Physical activity, body fat, and serum C-reactive protein in postmenopausal women with and without hormone replacement.
The objective was to determine whether higher physical activity is associated with lower serum C-reactive protein (CRP), independent of oral hormone replacement therapy (HRT) status and body fatness, in 133 postmenopausal women using a cross-sectional exploratory design at a university research laboratory. The subjects were 133 postmenopausal women, age 50-73 years, with no evidence of coronary artery disease or diabetes. The main outcome measures were: serum CRP, physical activity as measured by Stanford 7-day activity recall, body fat (both total and regional) as measured by dual energy X-ray absorptiometry (DXA), and anthropometry (waist and hip circumference). Secondary outcome measures included fasting plasma glucose and insulin as well as fasting serum triglycerides, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. Higher physical activity energy expenditures were significantly associated with lower serum CRP levels (r = -0.18, P = 0.041), independent of oral HRT use, age, smoking behavior, alcohol consumption, aspirin use, and statin use. However, in the complete multivariate model, which included body fat, older ages (P = 0.047), greater trunk fat masses (P < 0.001), any oral HRT use (P < 0.001), and unopposed oral estrogen use (P = 0.012) were the sole independent predictors of higher serum CRP levels. The complete multivariate model accounted for 58% of the variance in serum CRP. We conclude that the association between higher physical activity and lower serum CRP levels is dependent on the lower body fat of the more active women, yet independent of oral HRT use. Future intervention trials should determine whether diet- and exercise-related reductions in body fat may be effective ways to diminish the proinflammatory effects of oral HRT in postmenopausal women.
Manns PJ
,Williams DP
,Snow CM
,Wander RC
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《AMERICAN JOURNAL OF HUMAN BIOLOGY》
Metformin reduces weight, centripetal obesity, insulin, leptin, and low-density lipoprotein cholesterol in nondiabetic, morbidly obese subjects with body mass index greater than 30.
We studied 31 nondiabetic, habitually (> or =5 years) morbidly obese subjects (mean +/- SD body mass index [BMI] 43 +/- 8.7, median 43). Our specific aim was to determine whether metformin (2.55 g/d for 28 weeks) would ameliorate morbid obesity and reduce centripetal obesity; lipid and lipoprotein cholesterol, insulin, and leptin levels; and plasminogen activator inhibitor activity (PAI-Fx), risk factors for coronary heart disease (CHD). The patients were instructed to continue their prestudy dietary and exercise regimens without change. After 2 baseline visits 1 week apart, the 27 women and 4 men began receiving metformin, 2.55 g/d, which was continued for 28 weeks with follow-up visits at study weeks 5, 13, 21, and 29. Daily food intake was recorded by patients for 7 days before visits then reviewed with a dietitian. Kilocalories per day and per week were calculated. At each visit, fasting blood was obtained for measurement of lipid profile, insulin, leptin, and PAI-Fx. The mean +/- SD kilocalories consumed per day, 1,951 +/- 661 at entry, fell by week 29 to 1,719 +/- 493 (P =.014) but did not differ at weeks 5, 13, and 21 from that at week 29 (P >.2). Weight fell from 258 +/- 62 pounds at entry to 245 +/- 54 pounds at week 29 (P =.0001). Girth was reduced from 51.8 +/- 6.2 to 49.2 +/- 4.5 inches (P =.0001). Waist circumference fell from 44.0 +/- 6.4 inches to 41.3 +/- 5.9 (P =.0001). The waist/hip ratio fell from 0.85 +/- 0.09 to 0.84 +/- 0.09 (P =.04). Fasting serum insulin, 28 +/- 15 microU/mL at entry, fell to 21 +/- 11 microU/mL at week 29 (P =.0001), and leptin fell from 79 +/- 33 ng/mL to 55 +/- 27 ng/mL (P =.0001). On metformin, there were linear trends in decrements in weight, girth, waist circumference, waist/hip ratio, insulin, and leptin throughout the study period (P <.007). Low-density lipoprotein (LDL) cholesterol, 126 +/- 34 mg/dL at study entry, fell to 112 +/- 43 mg/dL at week 29 (P =.001), with a linear trend toward decreasing levels throughout (P =.036). By stepwise linear regression, the higher the entry weight, the larger the reduction in weight on metformin therapy (partial R(2) = 31%, P =.001). The greater the reduction in kilocalories consumed per day, the greater the decrease in weight on metformin therapy (partial R(2) = 15%, P =.011). The higher the waist/hip ratio at entry, the greater its reduction on metformin therapy (partial R(2) = 11%, P =.004). The higher the entry serum leptin, the greater its reduction on metformin therapy (partial R(2) = 29%, P =.002). The greater the reduction in insulin on metformin, the greater the reduction in leptin (partial R(2) = 8%, P =.03). The higher the entry PAI-Fx, the greater the reduction in PAI-Fx on metformin (partial R(2) = 43%, P =.0001). Metformin safely and effectively reduces CHD risk factors (weight, fasting insulin, leptin, LDL cholesterol, centripetal obesity) in morbidly obese, nondiabetic subjects with BMI > 30, probably by virtue of its insulin-sensitizing action.
Glueck CJ
,Fontaine RN
,Wang P
,Subbiah MT
,Weber K
,Illig E
,Streicher P
,Sieve-Smith L
,Tracy TM
,Lang JE
,McCullough P
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《METABOLISM-CLINICAL AND EXPERIMENTAL》