Endocrinol Metab.  2018 Mar;33(1):55-61. 10.3803/EnM.2018.33.1.55.

The Association between Persistent Hypertriglyceridemia and the Risk of Diabetes Development: The Kangbuk Samsung Health Study

Affiliations
  • 1Division of Endocrinology and Metabolism, Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea. hongsiri@hanmail.net
  • 2Department of Neurology, Soonchunhyang University Cheonan Hospital, Soonchunhyang University College of Medicine, Cheonan, Korea.

Abstract

BACKGROUND
Hypertriglyceridemia is known to have an association with increased risks of insulin resistance and diabetes. The aim of this study was to investigate the risk of diabetes mellitus, according to changes in the concentrations of triglycerides, over time.
METHODS
A total of 15,932 non-diabetic participants (mean age 43.2 years, 68% men) who attended five consecutive annual health check-ups at Kangbuk Samsung Hospital, between January 2010 and December 2014, were recruited. Participants were classified according to their triglyceride concentrations; normal ( < 150 mg/dL) and abnormal (≥150 mg/dL). According to the triglyceride levels in 2010 and 2012, subjects were divided into four groups: normal-normal, normal-abnormal, abnormal-normal, and abnormal-abnormal. The risk for incident diabetes was assessed in 2014.
RESULTS
Among the total subjects, 67.5% belonged to the normal-normal group, 8.6% to the normal-abnormal group, 9.4% to the abnormal-normal group, and 14.5% to the abnormal-abnormal group. A total of 234 subjects (1.5%) were newly diagnosed with diabetes, between 2010 and 2014. Over 4 years, 1%, 1.5%, 2.1%, and 3.0% of the subjects developed diabetes in the normal-normal, normal-abnormal, abnormal-normal, and abnormal-abnormal groups, respectively. When the risk for incident diabetes was analyzed in the groups, after adjusting the confounding variables, a 1.58-fold increase in the risk of diabetes (95% confidence interval [CI], 1.10 to 2.26) was observed in the participants with persistent hypertriglyceridemia (abnormal-abnormal group). This was attenuated by further adjustments for body mass index (BMI) (hazard ratio, 1.25; 95% CI, 0.86 to 1.80).
CONCLUSION
In this large study population, persistent hypertriglyceridemia, over a period of 2 years, was significantly associated with the risk of incident diabetes, which was attenuated after adjustment for BMI.

Keyword

Hypertriglyceridemia; Diabetes; Persistent

MeSH Terms

Body Mass Index
Confounding Factors (Epidemiology)
Diabetes Mellitus
Hypertriglyceridemia*
Insulin Resistance
Triglycerides
Triglycerides

Figure

  • Fig. 1 Incidences of diabetes in 2014, according to triglyceride levels in 2010 and 2012.


Cited by  4 articles

The Association between Persistent Hypertriglyceridemia and the Risk of Diabetes Development: The Kangbuk Samsung Health Study (Endocrinol Metab 2018;33:55–61, Yu Hyun Kwon et al.)
Mi Hae Seo
Endocrinol Metab. 2018;33(2):305-306.    doi: 10.3803/EnM.2018.33.2.305.

Response: The Association between Persistent Hypertriglyceridemia and the Risk of Diabetes Development: The Kangbuk Samsung Health Study (Endocrinol Metab 2018;33:55–61, Yu Hyun Kwon et al.)
Eun-Jung Rhee, Yu Hyun Kwon
Endocrinol Metab. 2018;33(3):425-426.    doi: 10.3803/EnM.2018.33.3.425.

Prevalence and Current Management of Cardiovascular Risk Factors in Korean Adults Based on Fact Sheets
Eun-Jung Rhee
Endocrinol Metab. 2020;35(1):85-94.    doi: 10.3803/EnM.2020.35.1.85.

Lipid Variability and Diabetes Mellitus
Jeongmin Lee, Seung-Hwan Lee
J Korean Diabetes. 2022;23(1):28-34.    doi: 10.4093/jkd.2022.23.1.28.


