ADAM SEAL, STEVEN K. MALIN, ANDREW SCHAFFNER, MICHAEL R. HUBBARD, SARAH K. KEADLE, HANNAH BRUNNER-GAYDOS, ALIA A. ORTIZ, JANE E. NAKAMURA, CLARA MCMAHON, RACHEL BARNETT, ANITA H. KELLEHER, KELLY A. BENNION, SUZANNE PHELAN, TODD HAGOBIAN
{"title":"17-OR:ADA 主席精选摘要:口服双酚 A 会降低健康成人的外周胰岛素敏感性","authors":"ADAM SEAL, STEVEN K. MALIN, ANDREW SCHAFFNER, MICHAEL R. HUBBARD, SARAH K. KEADLE, HANNAH BRUNNER-GAYDOS, ALIA A. ORTIZ, JANE E. NAKAMURA, CLARA MCMAHON, RACHEL BARNETT, ANITA H. KELLEHER, KELLY A. BENNION, SUZANNE PHELAN, TODD HAGOBIAN","doi":"10.2337/db24-17-or","DOIUrl":null,"url":null,"abstract":"Introduction: Bisphenol A (BPA) is a synthetic chemical widely used in consumer goods and is linked to Type 2 diabetes progression in observational studies. No experimental studies have examined whether BPA promotes reductions in peripheral insulin sensitivity. Objective: To determine the effects of oral BPA administration on peripheral insulin sensitivity. Methods: Forty non-habitually active, healthy adults (22 F, 18 M; 21.3 ± 2.5 yr; 22.1 ± 2.3 kg/m2; 85% Non-Hispanic White) completed a 2-day baseline energy balance diet low in bisphenols during which urine, blood, and peripheral insulin sensitivity (i.e., glucose infusion rate/steady-state plasma insulin) via 120 min euglycemic hyperinsulinemic clamp technique (40 mU/m2/min; 90 mg/dL) were assessed. Participants were then randomly assigned, in a double-blinded fashion, to a 4-day energy balance diet plus oral BPA administration at 50 μg/kg body weight (BPA-50) or 4-day energy balance diet plus oral placebo (PL) administration. Outcomes were reassessed using a repeated measures ANOVA adjusting for baseline sex, BMI, physical activity, and ethnicity. Results: From baseline to 4-days, body weight was not significantly (P>0.05) different between PL (mean ± SEM; 66.7 ± 2.5, 66.2 ± 2.5 kg) and BPA-50 (66.7 ± 2.5, 66.7± 2.5 kg). From baseline to 4-days, fasting blood glucose was not significantly (P > 0.05) different between PL (95 ± 2, 88 ± 2 mg/dL) and BPA-50 (92 ± 2, 92 ± 2 mg/dL). Compared to PL urine BPA was significantly higher (P<0.05) following BPA-50. From baseline to 4-days, peripheral insulin sensitivity significantly (P=0.01) decreased in BPA-50 (0.11 ± 0.01, 0.10 ± 0.01 mg/kg/min/uU/ml) and remained stable in PL (0.09 ± 0.01, 0.10 ± 0.01 mg/kg/min/uU/ml). Conclusion: BPA administration decreased peripheral insulin sensitivity after four days. These data provide the first experimental evidence that BPA administration may increase Type 2 diabetes risk. Supported by American Diabetes Association grant #1-19-ICTS-044. Disclosure A. Seal: None. S.K. Malin: None. A. Schaffner: None. M.R. Hubbard: None. S.K. Keadle: None. H. Brunner-Gaydos: None. A.A. Ortiz: None. J.E. Nakamura: None. C. McMahon: None. R. Barnett: None. A.H. Kelleher: None. K.A. Bennion: None. S. Phelan: Research Support; Weight Watchers International. T. Hagobian: None. Funding American Diabetes Association (1-19-ICTS-044)","PeriodicalId":11376,"journal":{"name":"Diabetes","volume":null,"pages":null},"PeriodicalIF":6.2000,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"17-OR: ADA Presidents' Select Abstract: Oral Bisphenol A Administration Decreased Peripheral Insulin Sensitivity in Healthy Adults\",\"authors\":\"ADAM SEAL, STEVEN K. MALIN, ANDREW SCHAFFNER, MICHAEL R. HUBBARD, SARAH K. KEADLE, HANNAH BRUNNER-GAYDOS, ALIA A. ORTIZ, JANE E. NAKAMURA, CLARA MCMAHON, RACHEL BARNETT, ANITA H. KELLEHER, KELLY A. BENNION, SUZANNE PHELAN, TODD HAGOBIAN\",\"doi\":\"10.2337/db24-17-or\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Introduction: Bisphenol A (BPA) is a synthetic chemical widely used in consumer goods and is linked to Type 2 diabetes progression in observational studies. No experimental studies have examined whether BPA promotes reductions in peripheral insulin sensitivity. Objective: To determine the effects of oral BPA administration on peripheral insulin sensitivity. Methods: Forty non-habitually active, healthy adults (22 F, 18 M; 21.3 ± 2.5 yr; 22.1 ± 2.3 kg/m2; 85% Non-Hispanic White) completed a 2-day baseline energy balance diet low in bisphenols during which urine, blood, and peripheral insulin sensitivity (i.e., glucose infusion rate/steady-state plasma insulin) via 120 min euglycemic hyperinsulinemic clamp technique (40 mU/m2/min; 90 mg/dL) were assessed. Participants were then randomly assigned, in a double-blinded fashion, to a 4-day energy balance diet plus oral BPA administration at 50 μg/kg body weight (BPA-50) or 4-day energy balance diet plus oral placebo (PL) administration. Outcomes were reassessed using a repeated measures ANOVA adjusting for baseline sex, BMI, physical activity, and ethnicity. Results: From baseline to 4-days, body weight was not significantly (P>0.05) different between PL (mean ± SEM; 66.7 ± 2.5, 66.2 ± 2.5 kg) and BPA-50 (66.7 ± 2.5, 66.7± 2.5 kg). From baseline to 4-days, fasting blood glucose was not significantly (P > 0.05) different between PL (95 ± 2, 88 ± 2 mg/dL) and BPA-50 (92 ± 2, 92 ± 2 mg/dL). Compared to PL urine BPA was significantly higher (P<0.05) following BPA-50. From baseline to 4-days, peripheral insulin sensitivity significantly (P=0.01) decreased in BPA-50 (0.11 ± 0.01, 0.10 ± 0.01 mg/kg/min/uU/ml) and remained stable in PL (0.09 ± 0.01, 0.10 ± 0.01 mg/kg/min/uU/ml). Conclusion: BPA administration decreased peripheral insulin sensitivity after four days. These data provide the first experimental evidence that BPA administration may increase Type 2 diabetes risk. Supported by American Diabetes Association grant #1-19-ICTS-044. Disclosure A. Seal: None. S.K. Malin: None. A. Schaffner: None. M.R. Hubbard: None. S.K. Keadle: None. H. Brunner-Gaydos: None. A.A. Ortiz: None. J.E. Nakamura: None. C. McMahon: None. R. Barnett: None. A.H. Kelleher: None. K.A. Bennion: None. S. Phelan: Research Support; Weight Watchers International. T. Hagobian: None. 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17-OR: ADA Presidents' Select Abstract: Oral Bisphenol A Administration Decreased Peripheral Insulin Sensitivity in Healthy Adults
Introduction: Bisphenol A (BPA) is a synthetic chemical widely used in consumer goods and is linked to Type 2 diabetes progression in observational studies. No experimental studies have examined whether BPA promotes reductions in peripheral insulin sensitivity. Objective: To determine the effects of oral BPA administration on peripheral insulin sensitivity. Methods: Forty non-habitually active, healthy adults (22 F, 18 M; 21.3 ± 2.5 yr; 22.1 ± 2.3 kg/m2; 85% Non-Hispanic White) completed a 2-day baseline energy balance diet low in bisphenols during which urine, blood, and peripheral insulin sensitivity (i.e., glucose infusion rate/steady-state plasma insulin) via 120 min euglycemic hyperinsulinemic clamp technique (40 mU/m2/min; 90 mg/dL) were assessed. Participants were then randomly assigned, in a double-blinded fashion, to a 4-day energy balance diet plus oral BPA administration at 50 μg/kg body weight (BPA-50) or 4-day energy balance diet plus oral placebo (PL) administration. Outcomes were reassessed using a repeated measures ANOVA adjusting for baseline sex, BMI, physical activity, and ethnicity. Results: From baseline to 4-days, body weight was not significantly (P>0.05) different between PL (mean ± SEM; 66.7 ± 2.5, 66.2 ± 2.5 kg) and BPA-50 (66.7 ± 2.5, 66.7± 2.5 kg). From baseline to 4-days, fasting blood glucose was not significantly (P > 0.05) different between PL (95 ± 2, 88 ± 2 mg/dL) and BPA-50 (92 ± 2, 92 ± 2 mg/dL). Compared to PL urine BPA was significantly higher (P<0.05) following BPA-50. From baseline to 4-days, peripheral insulin sensitivity significantly (P=0.01) decreased in BPA-50 (0.11 ± 0.01, 0.10 ± 0.01 mg/kg/min/uU/ml) and remained stable in PL (0.09 ± 0.01, 0.10 ± 0.01 mg/kg/min/uU/ml). Conclusion: BPA administration decreased peripheral insulin sensitivity after four days. These data provide the first experimental evidence that BPA administration may increase Type 2 diabetes risk. Supported by American Diabetes Association grant #1-19-ICTS-044. Disclosure A. Seal: None. S.K. Malin: None. A. Schaffner: None. M.R. Hubbard: None. S.K. Keadle: None. H. Brunner-Gaydos: None. A.A. Ortiz: None. J.E. Nakamura: None. C. McMahon: None. R. Barnett: None. A.H. Kelleher: None. K.A. Bennion: None. S. Phelan: Research Support; Weight Watchers International. T. Hagobian: None. Funding American Diabetes Association (1-19-ICTS-044)
期刊介绍:
Diabetes is a scientific journal that publishes original research exploring the physiological and pathophysiological aspects of diabetes mellitus. We encourage submissions of manuscripts pertaining to laboratory, animal, or human research, covering a wide range of topics. Our primary focus is on investigative reports investigating various aspects such as the development and progression of diabetes, along with its associated complications. We also welcome studies delving into normal and pathological pancreatic islet function and intermediary metabolism, as well as exploring the mechanisms of drug and hormone action from a pharmacological perspective. Additionally, we encourage submissions that delve into the biochemical and molecular aspects of both normal and abnormal biological processes.
However, it is important to note that we do not publish studies relating to diabetes education or the application of accepted therapeutic and diagnostic approaches to patients with diabetes mellitus. Our aim is to provide a platform for research that contributes to advancing our understanding of the underlying mechanisms and processes of diabetes.