Physical activity and incidence of noninsulin-dependent diabetes mellitus in women

Department of Nutrition , Harvard University, Cambridge, Massachusetts, United States
The Lancet (Impact Factor: 45.22). 10/1991; 338(8770):774-8. DOI: 10.1016/0140-6736(91)90664-B
Source: PubMed


The potential role of physical activity in the primary prevention of non-insulin-dependent diabetes mellitus (NIDDM) is largely unknown. We examined the association between regular vigorous exercise and the subsequent incidence of NIDDM in a prospective cohort of 87,253 US women aged 34-59 years and free of diagnosed diabetes, cardiovascular disease, and cancer in 1980. During 8 years of follow-up, we confirmed 1303 cases of NIDDM. Women who engaged in vigorous exercise at least once per week had an age-adjusted relative risk (RR) of NIDDM of 0.67 (p less than 0.0001) compared with women who did not exercise weekly. After adjustment for body-mass index, the reduction in risk was attenuated but remained statistically significant (RR = 0.84, p = 0.005). When analysis was restricted to the first 2 years after ascertainment of physical activity level and to symptomatic NIDDM as the outcome, age-adjusted RR of those who exercised was 0.5, and age and body-mass index adjusted RR was 0.69. Among women who exercised at least once per week, there was no clear dose-response gradient according to frequency of exercise. Family history of diabetes did not modify the effect of exercise, and risk reduction with exercise was evident among both obese and nonobese women. Multivariate adjustments for age, body-mass index, family history of diabetes, and other variables did not alter the reduced risk found with exercise. Our results indicate that physical activity may be a promising approach to the primary prevention of NIDDM.

