Adverse effects of obesity on β-cell function in Japanese subjects with normal glucose tolerance

Yuko Akehi, Keizo Anzai, Hitoshi Katsuta, Ryoko Yoshida, Kumiko Ohkubo, Takaaki Yamashita, Hironobu Kawashima, Junko Ono

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

The purpose of the present study was to elucidate the role of obesity in both early- and late-phase insulin secretion during an oral glucose tolerance test (OGTT) performed with 75 g glucose in Japanese subjects. This was performed using indices of β-cell function adjusted for insulin sensitivity. Of 155 subjects assessed, 68 had normal glucose tolerance (NGT) and 87 had impaired glucose tolerance (IGT). We used the homeostasis model assessment-insulin resistance (HOMA-IR) index as an indicator of insulin sensitivity. As indicators of β-cell function, we used the HOMA-β index, an insulinogenic index (ΔI30/ΔG30), and ΔAUC I/G(0-120), which were obtained in the OGTT. We then reevaluated the results after adjusting the β-cell function for insulin sensitivity ([ΔI30/ΔG30]/HOMA-IR index and [ΔAUC I/G(0-120)]/HOMA-IR index). β-Cell function was observed to reduce as the glucose tolerance deteriorated from NGT to IGT. However, when the effects of obesity were considered, the obese subjects with NGT already showed a decline in the (ΔAUC I/G(0-120))/HOMA-IR index value when compared with the nonobese subjects with NGT, despite the fact these subjects did not differ with regard to (ΔI30/ΔG30)/HOMA-IR index. As the glucose tolerance deteriorated to IGT, both (ΔI30/ΔG30)/HOMA-IR index and (ΔAUC I/G(0-120))/HOMA-IR index decreased to an identical extent in both subgroups. These data indicate that obesity causes a decrease in insulin secretion, especially during the late phase following a glucose load, even if the glucose tolerance remains normal.

Original languageEnglish
Pages (from-to)195-202
Number of pages8
JournalObesity Research and Clinical Practice
Volume2
Issue number3
DOIs
Publication statusPublished - Sep 1 2008
Externally publishedYes

Fingerprint

Insulin Resistance
Obesity
Glucose
Homeostasis
Area Under Curve
Glucose Intolerance
Glucose Tolerance Test
Insulin

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Nutrition and Dietetics

Cite this

Adverse effects of obesity on β-cell function in Japanese subjects with normal glucose tolerance. / Akehi, Yuko; Anzai, Keizo; Katsuta, Hitoshi; Yoshida, Ryoko; Ohkubo, Kumiko; Yamashita, Takaaki; Kawashima, Hironobu; Ono, Junko.

In: Obesity Research and Clinical Practice, Vol. 2, No. 3, 01.09.2008, p. 195-202.

Research output: Contribution to journalArticle

Akehi, Yuko ; Anzai, Keizo ; Katsuta, Hitoshi ; Yoshida, Ryoko ; Ohkubo, Kumiko ; Yamashita, Takaaki ; Kawashima, Hironobu ; Ono, Junko. / Adverse effects of obesity on β-cell function in Japanese subjects with normal glucose tolerance. In: Obesity Research and Clinical Practice. 2008 ; Vol. 2, No. 3. pp. 195-202.
@article{952cf0f690474c05afac11ee433815d1,
title = "Adverse effects of obesity on β-cell function in Japanese subjects with normal glucose tolerance",
abstract = "The purpose of the present study was to elucidate the role of obesity in both early- and late-phase insulin secretion during an oral glucose tolerance test (OGTT) performed with 75 g glucose in Japanese subjects. This was performed using indices of β-cell function adjusted for insulin sensitivity. Of 155 subjects assessed, 68 had normal glucose tolerance (NGT) and 87 had impaired glucose tolerance (IGT). We used the homeostasis model assessment-insulin resistance (HOMA-IR) index as an indicator of insulin sensitivity. As indicators of β-cell function, we used the HOMA-β index, an insulinogenic index (ΔI30/ΔG30), and ΔAUC I/G(0-120), which were obtained in the OGTT. We then reevaluated the results after adjusting the β-cell function for insulin sensitivity ([ΔI30/ΔG30]/HOMA-IR index and [ΔAUC I/G(0-120)]/HOMA-IR index). β-Cell function was observed to reduce as the glucose tolerance deteriorated from NGT to IGT. However, when the effects of obesity were considered, the obese subjects with NGT already showed a decline in the (ΔAUC I/G(0-120))/HOMA-IR index value when compared with the nonobese subjects with NGT, despite the fact these subjects did not differ with regard to (ΔI30/ΔG30)/HOMA-IR index. As the glucose tolerance deteriorated to IGT, both (ΔI30/ΔG30)/HOMA-IR index and (ΔAUC I/G(0-120))/HOMA-IR index decreased to an identical extent in both subgroups. These data indicate that obesity causes a decrease in insulin secretion, especially during the late phase following a glucose load, even if the glucose tolerance remains normal.",
author = "Yuko Akehi and Keizo Anzai and Hitoshi Katsuta and Ryoko Yoshida and Kumiko Ohkubo and Takaaki Yamashita and Hironobu Kawashima and Junko Ono",
year = "2008",
month = "9",
day = "1",
doi = "10.1016/j.orcp.2008.05.002",
language = "English",
volume = "2",
pages = "195--202",
journal = "Obesity Research and Clinical Practice",
issn = "1871-403X",
publisher = "Elsevier BV",
number = "3",

