Diabetes Metab J.  2015 Apr;39(2):147-153. 10.4093/dmj.2015.39.2.147.

Normal Glucose Tolerance with a High 1-Hour Postload Plasma Glucose Level Exhibits Decreased beta-Cell Function Similar to Impaired Glucose Tolerance

Affiliations
  • 1Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea. ymchomd@snu.ac.kr

Abstract

BACKGROUND
Subjects with normal glucose tolerance (NGT) who have a high 1-hour postload plasma glucose level (> or =155 mg/dL; NGT 1 hour-high) have been shown to be at higher risk for type 2 diabetes than subjects with NGT 1 hour-low postload plasma glucose level (<155 mg/dL). We compared beta-cell function in subjects with NGT 1 hour-high, NGT 1 hour-low, and impaired glucose tolerance (IGT).
METHODS
We classified subjects into NGT 1 hour-low (n=149), NGT 1 hour-high (n=43), and IGT (n=52). The beta-cell function was assessed based on insulinogenic index (IGI), oral disposition index (DI), and insulin secretion-sensitivity index-2 (ISSI-2).
RESULTS
Insulin sensitivity was comparable between the subjects with NGT 1 hour-high and NGT 1 hour-low. The beta-cell function with/without adjusting insulin sensitivity was significantly different among the three groups. The IGI (pmol/mmol) was 116.8+/-107.3 vs. 64.8+/-47.8 vs. 65.8+/-80.6 (P=0.141), oral DI was 3.5+/-4.2 vs. 1.8+/-1.4 vs. 1.8+/-3.1 (P<0.001), and ISSI-2 was 301.2+/-113.7 vs. 213.2+/-67.3 vs. 172.5+/-87.5 (P<0.001) in NGT 1 hour-low, NGT 1 hour-high, and IGT, respectively. Post hoc analyses revealed that oral DI and ISSI-2 were significantly different between NGT 1 hour-low and NGT 1 hour-high but comparable between NGT 1 hour-high and IGT.
CONCLUSION
Among Korean subjects with NGT, those who have a higher 1-hour postload glucose level have a compromised insulin-sensitivity adjusted beta-cell function to a similar degree as IGT subjects.

Keyword

beta-Cell function; Impaired glucose tolerance; Normal glucose tolerance; Oral glucose tolerance test

MeSH Terms

Blood Glucose*
Glucose Tolerance Test
Glucose*
Insulin
Insulin Resistance
Glucose
Insulin

Cited by  1 articles

Clinical Implications of Using Post-Challenge Plasma Glucose Levels for Early Diagnosis of Type 2 Diabetes Mellitus in Older Individuals
Kyong Hye Joung, Sang Hyun Ju, Ji Min Kim, Sorim Choung, Jae Min Lee, Kang Seo Park, Hyun Jin Kim, Bon Jeong Ku
Diabetes Metab J. 2018;42(2):147-154.    doi: 10.4093/dmj.2018.42.2.147.


