Mari Honda1,2, Ayaka Tsuboi3,4, Satomi Minato-Inokawa3,5, Kaori Kitaoka3,6, Mika Takeuchi3, Megumu Yano7, Miki Kurata3,7, Bin Wu1,8, Tsutomu Kazumi1,3,9, Keisuke Fukuo1,3,7. 1. Open Research Center for Studying of Lifestyle-Related Diseases, Mukogawa Women's University, Nishinomiya, Hyogo, Japan. 2. Department of Health, Sports, and Nutrition, Faculty of Health and Welfare, Kobe Women's University, Kobe, Hyogo, Japan. 3. Research Institute for Nutrition Sciences, Mukogawa Women's University, Nishinomiya, Hyogo, Japan. 4. Department of Nutrition, Osaka City Juso Hospital, Osaka, Japan. 5. Laboratory of Community Health and Nutrition, Department of Bioscience, Graduate School of Agriculture, Ehime University, Matsuyama, Ehime, Japan. 6. Department of Public Health, Shiga University of Medical Science, Otsu, Shiga, Japan. 7. Department of Food Sciences and Nutrition, School of Food Sciences and Nutrition, Mukogawa Women's University, Nishinomiya, Hyogo, Japan. 8. Department of Endocrinology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China. 9. Department of Medicine, Kohnan Kakogawa Hospital, Kakogawa, Hyogo, Japan.
Abstract
INTRODUCTION: We tested the hypothesis that family history of type 2 diabetes (FHD) is associated with reduced birth weight and reduced insulin secretion later in life. MATERIALS AND METHODS: Birth weight, body composition by whole-body dual-energy X-ray absorptiometry, and homeostasis model assessment-insulin resistance were compared between Japanese women aged 20 years with positive (n = 73) and negative (n = 258) FHD. A subsample of 153 women (57 with positive FHD) underwent a 75 g oral glucose tolerance test. Multivariate logistic regression analyses were used to identify the most important determinants of FHD. RESULTS: Women with positive as compared with negative FHD had lower birth weight (3132 ± 364 vs. 3238 ± 418 g, p = 0.04). However, the current fat mass index and trunk/leg fat ratio, sophisticated measures of general and abdominal fat accumulation, respectively, did not differ. Women with positive FHD had a lower insulinogenic index (2.4 ± 7.3 vs. 6.2 ± 16, p = 0.007) and higher area under the glucose curve (217 ± 47 vs. 198 ± 36 mg/dL/2 h, p = 0.006). However, fasting and postload insulinemia, homeostasis model assessment-insulin resistance, and Matsuda index did not differ. In multivariate logistic regression analysis, birth weight was marginally associated with FHD (odds ratio, 0.999; 95% confidential interval, 0.98-1.00000; p = 0.0509). CONCLUSIONS: FHD was associated not only with reduced birth weight but also with decreased early-phase insulin secretion and increased postload glucose concentrations in Japanese women aged 20 years. These findings may be in keeping with the fetal insulin hypothesis and provide some evidence that FHD can alter size at birth, probably through genetic and shared environmental components, which consequently resulted in decreased early-phase insulin secretion and increased glucose excursion in the early twenties. FHD was not related to sophisticated measures of general and abdominal adiposity and insulin resistance/sensitivity.
INTRODUCTION: We tested the hypothesis that family history of type 2 diabetes (FHD) is associated with reduced birth weight and reduced insulin secretion later in life. MATERIALS AND METHODS: Birth weight, body composition by whole-body dual-energy X-ray absorptiometry, and homeostasis model assessment-insulin resistance were compared between Japanese women aged 20 years with positive (n = 73) and negative (n = 258) FHD. A subsample of 153 women (57 with positive FHD) underwent a 75 g oral glucose tolerance test. Multivariate logistic regression analyses were used to identify the most important determinants of FHD. RESULTS: Women with positive as compared with negative FHD had lower birth weight (3132 ± 364 vs. 3238 ± 418 g, p = 0.04). However, the current fat mass index and trunk/leg fat ratio, sophisticated measures of general and abdominal fat accumulation, respectively, did not differ. Women with positive FHD had a lower insulinogenic index (2.4 ± 7.3 vs. 6.2 ± 16, p = 0.007) and higher area under the glucose curve (217 ± 47 vs. 198 ± 36 mg/dL/2 h, p = 0.006). However, fasting and postload insulinemia, homeostasis model assessment-insulin resistance, and Matsuda index did not differ. In multivariate logistic regression analysis, birth weight was marginally associated with FHD (odds ratio, 0.999; 95% confidential interval, 0.98-1.00000; p = 0.0509). CONCLUSIONS: FHD was associated not only with reduced birth weight but also with decreased early-phase insulin secretion and increased postload glucose concentrations in Japanese women aged 20 years. These findings may be in keeping with the fetal insulin hypothesis and provide some evidence that FHD can alter size at birth, probably through genetic and shared environmental components, which consequently resulted in decreased early-phase insulin secretion and increased glucose excursion in the early twenties. FHD was not related to sophisticated measures of general and abdominal adiposity and insulin resistance/sensitivity.
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