|
Diabetes Care, Vol 20, Issue 10 1562-1568, Copyright © 1997 by American Diabetes Association
Glucose tolerance, insulin secretion, and insulin sensitivity in nonobese and obese Japanese subjects
K Matsumoto, S Miyake, M Yano, Y Ueki, Y Yamaguchi, S Akazawa and Y Tominaga
Department of Internal Medicine, Sasebo Chuou Hospital, Sasebo City, Japan.
OBJECTIVE: To investigate the relative contributions of insulin secretion
and insulin resistance to the development of glucose intolerance in
Japanese subjects. RESEARCH DESIGN AND METHODS: A cross-sectional study of
756 Japanese subjects (530 nonobese, 226 obese) was performed. A 75-g oral
glucose tolerance test (OGTT) was given, and subjects were classified
according to the World Health Organization (WHO) criteria (normal glucose
tolerance [NGT], impaired glucose tolerance [IGT], and diabetes).
Early-phase insulin secretion was assessed by the insulinogenic index (the
ratio of the increment of insulin to that of plasma glucose [PG] 30 min
after a glucose load [delta IRI0-30 min/delta PG0-30 min]). Total insulin
secretion was assessed by mean immunoreactive insulin (IRI) during the
OGTT, and insulin resistance was assessed by use of the homeostasis model
[HOMA(R)]. RESULTS: Early-phase insulin secretion was significantly
decreased in IGT, compared with patients with NGT, in both the nonobese and
obese subjects (0.70 +/- 0.05 vs. 0.37 +/- 0.03, P < 0.01 and 1.36 +/-
0.19 vs. 0.73 +/- 0.08, P < 0.01, respectively). However, mean IRI and
HOMA(R) in both nonobese and obese subjects with IGT and NGT were not
statistically different. Subjects with diabetes showed a significant
decline in early-phase and total insulin secretion and a significantly
higher level of insulin resistance than did subjects with IGT. When the
fasting glucose (FPG) exceeded 100 mg/dl, early-phase insulin decreased
progressively. The graphed relationship between FPG and mean IRI did not
show an inverted U-shape, and mean IRI decreased progressively when FPG
exceeded 100-130 mg/dl. The pattern of changes in insulin secretion and
insulin resistance associated with the progression of glucose intolerance
was similar in both the nonobese and obese subjects. CONCLUSIONS: The
worsening from NGT to IGT in Japanese subjects may be associated with a
decrease in early-phase insulin secretion in nonobese as well as in obese
subjects. Hyperinsulinemia in IGT is not common. We suggest that impaired
early-phase insulin secretion may be the initial abnormality in the
development of glucose intolerance in Japanese people. Insulin resistance
may be a consequence of hyperglycemia and/or obesity.

CiteULike Del.icio.us Digg Reddit Technorati What's this?
This article has been cited by other articles:

|
 |

|
 |
 
K. A. McAuley, J. I. Mann, J. G. Chase, T. F. Lotz, and G. M. Shaw
Point: HOMA Satisfactory for the Time Being: HOMA: The best bet for the simple determination of insulin sensitivity, until something better comes along
Diabetes Care,
September 1, 2007;
30(9):
2411 - 2413.
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
Y. Song, J. E. Manson, L. Tinker, B. V. Howard, L. H. Kuller, L. Nathan, N. Rifai, and S. Liu
Insulin Sensitivity and Insulin Secretion Determined by Homeostasis Model Assessment and Risk of Diabetes in a Multiethnic Cohort of Women: The Women's Health Initiative Observational Study
Diabetes Care,
July 1, 2007;
30(7):
1747 - 1752.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
N. Rasouli, P. A Kern, E. A. Reece, and S. C. Elbein
Effects of pioglitazone and metformin on beta-cell function in nondiabetic subjects at high risk for type 2 diabetes
Am J Physiol Endocrinol Metab,
January 1, 2007;
292(1):
E359 - E365.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
N. Takashima, H. Tomoike, N. Iwai, C. Erikstrup, O. H. Mortensen, B. K. Pedersen, J. Oh, T. E. Graham, U. Smith, and B. B. Kahn
Retinol-Binding Protein 4 and Insulin Resistance.
N. Engl. J. Med.,
September 28, 2006;
355(13):
1392 - 1395.
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
A. V. Matveyenko, J. D. Veldhuis, and P. C. Butler
Mechanisms of impaired fasting glucose and glucose intolerance induced by a ~50% pancreatectomy.
Diabetes,
August 1, 2006;
55(8):
2347 - 2356.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
T. M. Wallace, J. C. Levy, and D. R. Matthews
Use and Abuse of HOMA Modeling
Diabetes Care,
June 1, 2004;
27(6):
1487 - 1495.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M. Sasahara, M. Nishi, H. Kawashima, K. Ueda, S. Sakagashira, H. Furuta, E. Matsumoto, T. Hanabusa, H. Sasaki, and K. Nanjo
Uncoupling Protein 2 Promoter Polymorphism -866G/A Affects Its Expression in {beta}-Cells and Modulates Clinical Profiles of Japanese Type 2 Diabetic Patients
Diabetes,
February 1, 2004;
53(2):
482 - 485.
[Abstract]
[Full Text]
|
 |
|

|
 |

|
 |
 
M. Maliqueo, I. Atwater, R. Lahsen, F. Perez-Bravo, B. Angel, and T. Sir-Petermann
Proinsulin serum concentrations in women with polycystic ovary syndrome: a marker of {beta}-cell dysfunction?
Hum. Reprod.,
December 1, 2003;
18(12):
2683 - 2688.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
H. Suzuki, M. Fukushima, M. Usami, M. Ikeda, A. Taniguchi, Y. Nakai, T. Matsuura, A. Kuroe, K. Yasuda, T. Kurose, et al.
Factors Responsible for Development From Normal Glucose Tolerance to Isolated Postchallenge Hyperglycemia
Diabetes Care,
April 1, 2003;
26(4):
1211 - 1215.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
H. Nagaretani, T. Nakamura, T. Funahashi, K. Kotani, M. Miyanaga, K. Tokunaga, M. Takahashi, H. Nishizawa, K. Kishida, H. Kuriyama, et al.
Visceral Fat Is a Major Contributor for Multiple Risk Factor Clustering in Japanese Men With Impaired Glucose Tolerance
Diabetes Care,
December 1, 2001;
24(12):
2127 - 2133.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
N. M. Wedick, E. J. Mayer-Davis, D. L. Wingard, C. L. Addy, and E. Barrett-Connor
Insulin Resistance Precedes Weight Loss in Adults without Diabetes : The Rancho Bernardo Study
Am. J. Epidemiol.,
June 15, 2001;
153(12):
1199 - 1205.
[Abstract]
[Full Text]
[PDF]
|
 |
|
Copyright © 1997 by the American Diabetes Association.
|
|
| |
|