Reference

1. Kim DJ. The epidemiology of diabetes in Korea. Diabetes Metab J. 2011; 35:303–308.
2. Shin CS, Lee HK, Koh CS, Kim YI, Shin YS, Yoo KY, Paik HY, Park YS, Yang BG. Risk factors for the development of NIDDM in Yonchon County, Korea. Diabetes Care. 1997; 20:1842–1846.
3. Song J, Oh JY, Sung YA, Pak YK, Park KS, Lee HK. Peripheral blood mitochondrial DNA content is related to insulin sensitivity in offspring of type 2 diabetic patients. Diabetes Care. 2001; 24:865–869.
4. Rhee SY, Kwon MK, Park BJ, Chon S, Jeong IK, Oh S, Ahn KJ, Chung HY, Kim SW, Kim JW, Kim YS, Woo JT. Differences in insulin sensitivity and secretory capacity based on OGTT in subjects with impaired glucose regulation. Korean J Intern Med. 2007; 22:270–274.
5. Choi ES, Rhee EJ, Kim JH, Won JC, Park CY, Lee WY, Oh KW, Park SW, Kim SW. Insulin sensitivity and insulin secretion determined by homeostasis model assessment and future risk of diabetes mellitus in Korean men. Korean Diabetes J. 2008; 32:498–505.
6. Ng MC, Park KS, Oh B, Tam CH, Cho YM, Shin HD, Lam VK, Ma RC, So WY, Cho YS, Kim HL, Lee HK, Chan JC, Cho NH. Implication of genetic variants near TCF7L2, SLC30A8, HHEX, CDKAL1, CDKN2A/B, IGF2BP2, and FTO in type 2 diabetes and obesity in 6,719 Asians. Diabetes. 2008; 57:2226–2233.
7. Cho YS, Chen CH, Hu C, Long J, Ong RT, Sim X, Takeuchi F, Wu Y, Go MJ, Yamauchi T, Chang YC, Kwak SH, Ma RC, Yamamoto K, Adair LS, Aung T, Cai Q, Chang LC, Chen YT, Gao Y, Hu FB, Kim HL, Kim S, Kim YJ, Lee JJ, Lee NR, Li Y, Liu JJ, Lu W, Nakamura J, Nakashima E, Ng DP, Tay WT, Tsai FJ, Wong TY, Yokota M, Zheng W, Zhang R, Wang C, So WY, Ohnaka K, Ikegami H, Hara K, Cho YM, Cho NH, Chang TJ, Bao Y, Hedman AK, Morris AP, McCarthy MI, Takayanagi R, Park KS, Jia W, Chuang LM, Chan JC, Maeda S, Kadowaki T, Lee JY, Wu JY, Teo YY, Tai ES, Shu XO, Mohlke KL, Kato N, Han BG, Seielstad M. DIAGRAM Consortium. MuTHER Consortium. Meta-analysis of genome-wide association studies identifies eight new loci for type 2 diabetes in east Asians. Nat Genet. 2012; 44:67–72.
8. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2014; 37:Suppl 1. S81–S90.
9. Meigs JB, Muller DC, Nathan DM, Blake DR, Andres R. Baltimore Longitudinal Study of Aging. The natural history of progression from normal glucose tolerance to type 2 diabetes in the Baltimore Longitudinal Study of Aging. Diabetes. 2003; 52:1475–1484.
10. Tirosh A, Shai I, Tekes-Manova D, Israeli E, Pereg D, Shochat T, Kochba I, Rudich A. Israeli Diabetes Research Group. Normal fasting plasma glucose levels and type 2 diabetes in young men. N Engl J Med. 2005; 353:1454–1462.
11. Kahn SE, Prigeon RL, McCulloch DK, Boyko EJ, Bergman RN, Schwartz MW, Neifing JL, Ward WK, Beard JC, Palmer JP, et al. Quantification of the relationship between insulin sensitivity and beta-cell function in human subjects. Evidence for a hyperbolic function. Diabetes. 1993; 42:1663–1672.
12. 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.
13. Abdul-Ghani MA, Lyssenko V, Tuomi T, DeFronzo RA, Groop L. Fasting versus postload plasma glucose concentration and the risk for future type 2 diabetes: results from the Botnia Study. Diabetes Care. 2009; 32:281–286.
14. Abdul-Ghani MA, Abdul-Ghani T, Ali N, Defronzo RA. Onehour plasma glucose concentration and the metabolic syndrome identify subjects at high risk for future type 2 diabetes. Diabetes Care. 2008; 31:1650–1655.
