Insulin secretion and insulin sensitivity at different stages of glucose tolerance: a cross-sectional study of Japanese type 2 diabetes

Fukushima, Mitsuo; Usami, Masaru; Ikeda, Masaki; Nakai, Yoshikatsu; Taniguchi, Ataru; Matsuura, Toshio; Suzuki, Haruhiko; Kurose, Takeshi; Yamada, Yoshio; Seino, Yutaka

doi:10.1016/j.metabol.2004.02.012

Cited by 199 publications

(178 citation statements)

References 41 publications

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“…The PAF of type 2 diabetes onset due to i-IIS was the highest (50.6%), indicating that IIS had a strong impact on the incidence of type 2 diabetes in this population. As Japanese individuals have low insulinsecreting ability [11], assessments of IIS are necessary so that groups at high risk of developing type 2 diabetes are not overlooked. Our findings may also be applicable to other Asian populations with similar genetic background.…”

Section: Discussionmentioning

confidence: 99%

“…Most white people with type 2 diabetes present with IR [9], which is strongly associated with obesity, whereas most Japanese patients with type 2 diabetes do not have IR [10]. Furthermore, insulin secretion in Japanese individuals is reported to be less than half that in whites [11,12]. To date, however, few cohort studies have investigated insulin secretion in Asian populations [13,14].…”

Section: Introductionmentioning

confidence: 99%

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Impact of impaired insulin secretion and insulin resistance on the incidence of type 2 diabetes mellitus in a Japanese population: the Saku study

et al. 2013

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Aims/hypothesis To assess the impact of impaired insulin secretion (IIS) and insulin resistance (IR) on type 2 diabetes incidence in a Japanese population. Methods This 4 year cohort study included 3,059 participants aged 30-69 without diabetes at baseline who underwent comprehensive medical check-ups between April 2006 and March 2007 at Saku Central Hospital. Based on their insulinogenic index and HOMA-IR values, participants were classified by the criteria of the Japan Diabetes Society into four categories: normal; isolated IIS (i-IIS); isolated IR (i-IR); and IIS plus IR. They were followed up until March 2011. The incidence of type 2 diabetes was determined from fasting and 2 h post-load plasma glucose concentrations and from receiving medical treatment for diabetes. Results At baseline, 1,550 individuals (50.7%) were classified as normal, 900 (29.4%) i-IIS, 505 (16.5%) i-IR, and 104 (3.4%) IIS plus IR. During 10,553 person-years of follow-up, 219 individuals developed type 2 diabetes, with 126 (57.5%) having i-IIS at baseline. Relative to the normal group, the multivariable-adjusted HRs for type 2 diabetes in the i-IIS, i-IR and IIS plus IR groups were 8.27 (95% CI 5.33, 12.83), 4.90 (95% CI 2. 94, 8.17) and 16.93 (95% CI 9.80, 29.25), respectively. The population-attributable fractions of type 2 diabetes onset due to i-IIS, i-IR, and IIS plus IR were 50.6% (95% CI 46.7%, 53.0%), 14.2% (95% CI 11.8%, 15.6%) and 12.9% (95% CI 12.3%, 13.2%), respectively. Conclusions/interpretation Compared with IR, IIS had a greater impact on the incidence of type 2 diabetes in a Japanese population.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Impact of impaired insulin secretion and insulin resistance on the incidence of type 2 diabetes mellitus in a Japanese population: the Saku study

et al. 2013

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“…Por ser estimado simplesmente a partir da determinação da insulinemia e da glicemia de jejum, vem sendo amplamente utilizado e referido na literatura, sobretudo em estudos populacionais (1,12,18,20,22,75,77) .…”

Section: Introductionunclassified

Índice HOMA (homeostasis model assessment) na prática clínica: uma revisão

Oliveira¹,

Souza²,

Lima³

2005

J. Bras. Patol. Med. Lab.

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“…Takeuchi et al [13] reported that cdkal1 was the best-replicated susceptibility locus and the strongest associated with T2D among several susceptibility loci, including KCNQ1, in the Japanese population. Asian-type T2D is characterized by a larger decrease in insulin secretion and less insulin resistance or obesity [14,15]. Thus, the variants of cdkal1 may be implicated in T2D in Asian populations.…”

Section: Association Of Variants In Cdkal1 With T2dmentioning

confidence: 99%

Functional loss of Cdkal1, a novel tRNA modification enzyme, causes the development of type 2 diabetes [Review]

Wei

Tomizawa

2011

Endocr J

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Abstract.A number of whole-genome association studies show the cdk5 regulatory associated protein 1-like 1 (cdkal1) gene to be one of the most reproducible risk genes in type 2 diabetes (T2D). Variations in the gene are associated with impaired insulin secretion but not insulin resistance or obesity. Although the physiological functions of Cdkal1 had been unclear, recent studies show that it is a tRNA modification enzyme, a mammalian methylthiotransferase that biosynthesizes 2-methylthio- A modification in tRNA Lys (UUU) is important for preventing the misreading of its cognate codons, especially when the rate of translation is relatively high. In both general and pancreatic β-cell-specific cdkal1-deficient mice, impaired mitochondrial ATP generation and first-phase insulin secretion are observed. Moreover, the β-cell-specific knockout mice show pancreatic islet hypertrophy and impaired blood glucose control. The mice are also hypersensitive to high-fat diet-induced endoplasmic reticulum (ER) stress. In this review, we provide an overview of the physiological functions of Cdkal1 and the molecular pathogenesis of T2D in patients carrying cdkal1 risk alleles.

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Insulin secretion and insulin sensitivity at different stages of glucose tolerance: a cross-sectional study of Japanese type 2 diabetes

Cited by 199 publications

References 41 publications

Impact of impaired insulin secretion and insulin resistance on the incidence of type 2 diabetes mellitus in a Japanese population: the Saku study

Impact of impaired insulin secretion and insulin resistance on the incidence of type 2 diabetes mellitus in a Japanese population: the Saku study

Índice HOMA (homeostasis model assessment) na prática clínica: uma revisão

Functional loss of Cdkal1, a novel tRNA modification enzyme, causes the development of type 2 diabetes [Review]

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