were correlated with BMI (P=0.03, r=0.281) and serum triglycerides (P=0.03, r=0.288). Patients with MetS had remarkably high EFT thickness [0.63(0.22) mm, P=0.043]. EFT thickness was correlated with age (P=0.008, r=0.397), weight (P=0042, r=0.308) and C-peptide (P=0.002, r=0.460) in patients with MetS.
Conclusion: EFT thickness and elevated C-peptide are independent risk factors influencing atherosclerosis. The strong association between EFT thickness and C-peptide demonstrated herein indicates that EFT may play an important role in C peptide secretion, possibly contributing to the cardiometabolic risk in patients with MetS.

Keywords

Metabolic syndrome, C-peptide, Epicardial fat tissue, Cardiovascular risk

References

1. Grundy SM. Metabolic syndrome pandemic. Arterioscler Thromb Vasc Biol. 2008;28(4):629-36. doi: 10.1161/ATVBAHA.107.151092.
2. Sherling DH, Perumareddi P, Hennekens CH. Metabolic Syndrome. J Cardiovasc Pharmacol Ther. 2017;22(4):365-7. doi: 10.1177/1074248416686187.
3. Robberecht H, Bruyne T, Hermans N. Biomarkers of the metabolic syndrome: Influence of minerals, oligo- and trace elements. J Trace Elem Med Biol. 2017;43:23-8. doi: 10.1016/j.jtemb.2016.10.005.
4. Kim BY, Jung CH, Mok JO, Kang SK, Kim CH. Association between serum C-peptide levels and chronic microvascular complications in Korean type 2 diabetic patients. Acta Diabetol. 2012;49(1):9-15. doi: 10.1007/s00592-010-0249-6.
5. Fitzgibbons TP, Czech MP. Epicardial and perivascular adipose tissues and their influence on cardiovascular disease: basic mechanisms and clinical associations. J Am Heart Assoc. 2014;3(2):e000582. doi: 10.1161/JAHA.113.000582. PMID: 24595191; PMCID: PMC4187500.
6. Baragetti A, Pisano G, Bertelli C, Garlaschelli K, Grigore L, Fracanzani AL, et al. Subclinical atherosclerosis is associated with Epicardial Fat Thickness and hepatic steatosis in the general population. Nutr Metab Cardiovasc Dis. 2016;26(2):141-53. doi: 10.1016/j.numecd.2015.10.013. Epub 2015 Nov 2. PMID: 26777475.
7. National Cholesterol Education Program. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final report. Circulation. 2002;106:3143–421. PMID:12485966.
8. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28(7):412-9. doi: 10.1007/BF00280883. PMID: 3899825.
9. Alberti KG, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120(16):1640-5.
10. Festa A, D'Agostino R Jr, Howard G, Mykkänen L, Tracy RP, Haffner SM. Chronic subclinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS). Circulation. 2000;102(1):42-7. doi: 10.1161/01.cir.102.1.42. PMID: 10880413.
11. Lann D, LeRoith D. Insulin resistance as the underlying cause for the metabolic syndrome. Med Clin North Am. 2007;91(6):1063-77. doi:10.1016/j.mcna.2007.06.012
12. Robberecht H, Hermans N. Biomarkers of Metabolic Syndrome: Biochemical Background and Clinical Significance. Metab Syndr Relat Disord. 2016;14(2):47-93. doi: 10.1089/met.2015.0113.
13. Fuentes E, Guzmán-Jofre L, Moore-Carrasco R, Palomo I. Role of PPARs in inflammatory processes associated with metabolic syndrome (Review). Mol Med Rep. 2013;8(6):1611-6. doi: 10.3892/mmr.2013.1714. Epub 2013 Oct 7. PMID: 24100795
14. Shafqat J, Melles E, Sigmundsson K, Johansson BL, Ekberg K, Alvelius G, et al. Proinsulin C-peptide elicits disaggregation of insulin resulting in enhanced physiological insulin effects. Cell Mol Life Sci. 2006;63(15):1805-11. doi: 10.1007/s00018-006-6204-6. PMID: 16845606; PMCID: PMC2773842.
15. Marx N, Walcher D, Raichle C, Aleksic M, Bach H, Grub M et al. C-peptide colocalizes with macrophages in early arteriosclerotic lesions of diabetic subjects and induces monocyte chemotaxis in vitro. Arterioscler Thromb Vasc Biol. 2004;24(3):540-5. doi:10.1161/01.ATV.0000116027.81513.68
16. Patel N, Taveira TH, Choudhary G, Whitlatch H, Wu WC. Fasting serum C-peptide levels predict cardiovascular and overall death in nondiabetic adults. J Am Heart Assoc. 2012;1(6):e003152. doi: 10.1161/JAHA.112.003152.
17. Li Y, Zhao D, Li Y, Meng L, Enwer G. Serum C-peptide as a key contributor to lipid-related residual cardiovascular risk in the elderly. Arch Gerontol Geriatr. 2017;73:263-268. doi: 10.1016/j.archger.2017.05.018.
18. Henrichot E, Juge-Aubry CE, Pernin A, Pache JC, Velebit V, Dayer JM, et al. Production of chemokines by perivascular adipose tissue: a role in the pathogenesis of atherosclerosis?. Arterioscler Thromb Vasc Biol. 2005;25(12):2594–2599. doi:10.1161/01.ATV.0000188508.40052.35
19. Fitzgibbons TP, Czech MP. Epicardial and perivascular adipose tissues and their influence on cardiovascular disease: basic mechanisms and clinical associations. J Am Heart Assoc. 2014;3(2):e000582. doi:10.1161/JAHA.113.000582
20. Ansaldo AM, Montecucco F, Sahebkar A, Dallegri F, Carbone F. Epicardial adipose tissue and cardiovascular diseases. Int J Cardiol. 2019;278:254-260. doi: 10.1016/j.ijcard.2018.09.089. Epub 2018 Oct 1. PMID: 30297191
21. Versteylen MO, Takx RA, Joosen IA, Nelemans PJ, Das M,Crijns HJ, et al. Epicardial adipose tissue volume as a predictor for coronary artery disease in diabetic, impaired fasting glucose, and non-diabetic patients presenting with chest pain. Eur Heart J Cardiovasc Imaging. 2012;13(6):517–523. doi:10.1093/ehjci/jes024.
22. Bachar GN, Dicker D, Kornowski R, Atar E. Epicardial adipose tissue as a predictor of coronary artery disease in asymptomatic subjects. Am J Cardiol. 2012;110(4):534–538. doi:10.1016/j.amjcard.2012.04.024
23. Iacobellis G, Singh N, Wharton S, Sharma AM. Substantial changes in epicardial fat thickness after weight loss in severely obese subjects. Obesity (Silver Spring). 2008;16(7):1693-7. doi: 10.1038/oby.2008.251. Epub 2008 May 1. PMID: 18451775.
24. González N, Moreno-Villegas Z, González-Bris A, Egido J, Lorenzo Ó. Regulation of visceral and epicardial adipose tissue for preventing cardiovascular injuries associated to obesity and diabetes. Cardiovasc Diabetol. 2017;16(1):44. doi: 10.1186/s12933-017-0528-4. PMID: 28376896; PMCID: PMC5379721.
25. Akyol B, Boyraz M, Aysoy C. Relationship of epicardial adipose tissue thickness with early indicators of atherosclerosis and cardiac functional changes in obese adolescents with metabolic syndrome. J Clin Res Pediatr Endocrinol 2013;5:156-163.
26. Wahren J, Larsson C. C-peptide: new findings and therapeutic possibilities. Diabetes Res Clin Pract. 2015;107(3):309-19. doi: 10.1016/j.diabres.2015.01.016

