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Behavioral Contributions to the Pathogenesis of Type 2 Diabetes

  • Pathogenesis of Type 2 Diabetes and Insulin Resistance (RM Watanabe, Section Editor)
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Abstract

Behavioral contributions to the pathogenesis of prediabetes and Type 2 diabetes (T2D) include lifestyle behaviors including dietary intake, exercise, sedentariness, sleep, and stress. The purpose of this paper is to review evidence for the metabolic pathways by which the behavior is linked to T2D. Evidence for interventions, which change each of the lifestyle behaviors, is discussed. The article will close with a brief discussion on how new technologies may provide opportunities to better understand relationships between moment-to-moment fluctuations in behaviors and diabetes pathogenesis, as well as provide opportunities to personalize and adapt interventions to achieve successful behavior change and maintenance of that change. Especially promising are new technologies, which assist in tracking lifestyle behaviors along with clinical and metabolic outcomes.

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Acknowledgements

This work was supported by the National Cancer Institute of the National Institutes of Health award number T32CA009492 and National Center for Research Resources and the Division of Program Coordination, Planning, and Strategic Initiatives of the National Institutes of Health through Grant Number R25RR032159. This work was also supported by a grant given to USC Keck School of Medicine.

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Donna Spruijt-Metz declares that she has no conflict of interest. Lauren Cook declares that she has no conflict of interest. Gillian A. O’Reilly declares that she has no conflict of interest. Kathleen A. Page declares that she has no conflict of interest. Charlene Quinn declares that she has no conflict of interest.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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This article is part of the Topical Collection on Pathogenesis of Type 2 Diabetes and Insulin Resistance

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Spruijt-Metz, D., O’Reilly, G.A., Cook, L. et al. Behavioral Contributions to the Pathogenesis of Type 2 Diabetes. Curr Diab Rep 14, 475 (2014). https://doi.org/10.1007/s11892-014-0475-3

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