46 research outputs found

    Physical Activity in the Prevention of Chronic Kidney Disease

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    Chronic kidney disease (CKD) is an important risk factor for cardiovascular disease (CVD) and mortality. The increase in CKD in recent decades has paralleled increases in obesity, diabetes, and the metabolic syndrome. Physical inactivity is a modifiable risk factor that may affect the development and course of CKD. It is well established that exercise training improves a number of metabolic factors, including blood pressure and insulin resistance, which would be expected to preserve renal function as well as lower CVD risk. Epidemiological studies have suggested that partaking in vigorous physical activity may protect against kidney disease. However, to date few studies have rigorously measured physical activity levels. Instead, investigators have relied on subjective measures of physical activity and patient recall. This is particularly problematic when attempting to capture low- and very-low-intensity physical activity and in quantifying sedentary behavior. Improvements in vascular endothelial function, insulin sensitivity, adipocytokine profiles, and oxidative stress likely mediate the benefits of physical activity on the kidney. While formal exercise recommendations have been published for diabetes and hypertension, guidelines regarding the optimal type, frequency, intensity and duration of physical activity for preventing CKD have yet to be formalized

    Inactivity induces increases in abdominal fat

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    Effect of Glucose or Fat Challenge on Aspirin Resistance in Diabetes

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    Aspirin has lower antiplatelet activity in diabetic patients. Our aim is to study the roles of acute hyperglycemia and hyperlipidemia on aspirin function in diabetic subjects with and without cardiovascular disease. Using urine thromboxane (pg/mg creatinine) and VerifyNow (Aspirin Resistance Measures-ARU), we investigated diabetic subjects during a 2-hour glucose challenge (n=49) or a 4-hour fat challenge (n=11). All subjects were currently taking aspirin (81 or 325 mg). After fat ingestion, urine thromboxane increased in all subjects (Mean ± SE before: after) (1209 ± 336: 1552 ±371, P=.01), while we noted a trend increase in VerifyNow measures (408±8: 431±18, P=.1). The response to glucose ingestion was variable. Diabetic subjects with cardiac disease and dyslipidemia increased thromboxane (1693±364: 2799 ± 513, P<.05) and VerifyNow (457.6 ± 22.3: 527.1 ± 25.8, P<.05) measures after glucose. We conclude that saturated fat ingestion increases in vivo thromboxane production despite aspirin therapy
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