15. Kodama K, Tojjar D, Yamada S, Toda K, Patel CJ, Butte AJ. Ethnic differences in the relationship between insulin sensitivity and insulin response: a systematic review and meta-analysis. Diabetes Care. 2013; 36:1789–1796.
16. 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; 28:412–419.
17. Seltzer HS, Allen EW, Herron AL Jr, Brennan MT. Insulin secretion in response to glycemic stimulus: relation of delayed initial release to carbohydrate intolerance in mild diabetes mellitus. J Clin Invest. 1967; 46:323–335.
18. Utzschneider KM, Prigeon RL, Faulenbach MV, Tong J, Carr DB, Boyko EJ, Leonetti DL, McNeely MJ, Fujimoto WY, Kahn SE. Oral disposition index predicts the development of future diabetes above and beyond fasting and 2-h glucose levels. Diabetes Care. 2009; 32:335–341.
19. Matsuda M, DeFronzo RA. Insulin sensitivity indices obtained from oral glucose tolerance testing: comparison with the euglycemic insulin clamp. Diabetes Care. 1999; 22:1462–1470.
20. Retnakaran R, Qi Y, Goran MI, Hamilton JK. Evaluation of proposed oral disposition index measures in relation to the actual disposition index. Diabet Med. 2009; 26:1198–1203.
21. Marini MA, Succurro E, Frontoni S, Mastroianni S, Arturi F, Sciacqua A, Lauro R, Hribal ML, Perticone F, Sesti G. Insulin sensitivity, beta-cell function, and incretin effect in individuals with elevated 1-hour postload plasma glucose levels. Diabetes Care. 2012; 35:868–872.
22. Kim DJ, Lee MS, Kim KW, Lee MK. Insulin secretory dysfunction and insulin resistance in the pathogenesis of korean type 2 diabetes mellitus. Metabolism. 2001; 50:590–593.
23. Sciacqua A, Maio R, Miceli S, Pascale A, Carullo G, Grillo N, Arturi F, Sesti G, Perticone F. Association between one-hour post-load plasma glucose levels and vascular stiffness in essential hypertension. PLoS One. 2012; 7:e44470.
24. Bianchi C, Miccoli R, Trombetta M, Giorgino F, Frontoni S, Faloia E, Marchesini G, Dolci MA, Cavalot F, Cavallo G, Leonetti F, Bonadonna RC, Del Prato S. GENFIEV Investigators. Elevated 1-hour postload plasma glucose levels identify subjects with normal glucose tolerance but impaired beta-cell function, insulin resistance, and worse cardiovascular risk profile: the GENFIEV study. J Clin Endocrinol Metab. 2013; 98:2100–2105.
25. Niijima K, Muranaka Y, Ando T, Okada S, Niijima Y, Hashimoto K, Yamada M, Ohshima K, Mori M, Ono K. Elevated 1-h plasma glucose following 75-g oral glucose load is a predictor of arterial stiffness in subjects with normal glucose tolerance. Diabet Med. 2012; 29:e457–e460.
26. Succurro E, Marini MA, Arturi F, Grembiale A, Lugara M, Andreozzi F, Sciacqua A, Lauro R, Hribal ML, Perticone F, Sesti G. Elevated one-hour post-load plasma glucose levels identifies subjects with normal glucose tolerance but early carotid atherosclerosis. Atherosclerosis. 2009; 207:245–249.
27. Priya M, Anjana RM, Chiwanga FS, Gokulakrishnan K, Deepa M, Mohan V. 1-hour venous plasma glucose and incident prediabetes and diabetes in Asian indians. Diabetes Technol Ther. 2013; 15:497–502.
28. Kim YG, Hahn S, Oh TJ, Kwak SH, Park KS, Cho YM. Differences in the glucose-lowering efficacy of dipeptidyl peptidase-4 inhibitors between Asians and non-Asians: a systematic review and meta-analysis. Diabetologia. 2013; 56:696–708.
29. Strandberg AY, Pienimaki T, Pitkala KH, Tilvis RS, Salomaa VV, Strandberg TE. Comparison of normal fasting and one-hour glucose levels as predictors of future diabetes during a 34-year follow-up. Ann Med. 2013; 45:336–340.
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