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Insulin‐secretion capacity in normal glucose tolerance, impaired glucose tolerance, and diabetes in obese and non‐obese Japanese patients

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      Abstract

      Aims/Introduction:  Pronounced reduction of insulin secretion in response to a rise in glucose level has been reported in Japanese patients compared with Caucasian patients, but the mean body mass index (BMI) is also lower in Japanese patients. As BMI is a determinant of insulin secretion, we examined insulin‐secretion capacity in obese and non‐obese Japanese patients.

      Materials and Methods:  Using the oral glucose tolerance test (OGTT), we estimated the insulin‐secreting capacity in obese (BMI ≥ 25) and non‐obese (BMI < 25) Japanese patients, including 1848 patients with normal glucose tolerance (NGT), 321 patients with impaired glucose tolerance (IGT) and 69 diabetes (DM) patients.

      Results:  The insulinogenic index (I.I.), calculated by dividing the increment in serum insulin by the increment in plasma glucose from 0 to 30 min during OGTT, decreased from NGT to IGT and to DM in patients with and without obesity. In patients with NGT, IGT and DM, the I.I. values of obese patients were higher than those of the non‐obese patients. The peak of insulin concentration in OGTT appeared at 60 min in NGT and at 120 min in IGT in both obese and non‐obese patients, but in DM it was observed at 120 min in obese patients and at 60 min in non‐obese patients.

      Conclusions:  These results show that early‐phase insulin secretion in obese Japanese patients is higher than in non‐obese patients in all stages of glucose tolerance, and delayed insulin‐secretion capacity is also conserved in obese Japanese patients, even in IGT and DM, which is similar to Caucasian patients. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2011.00180.x , 2011)

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      Most cited references 10

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      Follow-up report on the diagnosis of diabetes mellitus.

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        The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes.

         S. J. Kahn (2002)
        The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes have been debated extensively. The concept that a feedback loop governs the interaction of the insulin-sensitive tissues and the beta cell as well as the elucidation of the hyperbolic relationship between insulin sensitivity and insulin secretion explains why insulin-resistant subjects exhibit markedly increased insulin responses while those who are insulin-sensitive have low responses. Consideration of this hyperbolic relationship has helped identify the critical role of beta-cell dysfunction in the development of Type 2 diabetes and the demonstration of reduced beta-cell function in high risk subjects. Furthermore, assessments in a number of ethnic groups emphasise that beta-cell function is a major determinant of oral glucose tolerance in subjects with normal and reduced glucose tolerance and that in all populations the progression from normal to impaired glucose tolerance and subsequently to Type 2 diabetes is associated with declining insulin sensitivity and beta-cell function. The genetic and molecular basis for these reductions in insulin sensitivity and beta-cell function are not fully understood but it does seem that body-fat distribution and especially intra-abdominal fat are major determinants of insulin resistance while reductions in beta-cell mass contribute to beta-cell dysfunction. Based on our greater understanding of the relative roles of insulin resistance and beta-cell dysfunction in Type 2 diabetes, we can anticipate advances in the identification of genes contributing to the development of the disease as well as approaches to the treatment and prevention of Type 2 diabetes.
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          Insulin secretion capacity in the development from normal glucose tolerance to type 2 diabetes.

          We have examined the contribution of insulin secretion and insulin resistance to glucose intolerance in Japanese. Some indices of insulin secretion and insulin sensitivity based on the results of OGTT were used. The decline of insulin secretion capacity was significant throughout the development of glucose intolerance from NGT via IGT to DM. Decreased insulinogenic indices were conspicuous when it is compared with other types of diabetes. Slight impairment of insulin secretion has begun in subjects with NGT. The progression from NGT via isolated IGT to isolated post-challenge hyperglycemia was considered mostly due to the deterioration of early-phase insulin secretion. It is summarized that decreased insulin secretion capacity takes a definite role in the development from NGT to type 2 diabetes in Japan.
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            Author and article information

            Affiliations
            [ 1 ]Departments of Metabolic Medicine
            [ 2 ]Social and Environmental Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka
            [ 3 ]Amagasaki City Office, Amagasaki, Hyogo Japan
            Author notes
            [* ] Hiromi Iwahashi Tel.: +81‐6‐6879‐3736 Fax: +81‐6‐6879‐3739 E‐mail address: iwahashi@ 123456endmet.med.osaka-u.ac.jp
            Journal
            J Diabetes Investig
            J Diabetes Investig
            10.1111/(ISSN)2040-1124
            JDI
            ST
            Journal of Diabetes Investigation
            Blackwell Publishing Ltd (Oxford, UK )
            2040-1116
            2040-1124
            06 June 2012
            29 November 2011
            : 3
            : 3 ( doiID: 10.1111/jdi.2012.3.issue-3 )
            : 271-275
            4014949
            10.1111/j.2040-1124.2011.00180.x
            JDI180
            © 2011 Asian Association for the Study of Diabetes and Blackwell Publishing Asia Pty Ltd
            Counts
            Figures: 4, Tables: 1, Pages: 5
            Product
            Categories
            Articles
            Clinical Science and Care
            Original Article
            Custom metadata
            2.0
            June 2012
            Converter:WILEY_ML3GV2_TO_NLM version:3.9.3 mode:remove_FC converted:04.02.2014

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