Nutritional status of COPD patients with acute exacerbation.

The prevalence and features of nutritional status in patients with chronic obstructive pulmonary disease (COPD) have been studied extensively in stable conditions, but are poorly defined in the presence of an acute exacerbation. The aim of this study is to evaluate the nutritional status of COPD patients with acute exacerbation and possible relationship between nutritional parameters and pulmonary functions. The study group consisted of 53 COPD patients acutely admitted to the hospital for standardized medical treatment. The nutritional status of patients was assessed by anthropometric measurements, biochemical analysis, and immunologic testing. The patients were divided into two groups as having severe (FEV1 < 50%) and mild to moderate (FEV1 ? 50%) COPD and weight loss greater than 5% for the comparison of the study parameters. Ideal body weight (IBW%) was found as 104.42 +/- 4.30 in severe COPD, where as it was 115.31 +/- 7.28 in mild to moderate COPD group (p= 0.07). There was no relationship demonstrated between IBW% and FEV1. IBW% was correlated with DLCO for the total study population (r= 0.353, p= 0.035). weight loss greater than 5% of body weight (BW) was observed in 54% of patients. Comparison of the patient's actual weight to their usual weight revealed statistically significant weight loss (p< 0.01). Mean values of serum albumin, transferrin were found in normal range. Delayed type hypersensitivity skin test revealed normal immune status. When the study parameters were compared, no any statistically significant differences in parameters related to nutritional status were detected, between severe and mild to moderate COPD groups. As a statistically significant weight loss was found between the actual and usual weights of the patients, monitoring of nutritional parameters and eventual dietetic treatment should also be included in the goals of the medical treatment of patients with COPD in acute exacerbation.

Relationship of a large weight loss to long-term weight change among young and middle-aged US women.

OBJECTIVE: To assess the prevalence of clinically significant weight loss among women and whether this is associated with smaller long-term weight gains. DESIGN: Six-year follow-up of young and middle-aged women in the Nurses' Health Study II. SUBJECTS: A total of 47,515 women who did not report a pregnancy, or a diagnosis of cancer or cardiovascular disease any time between 1989 and 1995. MEASUREMENTS: Self-reported weights in 1989, 1991, 1993 and 1995, dietary intake, physical activity, inactivity, history of weight cycling and smoking. RESULTS: Between 1989 and 1991, 9% of the women lost > or =5% of their 1989 weight (6% lost 5--9.9% and 3% lost > or =10%). The proportion who lost > or =10% of their weight increased with category of body mass index (BMI, kg/m(2)) from 0.4% among women with a BMI <22 to 9% among women with a BMI > or =30 in 1989. Women who lost > or =5% of their weight between 1989 and 1991 gained more weight between 1991 and 1995 than their peers and the difference increased across categories of BMI in 1989. However, due to their large weight losses, women who lost > or =5% of their weight between 1989 and 1991 overall gained less weight than their peers between 1989 and 1995 (P<0.001). Moreover, women who engaged in 5 or more hours per week of vigorous physical activity gained approximately 0.5 kg less than their inactive peers (P<0.001). CONCLUSION: Although most women who lost a clinically significant amount of weight regained most of it, they gained less weight over the entire 6 y period than their peers.

Relationship between different subcutaneous adipose tissue layers, fat mass, and leptin in response to short-term energy restriction in obese girls.