Reference

1. Seuring T, Archangelidi O, Suhrcke M. The economic costs of type 2 diabetes: a global systematic review. Pharmacoeconomics. 2015; 33:811–831.
Article
2. Shaw JE, Sicree RA, Zimmet PZ. Global estimates of the prevalence of diabetes for 2010 and 2030. Diabetes Res Clin Pract. 2010; 87:4–14.
Article
3. Ohn JH, Kwak SH, Cho YM, Lim S, Jang HC, Park KS, et al. 10-Year trajectory of β-cell function and insulin sensitivity in the development of type 2 diabetes: a community-based prospective cohort study. Lancet Diabetes Endocrinol. 2016; 4:27–34.
Article
4. Abdul-Ghani MA, Williams K, DeFronzo RA, Stern M. What is the best predictor of future type 2 diabetes? Diabetes Care. 2007; 30:1544–1548.
Article
5. Gutch M, Kumar S, Razi SM, Gupta KK, Gupta A. Assessment of insulin sensitivity/resistance. Indian J Endocrinol Metab. 2015; 19:160–164.
Article
6. Roberts CK, Hevener AL, Barnard RJ. Metabolic syndrome and insulin resistance: underlying causes and modification by exercise training. Compr Physiol. 2013; 3:1–58.
Article
7. Verges B. Pathophysiology of diabetic dyslipidaemia: where are we? Diabetologia. 2015; 58:886–899.
Article
8. Sandhofer A, Kaser S, Ritsch A, Laimer M, Engl J, Paulweber B, et al. Cholesteryl ester transfer protein in metabolic syndrome. Obesity (Silver Spring). 2006; 14:812–818.
Article
9. Bardini G, Rotella CM, Giannini S. Dyslipidemia and diabetes: reciprocal impact of impaired lipid metabolism and beta-cell dysfunction on micro- and macrovascular complications. Rev Diabet Stud. 2012; 9:82–93.
Article
10. Tchernof A, Despres JP. Pathophysiology of human visceral obesity: an update. Physiol Rev. 2013; 93:359–404.
Article
11. Galic S, Oakhill JS, Steinberg GR. Adipose tissue as an endocrine organ. Mol Cell Endocrinol. 2010; 316:129–139.
Article
12. Dotevall A, Johansson S, Wilhelmsen L, Rosengren A. Increased levels of triglycerides, BMI and blood pressure and low physical activity increase the risk of diabetes in Swedish women. A prospective 18-year follow-up of the BEDA study. Diabet Med. 2004; 21:615–622.
13. Seo MH, Bae JC, Park SE, Rhee EJ, Park CY, Oh KW, et al. Association of lipid and lipoprotein profiles with future development of type 2 diabetes in nondiabetic Korean subjects: a 4-year retrospective, longitudinal study. J Clin Endocrinol Metab. 2011; 96:E2050–E2054.
Article
14. Tirosh A, Shai I, Bitzur R, Kochba I, Tekes-Manova D, Israeli E, et al. Changes in triglyceride levels over time and risk of type 2 diabetes in young men. Diabetes Care. 2008; 31:2032–2037.
Article
15. Rhee EJ, Han K, Ko SH, Ko KS, Lee WY. Increased risk for diabetes development in subjects with large variation in total cholesterol levels in 2,827,950 Koreans: a nationwide population-based study. PLoS One. 2017; 12:e0176615.
Article
16. Schwartz KL, Monsur JC, Bartoces MG, West PA, Neale AV. Correlation of same-visit HbA1c test with laboratory-based measurements: a MetroNet study. BMC Fam Pract. 2005; 6:28.
Article
17. Marathe PH, Gao HX, Close KL. American Diabetes Association standards of medical care in diabetes 2017. J Diabetes. 2017; 9:320–324.
Article
