Physical activity and incidence of noninsulin-dependent diabetes mellitus in women
ABSTRACT 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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- "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). "
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 · 1.93 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 . 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 . 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   . "
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 · 1.52 Impact Factor
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- "For cases diagnosed in 1998 and later, the fasting plasma glucose threshold was lowered to 126 mg/dl according to the American Diabetes Association criteria (Gavin et al., 1997). The validity of the supplementary questionnaire has been demonstrated previously in the NHS (Manson et al., 1991; Field et al., 2001). Only cases confirmed by the supplemental questionnaires were included in the current analysis. "
ABSTRACT: Emotional stress may be a risk factor for type 2 diabetes (T2D), but the relation between phobic anxiety symptom scores and risk of T2D is uncertain. To evaluate prospectively the association between phobic anxiety symptom scores and incident T2D in three cohorts of US men and women. We followed 30,830 men in the Health Professional's Follow-Up Study (HPFS) (1988-2008), 69,336 women in the Nurses' Health Study (NHS) (1988-2008), and 80,120 women in the Nurses' Health Study II (NHS II) (1993-2011). Phobic anxiety symptom scores, as measured by the Crown-Crisp index (CCI), calculated from 8 questions, was administered at baseline and updated in 2004 for NHS, in 2005 for NHS II, and in 2000 for HPFS. Incident T2D was confirmed by a validated supplementary questionnaire. We used Cox proportional hazards analysis to evaluate associations with incident T2D. During 3,110,248 person-years of follow-up, we documented 12,876 incident T2D cases. In multivariable Cox regression models with adjustment for major lifestyle and dietary risk factors,the HRs of T2D across categories of increasing levels ofCCI (scores= 2-<3, 3-<4, 4-<6, ⩾6), compared with a score of <2, were increased significantly by 6%, 10%, 11% and 13% (Ptrend =0.0005) for NHS; and by 19%, 11%, 22%, and 29% (Ptrend <0.0001) for NHS II. Each score increment in CCI was associated with 3% higher risk of T2D in NHS (HRs, 1.03, 95%CI:1.02-1.04) and 4% higher risk of T2D in NHS II (HRs, 1.04, 95%CI:1.03-1.05). Further adjustment for self-reported depression and antidepressant use did not change the results. In HPFS, the association between CCI and T2D was not significant after adjusting for lifestyle variables. Our results suggest that higher phobic anxiety symptom scores are associated with an increased risk of T2D in women.Brain Behavior and Immunity 10/2013; 36. DOI:10.1016/j.bbi.2013.10.025 · 6.13 Impact Factor