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      Self-Reported Physical Activity and Relations to Growth and Neurotrophic Factors in Diabetes Mellitus: The Framingham Offspring Study

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          Abstract

          Aims

          Circulating insulin-like growth factor- (IGF-) 1, vascular endothelial growth factor (VEGF), and brain-derived neurotrophic factor (BDNF) levels are often lower in individuals with diabetes mellitus (DM) and are important for repairing vascular and neuronal dysfunction. The purpose of this investigation was to determine the cross-sectional relations of physical activity to circulating concentrations of IGF-1, VEGF, and BDNF in individuals with and without DM.

          Methods

          In 1730 participants from the Framingham Offspring Study examination cycle 7, including those with DM ( n = 179, mean age 64 years, 39% women) and without DM ( n = 1551, mean age 60 years, 46% women), we related self-reported physical activity variables to circulating concentrations of IGF-1, VEGF, and BDNF using linear multivariable regression models. We also tested for interactions by age. Participants with prevalent cardiovascular disease, stroke, and dementia or taking hormone replacement therapy were excluded.

          Results

          In participants with DM, more ambulatory physical activity was associated with higher IGF-1 levels ( β ± standard error (SE) = 0.22 ± 0.08, p = 0.009), and more total physical activity was related to higher BDNF levels ( β ± SE = 0.18 ± 0.08, p = 0.035), but physical activity was not significantly related to circulating VEGF. In participants without DM, no associations were observed. Moreover, in the examination of interactions by age, the association of ambulatory physical activity with IGF-1 levels was only observed in older adults with DM (age ≥ 60 years, β ± SE = 0.23 ± 0.11, p = 0.042) but not in middle-aged adults with DM (age < 60 years, β ± SE = 0.06 ± 0.13, p = 0.645).

          Conclusion

          Our results suggest that more physical activity is associated with higher circulating IGF-1 and BDNF in participants with DM. These results, dissecting interactions by both age and DM status, may also help to explain some of the inconsistent results in studies relating physical activity to growth and neurotrophic factors.

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          Most cited references49

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          The intersection between aging and cardiovascular disease.

          The average lifespan of humans is increasing, and with it the percentage of people entering the 65 and older age group is growing rapidly and will continue to do so in the next 20 years. Within this age group, cardiovascular disease will remain the leading cause of death, and the cost associated with treatment will continue to increase. Aging is an inevitable part of life and unfortunately poses the largest risk factor for cardiovascular disease. Although numerous studies in the cardiovascular field have considered both young and aged humans, there are still many unanswered questions as to how the genetic pathways that regulate aging in model organisms influence cardiovascular aging. Likewise, in the molecular biology of aging field, few studies fully assess the role of these aging pathways in cardiovascular health. Fortunately, this gap is beginning to close, and these two fields are merging together. We provide an overview of some of the key genes involved in regulating lifespan and health span, including sirtuins, AMP-activated protein kinase, mammalian target of rapamycin, and insulin-like growth factor 1 and their roles regulating cardiovascular health. We then discuss a series of review articles that will appear in succession and provide a more comprehensive analysis of studies carried out linking genes of aging and cardiovascular health, and perspectives of future directions of these two intimately linked fields.
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            Diabetes and Cardiovascular Disease: A Statement for Healthcare Professionals From the American Heart Association

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              An investigation of coronary heart disease in families. The Framingham offspring study.

              The Framingham Heart Study (FHS) was started in 1948 as a prospective investigation of cardiovascular disease in a cohort of adult men and women. Continuous surveillance of this sample of 5209 subjects has been maintained through biennial physical examinations. In 1971 examinations were begun on the children of the FHS cohort. This study, called the Framingham Offspring Study (FOS), was undertaken to expand upon knowledge of cardiovascular disease, particularly in the area of familial clustering of the disease and its risk factors. This report reviews the sampling design of the FHS and describes the nature of the FOS sample. The FOS families appear to be of typical size and age structure for families with parents born in the late 19th or early 20th century. In addition, there is little evidence that coronary heart disease (CHD) experience and CHD risk factors differ in parents of those who volunteered for this study and the parents of those who did not volunteer.
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                Author and article information

                Contributors
                Journal
                J Diabetes Res
                J Diabetes Res
                JDR
                Journal of Diabetes Research
                Hindawi
                2314-6745
                2314-6753
                2019
                9 January 2019
                : 2019
                : 2718465
                Affiliations
                1Department of Endocrinology, Diabetes, Nutrition & Weight Management, Boston University School of Medicine (BUSM), Boston, MA, USA
                2Framingham Heart Study, Framingham, MA, USA
                3Department of Biostatistics, Boston University School of Public Health (BUSPH), Boston, MA, USA
                4Department of Neurology, BUSM, Boston, MA, USA
                5Departments of Medicine and Epidemiology, BUSM and BUSPH, Boston, MA, USA
                6Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, University of Texas Health Sciences Center, San Antonio, TX, USA
                Author notes

                Academic Editor: Bernard Portha

                Author information
                http://orcid.org/0000-0002-0724-8629
                Article
                10.1155/2019/2718465
                6343169
                30729134
                71336e60-cb0d-4b92-9999-bf268bfb5d4e
                Copyright © 2019 Nicole L. Spartano et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 28 May 2018
                : 28 November 2018
                : 3 December 2018
                Funding
                Funded by: National Heart, Lung, and Blood Institute
                Award ID: N01-HC25195
                Award ID: HHSN268201500001I
                Funded by: National Institutes of Health
                Award ID: R01 AG031287
                Award ID: R01 AG054076
                Award ID: R01 AG033040
                Award ID: R01 AG049607
                Award ID: R01 NS017950
                Award ID: UH2 NS100605
                Award ID: R01 AG047645
                Award ID: R01 HL131029
                Award ID: R01 DK080739
                Award ID: R56 AG029451
                Funded by: American Heart Association
                Award ID: 15GPSGC24800006
                Award ID: 16MCPRP30310001
                Funded by: Evans Medical Foundation
                Funded by: Boston University School of Medicine
                Categories
                Research Article

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