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    • "At baseline and on all biennial follow-up questionnaires, participants were asked whether they had received a physician-diagnosis of diabetes. Those reporting a diabetes diagnosis were sent a supplementary questionnaire (Manson et al. 1991) regarding any symptoms, diagnostic tests, and treatment. We used one of the following American Diabetes Association 1998 criteria to confirm self-reported T2D diagnosis: a) an elevated glucose concentration (fasting plasma glucose ≥ 7.0 mmol/L, random plasma glucose ≥ 11.1 mmol/L, or plasma glucose ≥ 11.1 mmol/L after an oral glucose load) and at least one symptom (excessive thirst, polyuria, weight loss, or hunger) related to diabetes; b) no symptoms, but elevated glucose concentrations on two separate occasions; or c) treatment with insulin or oral hypoglycemic medication. "
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    ABSTRACT: Prospective evidence regarding associations for exposures to bisphenol A (BPA) and phthalates with type 2 diabetes (T2D) is lacking. To prospectively examine urinary concentrations of BPA and phthalate metabolites with T2D risk. BPA and eight major phthalate metabolites were measured among 971 incident T2D case-control pairs from the Nurses' Health Study (NHS; mean age 65.6) and NHSII (mean age 45.6). In the NHSII, BPA levels were not associated with incident T2D in multivariate-adjusted analysis until body mass index was adjusted: odds ratio (OR) comparing extreme BPA quartiles increased from 1.40 (95% CI: 0.91, 2.15) to 2.08 (95% CI: 1.17, 3.69; Ptrend = 0.02) with such an adjustment. In contrast, BPA concentrations were not associated with T2D in the NHS (OR 0.81; 95% CI 0.48, 1.38; Ptrend = 0.45). Likewise, urinary concentrations of total phthalate metabolites were associated with T2D in the NHSII (OR comparing extreme quartiles 2.14; 95% CI 1.19, 3.85; Ptrend = 0.02), but not in the NHS (OR 0.87; 95% CI 0.49, 1.53; Ptrend = 0.29). Summed metabolites of butyl phthalates or di-(2-ethylhexyl) phthalates were significantly associated with T2D in the NHSII only; ORs comparing extreme quartiles were 3.16 (95% CI: 1.68, 5.95; Ptrend = 0.0002) and 1.91 (95% CI: 1.04, 3.49; Ptrend = 0.20), respectively. These results suggest that BPA and phthalate exposures may be associated with the risk of T2D among middle-aged women, but not older women. The divergent findings between the two cohorts might be explained by menopausal status or simply by chance. Clearly, these results need to be interpreted with caution and should be replicated in future studies, ideally with multiple urine samples collected prospectively to improve the measurement of these exposures with short half-lives.
    Environmental Health Perspectives 03/2014; 122(6). DOI:10.1289/ehp.1307201 · 7.98 Impact Factor
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    • "High body mass index (BMI; Ohlson et al., 1985; Colditz et al., 1990; Chan et al., 1994; Carey et al., 1997; Hu et al., 2001b), which reflects a positive energy balance, has been positively associated with T2D. High physical activity, another component of the energy balance equation, has been associated with lower incidence of T2D (Helmrich et al., 1991; Manson et al., 1991; Wei et al., 1999; Hu et al., 2001a; Annals of Human Genetics (2014) 78,23–32 23 R. Villegas et al. Sigal et al., 2004). "
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    ABSTRACT: We used a two-stage study design to evaluate whether variations in the peroxisome proliferator-activated receptors (PPAR) and the PPAR gamma co-activator 1 (PGC1) gene families (PPARA, PPARG, PPARD, PPARGC1A, and PPARGC1B) are associated with type 2 diabetes (T2D) risk. Stage I used data from a genome-wide association study (GWAS) from Shanghai, China (1019 T2D cases and 1709 controls) and from a meta-analysis of data from the Asian Genetic Epidemiology Network for T2D (AGEN-T2D). Criteria for selection of single nucleotide polymorphisms (SNPs) for stage II were: (1) P < 0.05 in single marker analysis in Shanghai GWAS and P < 0.05 in the meta-analysis or (2) P < 10(-3) in the meta-analysis alone and (3) minor allele frequency ≥ 0.10. Nine SNPs from the PGC1 family were assessed in stage II (an independent set of middle-aged men and women from Shanghai with 1700 T2D cases and 1647 controls). One SNP in PPARGC1B, rs251464, was replicated in stage II (OR = 0.87; 95% CI: 0.77-0.99). Gene-body mass index (BMI) and gene-exercise interactions and T2D risk were evaluated in a combined dataset (Shanghai GWAS and stage II data: 2719 cases and 3356 controls). One SNP in PPARGC1A, rs12640088, had a significant interaction with BMI. No interactions between the PPARGC1B gene and BMI or exercise were observed.
    Annals of Human Genetics 01/2014; 78(1):23-32. DOI:10.1111/ahg.12044 · 2.21 Impact Factor
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    • "Furthermore, a study that followed 21,271 male U.S. doctors over five years revealed that even a once-weekly bout of exercise at an intensity that is sufficient to cause sweating reduced the risk of developing diabetes [7]. In addition, results from a study that followed 87,253 female U.S. nurses over eight years showed that the group that exercised at least once a week at an intensity sufficient to cause sweating had a relative risk of developing diabetes of 0.84 compared with a group that exercised less than once a week [8]. Although WAT was once considered to be merely a site for energy storage, in recent years it has become better understood at the molecular level; for example, how WAT secretes physiologically active substances, collectively known as adipokines, and how obesity-induced dysregulated expression of adipokines in WAT causes insulin resistance, which is the pathogenesis of diabetes [9] [10] [11]. "
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    ABSTRACT: Obesity is recognized as a risk factor for lifestyle-related diseases such as type 2 diabetes and cardiovascular disease. White adipose tissue (WAT) is not only a static storage site for energy; it is also a dynamic tissue that is actively involved in metabolic reactions and produces humoral factors, such as leptin and adiponectin, which are collectively referred to as adipokines. Additionally, because there is much evidence that obesity-induced inflammatory changes in WAT, which is caused by dysregulated expression of inflammation-related adipokines involving tumor necrosis factor- α and monocyte chemoattractant protein 1, contribute to the development of insulin resistance, WAT has attracted special attention as an organ that causes diabetes and other lifestyle-related diseases. Exercise training (TR) not only leads to a decrease in WAT mass but also attenuates obesity-induced dysregulated expression of the inflammation-related adipokines in WAT. Therefore, TR is widely used as a tool for preventing and improving lifestyle-related diseases. This review outlines the impact of TR on the expression and secretory response of adipokines in WAT.
    International Journal of Endocrinology 12/2013; 2013(3):801743. DOI:10.1155/2013/801743 · 1.95 Impact Factor
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