There are 26 citations in total.

Details

Primary Language	English
Subjects	Endocrinology
Journal Section	Research article
Authors	Hande Erman 0000-0001-7213-9624 Banu Böyük 0000-0001-7794-4411 Seher Irem Cetın 0000-0003-2325-7776 Samet Sevınc 0000-0001-6166-1708 Umit Bulut 0000-0002-7686-5356 Osman Maviş 0000-0002-9580-6124
Publication Date	October 1, 2021
Published in Issue	Year 2021 Volume: 5 Issue: 10

Cite

APA	Erman, H., Böyük, B., Cetın, S. I., Sevınc, S., et al. (2021). Beta cell function as an assessment tool for cardiovascular risk in patients with metabolic syndrome. Journal of Surgery and Medicine, 5(10), 1002-1006. https://doi.org/10.28982/josam.847350
AMA	Erman H, Böyük B, Cetın SI, Sevınc S, Bulut U, Maviş O. Beta cell function as an assessment tool for cardiovascular risk in patients with metabolic syndrome. J Surg Med. October 2021;5(10):1002-1006. doi:10.28982/josam.847350
Chicago	Erman, Hande, Banu Böyük, Seher Irem Cetın, Samet Sevınc, Umit Bulut, and Osman Maviş. “Beta Cell Function As an Assessment Tool for Cardiovascular Risk in Patients With Metabolic Syndrome”. Journal of Surgery and Medicine 5, no. 10 (October 2021): 1002-6. https://doi.org/10.28982/josam.847350.
EndNote	Erman H, Böyük B, Cetın SI, Sevınc S, Bulut U, Maviş O (October 1, 2021) Beta cell function as an assessment tool for cardiovascular risk in patients with metabolic syndrome. Journal of Surgery and Medicine 5 10 1002–1006.
IEEE	H. Erman, B. Böyük, S. I. Cetın, S. Sevınc, U. Bulut, and O. Maviş, “Beta cell function as an assessment tool for cardiovascular risk in patients with metabolic syndrome”, J Surg Med, vol. 5, no. 10, pp. 1002–1006, 2021, doi: 10.28982/josam.847350.
ISNAD	Erman, Hande et al. “Beta Cell Function As an Assessment Tool for Cardiovascular Risk in Patients With Metabolic Syndrome”. Journal of Surgery and Medicine 5/10 (October 2021), 1002-1006. https://doi.org/10.28982/josam.847350.
JAMA	Erman H, Böyük B, Cetın SI, Sevınc S, Bulut U, Maviş O. Beta cell function as an assessment tool for cardiovascular risk in patients with metabolic syndrome. J Surg Med. 2021;5:1002–1006.
MLA	Erman, Hande et al. “Beta Cell Function As an Assessment Tool for Cardiovascular Risk in Patients With Metabolic Syndrome”. Journal of Surgery and Medicine, vol. 5, no. 10, 2021, pp. 1002-6, doi:10.28982/josam.847350.
Vancouver	Erman H, Böyük B, Cetın SI, Sevınc S, Bulut U, Maviş O. Beta cell function as an assessment tool for cardiovascular risk in patients with metabolic syndrome. J Surg Med. 2021;5(10):1002-6.

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