Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Original Article
  • Published:

Exacerbation of insulin resistance and postprandial triglyceride response in newly diagnosed hypertensive patients with hypertriglyceridaemia

Abstract

The purpose of the study is to examine the differences in insulin resistance and postprandial triglyceride (TG) response between hypertensive patients with or without hypertriglyceridaemia. The study is a comparative cohort study with matching. Thirty-one newly diagnosed hypertensive patients without any medication were recruited from a health survey. The participants were further divided into two groups: those with fasting TG <2.26 mmol/L, and those with TG between 2.26 and 5.65 mmol/L. Both groups were matched in age, sex, body mass index and waist circumference. Each patient received a 75-g oral glucose tolerance test, an insulin suppression test, and a 1000 kcal high fat mixed meal test. The hypertriglyceridaemic hypertensive patients had significantly higher fasting insulin, 2-h plasma glucose, 2-h insulin, and steady-state plasma glucose (SSPG) (13.16 ± 1.87 vs 9.76 ± 3.18 mmol/L). They also had a greater postprandial TG response to the challenge of mixed meal (ΔAUC 20.76 ± 10.06 vs 7.97 ± 3.18 mmol 8 h/L). The postprandial TG response was closely correlated (r = 0.72–0.95, P < 0.0001) with fasting TG in all hypertensive patients. Both fasting TG levels and postprandial TG response were significantly (P < 0.05) correlated with SSPG. In conclusion, the hypertensive patients with hypertriglyceridaemia were more insulin resistant than those without it. Exacerbation of postprandial hypertriglyceridaemia was identified in these patients. The TG response to the challenge of high fat meal was significantly correlated with fasting TG and insulin resistant in them. The results provide a rationale for the alleviation of insulin resistance and hypertriglyceridaemia in these atherosclerosis-prone hypertensive patients.

This is a preview of subscription content, access via your institution

Access options

Rent or buy this article

Prices vary by article type

from$1.95

to$39.95

Prices may be subject to local taxes which are calculated during checkout

Figure 1
Figure 2
Figure 3

Similar content being viewed by others

References

  1. DeFronzo RA, Ferrannini E . Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease Diabetes Care 1991; 14: 173–194

    Article  CAS  Google Scholar 

  2. Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. The Six Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI) Arch Intern Med 1997; 157: 2413–2446

  3. Ferrannini E et al. Insulin resistance in essential hypertension N Engl J Med 1987; 317: 350–357

    Article  CAS  Google Scholar 

  4. Lind L, Berne C, Lithell H . Prevalence of insulin resistance in essential hypertension J Hypertens 1995; 13: 1457–1462

    CAS  PubMed  Google Scholar 

  5. Grundy SM . Hypertriglyceridemia, insulin resistance, and the metabolic syndrome Am J Cardiol 1999; 83: 25F–29F

    Article  CAS  Google Scholar 

  6. Bonora E et al. Prevalence of insulin resistance in metabolic disorders: the Bruneck Study Diabetes 1998; 47: 1643–1649

    Article  CAS  Google Scholar 

  7. Stern N et al. Risk factor clustering in hypertensivepatients: impact of the reports of NCEP-II and second joint task force on coronary prevention on JNC-VI guidelines J Int Med 2000; 248: 203–210

    Article  CAS  Google Scholar 

  8. Després J-P et al. Hyperinsulinemia as an independent risk factor for ischemic heart disease N Engl J Med 1996; 334: 952–957

    Article  Google Scholar 

  9. Grundy SM . Hypertriglyceridemia, atherogenic dyslipidemia, and the metabolic syndrome Am J Cardiol 1998; 81: 18B–25B

    Article  CAS  Google Scholar 

  10. Zilversmit DB . Atherogenesis: a postprandial phenomenon Circulation 1979; 60: 473–485

    Article  CAS  Google Scholar 

  11. Karpe F, Hellenius ML, Hamsten A . Differences in postprandial concentrations of very-low-density lipoprotein and chylomicron remnants between normotriglyceridemic and hypertriglyceridemic men with and without coronary heart disease Metabolism 1999; 48: 301–307

    Article  CAS  Google Scholar 

  12. Couillard C et al. Postprandial triglyceride response in visceral obesity in men Diabetes 1998; 47: 953–960

    Article  CAS  Google Scholar 

  13. Lewis GF et al. Fasting hypertriglyceridemia in noninsulin-dependent diabetes mellitus is an important predictor of postprandial lipid and lipoprotein abnormalities J Clin Endocrinol Metab 1991; 72: 934–944