}

TY - JOUR

T1 - Adverse effects of obesity on β-cell function in Japanese subjects with normal glucose tolerance

AU - Akehi, Yuko

AU - Anzai, Keizo

AU - Katsuta, Hitoshi

AU - Yoshida, Ryoko

AU - Ohkubo, Kumiko

AU - Yamashita, Takaaki

AU - Kawashima, Hironobu

AU - Ono, Junko

PY - 2008/9/1

Y1 - 2008/9/1

N2 - The purpose of the present study was to elucidate the role of obesity in both early- and late-phase insulin secretion during an oral glucose tolerance test (OGTT) performed with 75 g glucose in Japanese subjects. This was performed using indices of β-cell function adjusted for insulin sensitivity. Of 155 subjects assessed, 68 had normal glucose tolerance (NGT) and 87 had impaired glucose tolerance (IGT). We used the homeostasis model assessment-insulin resistance (HOMA-IR) index as an indicator of insulin sensitivity. As indicators of β-cell function, we used the HOMA-β index, an insulinogenic index (ΔI30/ΔG30), and ΔAUC I/G(0-120), which were obtained in the OGTT. We then reevaluated the results after adjusting the β-cell function for insulin sensitivity ([ΔI30/ΔG30]/HOMA-IR index and [ΔAUC I/G(0-120)]/HOMA-IR index). β-Cell function was observed to reduce as the glucose tolerance deteriorated from NGT to IGT. However, when the effects of obesity were considered, the obese subjects with NGT already showed a decline in the (ΔAUC I/G(0-120))/HOMA-IR index value when compared with the nonobese subjects with NGT, despite the fact these subjects did not differ with regard to (ΔI30/ΔG30)/HOMA-IR index. As the glucose tolerance deteriorated to IGT, both (ΔI30/ΔG30)/HOMA-IR index and (ΔAUC I/G(0-120))/HOMA-IR index decreased to an identical extent in both subgroups. These data indicate that obesity causes a decrease in insulin secretion, especially during the late phase following a glucose load, even if the glucose tolerance remains normal.

AB - The purpose of the present study was to elucidate the role of obesity in both early- and late-phase insulin secretion during an oral glucose tolerance test (OGTT) performed with 75 g glucose in Japanese subjects. This was performed using indices of β-cell function adjusted for insulin sensitivity. Of 155 subjects assessed, 68 had normal glucose tolerance (NGT) and 87 had impaired glucose tolerance (IGT). We used the homeostasis model assessment-insulin resistance (HOMA-IR) index as an indicator of insulin sensitivity. As indicators of β-cell function, we used the HOMA-β index, an insulinogenic index (ΔI30/ΔG30), and ΔAUC I/G(0-120), which were obtained in the OGTT. We then reevaluated the results after adjusting the β-cell function for insulin sensitivity ([ΔI30/ΔG30]/HOMA-IR index and [ΔAUC I/G(0-120)]/HOMA-IR index). β-Cell function was observed to reduce as the glucose tolerance deteriorated from NGT to IGT. However, when the effects of obesity were considered, the obese subjects with NGT already showed a decline in the (ΔAUC I/G(0-120))/HOMA-IR index value when compared with the nonobese subjects with NGT, despite the fact these subjects did not differ with regard to (ΔI30/ΔG30)/HOMA-IR index. As the glucose tolerance deteriorated to IGT, both (ΔI30/ΔG30)/HOMA-IR index and (ΔAUC I/G(0-120))/HOMA-IR index decreased to an identical extent in both subgroups. These data indicate that obesity causes a decrease in insulin secretion, especially during the late phase following a glucose load, even if the glucose tolerance remains normal.

UR - http://www.scopus.com/inward/record.url?scp=50649117101&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=50649117101&partnerID=8YFLogxK

U2 - 10.1016/j.orcp.2008.05.002

DO - 10.1016/j.orcp.2008.05.002

M3 - Article

AN - SCOPUS:50649117101

VL - 2

SP - 195

EP - 202

JO - Obesity Research and Clinical Practice

JF - Obesity Research and Clinical Practice

SN - 1871-403X

IS - 3

ER -