18. Sommariva D, Tirrito M, Bellintani L, Bonfiglioli D, Branchi A, Pogliaghi I, et al. Interrelationships between body mass and lipid and lipoprotein triglycerides and cholesterol in obese women. Ric Clin Lab. 1986; 16:481–488.
19. Shimada A, Kimura H, Oida K, Kanehara H, Bando Y, Sakamoto S, et al. Serum CETP status is independently associated with reduction rates in LDL-C in pitavastatin-treated diabetic patients and possible involvement of LXR in its association. Lipids Health Dis. 2016; 15:57.
Article
20. Ginsberg HN, Zhang YL, Hernandez-Ono A. Regulation of plasma triglycerides in insulin resistance and diabetes. Arch Med Res. 2005; 36:232–240.
Article
21. Muacevic-Katanec D, Reiner Z. Diabetic dyslipidemia or ‘diabetes lipidus’? Expert Rev Cardiovasc Ther. 2011; 9:341–348.
22. Hagman DK, Hays LB, Parazzoli SD, Poitout V. Palmitate inhibits insulin gene expression by altering PDX-1 nuclear localization and reducing MafA expression in isolated rat islets of Langerhans. J Biol Chem. 2005; 280:32413–32418.
Article
23. Shimabukuro M, Higa M, Zhou YT, Wang MY, Newgard CB, Unger RH. Lipoapoptosis in beta-cells of obese prediabetic fa/fa rats. Role of serine palmitoyltransferase overexpression. J Biol Chem. 1998; 273:32487–32490.
24. Cunha DA, Hekerman P, Ladriere L, Bazarra-Castro A, Ortis F, Wakeham MC, et al. Initiation and execution of lipotoxic ER stress in pancreatic beta-cells. J Cell Sci. 2008; 121(Pt 14):2308–2318.
25. Poitout V, Hagman D, Stein R, Artner I, Robertson RP, Harmon JS. Regulation of the insulin gene by glucose and fatty acids. J Nutr. 2006; 136:873–876.
Article
26. Kruit JK, Wijesekara N, Fox JE, Dai XQ, Brunham LR, Searle GJ, et al. Islet cholesterol accumulation due to loss of ABCA1 leads to impaired exocytosis of insulin granules. Diabetes. 2011; 60:3186–3196.
Article
27. Hao M, Head WS, Gunawardana SC, Hasty AH, Piston DW. Direct effect of cholesterol on insulin secretion: a novel mechanism for pancreatic beta-cell dysfunction. Diabetes. 2007; 56:2328–2338.
28. Warram JH, Martin BC, Krolewski AS, Soeldner JS, Kahn CR. Slow glucose removal rate and hyperinsulinemia precede the development of type II diabetes in the offspring of diabetic parents. Ann Intern Med. 1990; 113:909–915.
Article
29. Lillioja S, Mott DM, Howard BV, Bennett PH, Yki-Jarvinen H, Freymond D, et al. Impaired glucose tolerance as a disorder of insulin action. Longitudinal and cross-sectional studies in Pima Indians. N Engl J Med. 1988; 318:1217–1225.
30. Ginsberg HN. Effects of statins on triglyceride metabolism. Am J Cardiol. 1998; 81:32B–35B.
Article
31. Shah RV, Goldfine AB. Statins and risk of new-onset diabetes mellitus. Circulation. 2012; 126:e282–e284.
Article
32. Chogtu B, Magazine R, Bairy KL. Statin use and risk of diabetes mellitus. World J Diabetes. 2015; 6:352–357.
Article
33. Rhee EJ, Lee MK, Kim JD, Jeon WS, Bae JC, Park SE, et al. Metabolic health is a more important determinant for diabetes development than simple obesity: a 4-year retrospective longitudinal study. PLoS One. 2014; 9:e98369.
Article
Full Text Links
  • ENM
Actions
Cited
CITED
export Copy
Close
Share
  • Twitter
  • Facebook
Similar articles
Copyright © 2024 by Korean Association of Medical Journal Editors. All rights reserved.     E-mail: koreamed@kamje.or.kr