Tae Jung Oh; Se Hee Min; Chang Ho Ahn; Eun Ky Kim; Soo Heon Kwak; Hye Seung Jung; Kyong Soo Park; Young Min Cho

doi:10.4093/dmj.2015.39.3.270

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Response Response: Normal Glucose Tolerance with a High 1-Hour Postload Plasma Glucose Level Exhibits Decreased β-Cell Function Similar to Impaired Glucose Tolerance (Diabetes Metab J 2015;39:147-53): Tae Jung Oh, Se Hee Min, Chang Ho Ahn, Eun Ky Kim, Soo Heon Kwak, Hye Seung Jung, Kyong Soo Park, Young Min Cho; Diabetes & Metabolism Journal 2015;39(3):270-271.
DOI: https://doi.org/10.4093/dmj.2015.39.3.270
Published online: June 15, 2015

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Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.

Corresponding author: Young Min Cho. Department of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul 110-744, Korea. ymchomd@snu.ac.kr

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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REFERENCES

We appreciate Dr. Hee Kyung Kim's comments on our study entitled "Normal glucose tolerance with a high 1-hour postload plasma glucose level exhibits decreased β-cell function similar to impaired glucose tolerance," which was published in Diabetes and Metabolism Journal [1]. Our responses to Dr. Kim's comments are below.

First, in our study, insulin resistance or insulin sensitivity presented by the homeostasis model assessment for insulin resistance (HOMA-IR) and Matsuda index was not different between the subjects who had 1-hour glucose levels of ≥155 mg/dL with normal glucose tolerance (NGT 1 hour-high) and the subjects with NGT 1 hour-low (<155 mg/dL). In addition, simple indices representing β-cell function such as HOMA-β cell function (HOMA-β) and insulinogenic index were also comparable between the two groups. However, β-cell function should be viewed in the context of insulin sensitivity to reflect the β-cell capacity of compensation for insulin resistance [2]. As such, indices of β-cell function adjusted by insulin sensitivity (e.g., oral disposition index and insulin secretion-sensitivity index-2) were different between the NGT 1 hour-high and NGT 1 hour-low subjects. Therefore, the data presented in our study indicated that insulin resistance (or sensitivity) and simple β-cell function indices were not different, but indices for β-cell function adjusted by insulin sensitivity were different, which consistently substantiated our conclusion.

Second, we did not compare NGT 1 hour-high with impaired fasting glucose (IFG). Because there are different metabolic abnormalities between IFG and IGT [3], it would be worthwhile to examine the differences in insulin sensitivity and β-cell function between NGT 1 hour-high and IFG.

Lastly, Dr. Kim suggested an important implication of our study: NGT 1 hour-high subjects may be associated with non-alcoholic fatty liver disease and dyslipidemia and could be potential candidates for pharmacological or non-pharmacological intervention even though they are classified as normal based on fasting plasma glucose and 2-hour postload plasma glucose levels. Indeed, we showed that fasting plasma glucose and triglyceride levels were significantly higher in NGT 1 hour-high subjects than in NGT 1 hour-low subjects. These parameters are components of metabolic syndrome, which is considered as a risk factor for type 2 diabetes [4]. Further studies are necessary regarding the cost-effectiveness of testing 1-hour postload glucose levels during the standard 75 g oral glucose tolerance test. We all appreciate Dr. Kim's valuable comments and suggestions.

NOTES

CONFLICTS OF INTEREST: No potential conflict of interest relevant to this article was reported.

REFERENCES

1. Oh TJ, Min SH, Ahn CH, Kim EK, Kwak SH, Jung HS, Park KS, Cho YM. Normal glucose tolerance with a high 1-hour postload plasma glucose level exhibits decreased β-cell function similar to impaired glucose tolerance. Diabetes Metab J 2015;39:147-153. Article PubMed PMC
2. Bergman RN. Orchestration of glucose homeostasis: from a small acorn to the California oak. Diabetes 2007;56:1489-1501. PubMed
3. Abdul-Ghani MA, Tripathy D, DeFronzo RA. Contributions of beta-cell dysfunction and insulin resistance to the pathogenesis of impaired glucose tolerance and impaired fasting glucose. Diabetes Care 2006;29:1130-1139. Article PubMed
4. Lorenzo C, Okoloise M, Williams K, Stern MP, Haffner SM. San Antonio Heart Study. The metabolic syndrome as predictor of type 2 diabetes: the San Antonio heart study. Diabetes Care 2003;26:3153-3159. PubMed

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Prevalence of Impaired Glucose Tolerance/Prediabetes in Local Adult Obese Population Presenting to A Tertiary Care Hospital
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Response: Normal Glucose Tolerance with a High 1-Hour Postload Plasma Glucose Level Exhibits Decreased β-Cell Function Similar to Impaired Glucose Tolerance (Diabetes Metab J 2015;39:147-53)

Diabetes Metab J. 2015;39(3):270-271. Published online June 15, 2015

DOI: https://doi.org/10.4093/dmj.2015.39.3.270

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