This study addresses whether the expected relationship of 15 specified subcutaneous adipose tissue layers (SAT layers) from 1-neck to 15-calf and body fat mass (FM) with leptin was influenced by a weight-loss program. In 30 obese girls (10 prepubertal, 15 pubertal, and 5 late/postpubertal) SAT layers were measured by means of the optical device Lipometer. Fat mass (FM) was estimated indirectly by means of bioelectrical impedance. Leptin and insulin were determined by means of radioimmunoassays. All measurements were performed before (pre) and after (post) 3 weeks of low-caloric diet and physical training. At the beginning of the study, there were significant correlations for all estimates of adiposity and leptin (0.67 to 0.79; P < 0.0001). Five SAT layers from the upper body and the trunk (0.48 to 0.67; P < 0.01) but none from the abdominal region and lower extremities were correlated with leptin. FM together with SAT layers 4-upper back and 8-lower abdomen (negative slope) explained 79% of the variation in pre leptin values (P < 0.0001). The weight-loss program significantly reduced leptin (P < 0.0001), insulin (P = 0.04), estimates of adiposity (P < 0.0001), and SAT layers 4-upper back (P = 0.0006), 11-front thigh, 13-rear thigh, and 14-inner thigh (P between <0.03 and <0.01). Although significant, the reductions in the four SAT layers were small. Estimated fat-free mass was significantly increased after three weeks (P < 0.05). Changes in SAT layers from the upper extremities and from the trunk were inversely correlated to the decrease in leptin (P between <0.05 and <0.001). Initial leptin was the best correlate of the decrease in leptin (adj. R(2) = 0.815; P < 0.0001). However, when only changes in adiposity and insulin were considered in the regression model, changes in insulin contributed to the fall in leptin (adj. R(2) = 0.23; P = 0.004). When changes in SAT layers were added to the model, changes in SAT layers 2-triceps and 10-hip (negative slopes) contributed to the decrease in leptin (adj. R(2) = 0.48; P < 0.0001). After weight loss, correlations between estimates of post adiposity and post leptin (0.40, P = 0.01 to 0.57, P = 0.0005) were lower compared with pre values. SAT layers 4-upper back and 3-biceps contributed independently to post leptin values (adj. R(2) = 0.50; P < 0.0001). It is suggested that fat mass and SAT layers from the upper body are the main determinants of leptin in obese girls before weight loss. The diet and sports intervention program reduced leptin independent of the reduction in adiposity. The distribution of subcutaneous fat might be a stable correlate of circulating leptin after a short-term reduction in energy intake. Am. J. Hum. Biol. 12:803-813, 2000. Copyright 2000 Wiley-Liss, Inc.

Regulation of adiponectin by adipose tissue-derived cytokines: in vivo and in vitro investigations in humans.

Adiponectin is an adipose tissue-specific protein that is abundantly present in the circulation and suggested to be involved in insulin sensitivity and development of atherosclerosis. Because cytokines are suggested to regulate adiponectin, the aim of the present study was to investigate the interaction between adiponectin and three adipose tissue-derived cytokines (IL-6, IL-8, and TNF-alpha). The study was divided into three substudies as follows: 1) plasma adiponectin and mRNA levels in adipose tissue biopsies from obese subjects [mean body mass index (BMI): 39.7 kg/m2, n = 6] before and after weight loss; 2) plasma adiponectin in obese men (mean BMI: 38.7 kg/m2, n = 19) compared with lean men (mean BMI: 23.4 kg/m2, n = 10) before and after weight loss; and 3) in vitro direct effects of IL-6, IL-8, and TNF-alpha on adiponectin mRNA levels in adipose tissue cultures. The results were that 1) weight loss resulted in a 51% (P < 0.05) increase in plasma adiponectin and a 45% (P < 0.05) increase in adipose tissue mRNA levels; 2) plasma adiponectin was 53% (P < 0.01) higher in lean compared with obese men, and plasma adiponectin was inversely correlated with adiposity, insulin sensitivity, and IL-6; and 3) TNF-alpha (P < 0.01) and IL-6 plus its soluble receptor (P < 0.05) decreased adiponectin mRNA levels in vitro. The inverse relationship between plasma adiponectin and cytokines in vivo and the cytokine-induced reduction in adiponectin mRNA in vitro suggests that endogenous cytokines may inhibit adiponectin. This could be of importance for the association between cytokines (e.g., IL-6) and insulin resistance and atherosclerosis.