    Article  CAS  Google Scholar 

  14. Singer P et al. Postprandial hyperinsulinemia inpatients with mild essential hypertension Hypertension 1985; 7: 182–186

    Article  CAS  Google Scholar 

  15. Hwu CM et al. Growth hormone (GH) replacement reduces total body fat and normalizes insulin sensitivity in GH-deficient adults: a report of one-year clinical experience J Clin Endocrinol Metab 1997; 82: 3285–3292

    CAS  PubMed  Google Scholar 

  16. Segal KR et al. Lean body mass estimation by bioelectrical impedance analysis: a four site cross-validation study Am J Clin Nutr 1988; 47: 7–14

    Article  CAS  Google Scholar 

  17. Ho LT et al. Insulin insensitivity in offspring of parents with type 2 diabetes mellitus Diabetic Med 1990; 7: 31–34

    Article  CAS  Google Scholar 

  18. Hwu CM et al. A comparison of insulin suppression tests performed with somatostatin and octreotide with particular reference to tolerability Diabetes Res Clin Practice 2001; 51: 187–193

    Article  CAS  Google Scholar 

  19. Chen HS et al. Insulin sensitivity in normotensive offspring of hypertensive parents Horm Metab Res 2000; 32: 110–114

    Article  CAS  Google Scholar 

  20. Tai MM . A mathematical model for the determination of total area under glucose tolerance and other metabolic curves Diabetes Care 1994; 17: 152–154

    Article  CAS  Google Scholar 

  21. Williams RR et al. Familial dyslipidemic hypertension: evidence from 58 Utah families for a syndrome present in approximately 12% ofpatients with essential hypertension JAMA 1988; 259: 3579–3586

    Article  CAS  Google Scholar 

  22. Williams RR et al. Familial dyslipidaemic hypertension and other multiple metabolic syndromes Ann Med 1992; 24: 469–475

    Article  CAS  Google Scholar 

  23. Andersson PE, Lithell H . Metabolic effects of doxazosin and enalapril in hypertriglyceridemic, hypertensive men: relationship to changes in skeletal muscle blood flow Am J Hypertens 1996; 9: 323–333

    Article  CAS  Google Scholar 

  24. Kahn BB, Flier JS . Obesity and insulin resistance J Clin Invest 2000; 106: 473–481

    Article  CAS  Google Scholar 

  25. Jeppesen J et al. Relation between insulin resistance, hyperinsulinemia, postheparin plasma lipoprotein lipase activity, and postprandial lipemia Arterioscler Thromb Vasc Biol 1995; 15: 320–324

    Article  CAS  Google Scholar 

  26. Byrne CD et al. Is an exaggerated postprandial triglyceride response associated with the component features of the insulin resistance syndrome? Diabet Med 1997; 14: 942–950

    Article  CAS  Google Scholar 

  27. O'Meara NM et al. Role of basal triglyceride and high density lipoprotein in determination of postprandial lipid and lipoprotein responses J Clin Endocrinol Metab 1992; 75: 465–471

    CAS  PubMed  Google Scholar 

  28. Karamanos BG, Thanopoulou AC, Rousi-Penesi DP . Maximal post-prandial triglyceride increase reflects post-prandial hypertriglyceridaemia and is associated with the insulin resistance syndrome Diabet Med 2001; 18: 32–39

    Article  CAS  Google Scholar 

  29. Brunzell JD, Hazzard WR, Porte D Jr, Bierman EL . Evidence for a common, saturable, triglyceride removal mechanism for chylomicrons and very low density lipoproteins in man J Clin Invest 1973; 52: 1578–1585

    Article  CAS  Google Scholar 

Download references

Acknowledgements

The study was supported by the National Health Research Institute ROC (DDH-87-HR-616 and DD-01-86-IX-MG-608S) and Taipei Veterans General Hospital (VAC-86-43 and VAC-89-404-4). Dr Chii-Min Hwu is now a postgraduate scholar supported in part by exchange programs from the Division of Clinical Epidemiology and Preventive Medicine, UCLA and the Choh Hao Li Memorial Fund for Hormone Research, ABMAC.

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to L T Ho.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Hwu, C., Kwok, C., Kuo, C. et al. Exacerbation of insulin resistance and postprandial triglyceride response in newly diagnosed hypertensive patients with hypertriglyceridaemia. J Hum Hypertens 16, 487–493 (2002). https://doi.org/10.1038/sj.jhh.1001426

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/sj.jhh.1001426

Keywords

This article is cited by

Search

Quick links