An evaluation of resting energy expenditure in hospitalized, severely underweight patients.

A prospective trial was conducted with 14 hospitalized patients who were severely underweight with a mean weight of 40.9+/-5.1 kg and 70.7+/-7.8% of ideal body weight, to compare estimates of resting energy expenditure (REE) with measured values. The 9 women and 3 men, whose mean age was 66.5+/-13.9 y, underwent nutritional assessment and measurement of their REE by indirect calorimetry using the Sensormedics Deltatrac MBM100 indirect calorimeter. Their REE was also estimated by the Harris-Benedict formula (mean 1032+/-66 kcal/d) as well as a previously established empirical formula where REE = 25 x body weight in kg (mean 1023+/-129 kcal/d). Results by both estimates were significantly lower than the measured resting energy expenditure (MREE) in this group of patients (P<0.0001). The percentage difference between MREE and estimated REE by the Harris-Benedict formula was 18.4+/-9.4% and 20.9+/-7.5% by the empirical formula. The MREE exceeded the estimated REE in each individual. The correlation between MREE and body weight (r2 = 0.558, r = 0.005) was better than that between MREE and estimated REE by Harris-Benedict formula (r2 = 0.275, P = 0.08) suggesting that weight was the principal determinant rather than the other components (height, age, sex) of the Harris-Benedict formula. Our data shows that commonly employed formulae routinely underestimate the energy needs of severely underweight patients below 50 kg in body weight. The Harris-Benedict equation had limited predictive value for the individual, explaining approximately 25% of the variance in energy expenditure. Given the particular importance of matching energy intake to needs in this group of patients with limited reserves, many of whom are critically ill, we suggest an empirical equation using 30-32 kcal/kg be used to estimate the energy requirements of severely underweight patients when direct measurements are unavailable or clinically less imperative.     

Greater whole-body myofibrillar protein breakdown in cachectic patients with chronic obstructive pulmonary disease

BACKGROUND: Experimental studies indicate that greater skeletal muscle protein breakdown is a trigger for the cachexia that often is prevalent in chronic obstructive pulmonary disease (COPD). OBJECTIVE: We compared myofibrillar protein breakdown (MPB) with whole-body (WB) protein breakdown (PB) in 9 cachectic COPD patients [x +/- SEM forced expiratory volume in 1 s (FEV(1)): 48 +/- 4% of predicted], 7 noncachectic COPD patients (FEV(1): 53 +/- 5% of predicted), and 7 age-matched healthy control subjects, who were matched by body mass index with the noncachectic patients. DESIGN: After the subjects fasted overnight (10 h) and discontinued the maintenance medication, a primed constant and continuous infusion protocol was used to infuse L-[ring-(2)H(5)]-phenylalanine and L-[ring-(2)H(2)]-tyrosine to measure WB protein turnover and L-[(2)H(3)]-3-methylhistidine to measure WB MPB. Three arterialized venous blood samples were taken between 80 and 90 min of infusion to measure amino acid concentrations and tracer enrichments. RESULTS: Body composition, WB protein turnover, and WB MPB did not differ significantly between the noncachectic COPD and control subjects. Cachectic COPD patients had lower fat mass and fat-free mass values (both: P < 0.01) than did the noncachectic COPD patients. WB MPB was significantly (P < 0.05) higher in the cachectic COPD group (18 +/- 3 nmol . kg(-1) . min(-1)) than in the combined control and noncachectic COPD groups (10 +/- 1 nmol . kg(-1) . min(-1)), but WB protein turnover did not differ significantly between the groups. Correlations with fat-free mass were significant (P < 0.05) for plasma glutamate and branched-chain amino acids, and that for WB MPB trended toward significance (P = 0.07). CONCLUSION: Cachexia in clinically stable patients with moderate COPD is characterized by increased WB MPB, which indicates that myofibrillar protein wasting is an important target for nutritional and pharmacologic modulation.     

Association of household rice expenditure with child nutritional status indicates a role for macroeconomic food policy in combating malnutrition

Macroeconomic food policies have the potential to reduce malnutrition by improving access to food, a determinant of nutritional status. However, very little is understood about the mechanisms and the magnitude of the effects of macroeconomic food policies such as food price policies on nutritional status. Data collected by the Nutritional Surveillance Project on a total of 81,337 children aged 6-59 mo in rural Bangladesh between 1992 and 2000 were used to examine how changes in rice price affect child underweight. Rice consumption per capita declined only slightly during the period but rice expenditure per capita varied widely due to fluctuations in rice price. Rice expenditure was positively correlated with the percentage of underweight children (r = 0.91, P = 0.001). Households were found to spend more on nonrice foods as their rice expenditure declined, and nonrice expenditure per capita was negatively correlated with the percentage of underweight children (r = -0.91, P = 0.001). Expenditure on nonrice foods per capita increased with the frequency with which nonrice foods were consumed (P < 0.05) and with the diversity of the diet (P < 0.001). The findings suggest that the percentage of underweight children declined when rice expenditure fell because households were able to spend more on nonrice foods and thereby increase the quantity and quality of their diet. We hypothesize that macroeconomic food policies that keep the price of food staples low can contribute toward reducing child underweight.     

Branched-chain alpha-ketoacids and related acids in thiamin-deprived rats

We showed elevated plasma levels of branched-chain amino acids, alpha-ketoacids, alpha-hydroxyacids in thiamin-deprived rats, which had decreased liver thiamin levels (2.4% of control) after 4 weeks of feeding of thiamin-deficient diet. The ratios of mean levels of these acids in thiamin-deficient rats to those in control rats were as follows: total branched-chain amino acids 1.6; total branched-chain alpha-ketoacids 2.7; total branched-chain alpha-hydroxyacids 3.6; pyruvic acid 1.6. The plasma level of total branched-chain alpha-hydroxyacids was correlated to liver thiamin concentration (r = -0.67, p less than 0.01), but those of the other two acids were not correlated. Although the increased levels of branched-chain acids in thiamin-deprived rats were less remarkable than those of ill patients with maple syrup urine disease, they reflect the reportedly decreased branched-chain alpha-ketoacid dehydrogenase activities (about 40% of control), and we discussed whether the toxic effects of individual branched-chain acid could be demonstrated by its administration to the thiamin-deprived rats.     

Altered postprandial glucose, insulin, leptin, and ghrelin in liver cirrhosis: correlations with energy intake and resting energy expenditure

BACKGROUND: Liver cirrhosis is associated with reduced energy intake and increased resting energy expenditure. OBJECTIVE: We aimed to investigate the possible role of glucose, insulin, leptin, and ghrelin in the pathogenesis of these alterations. DESIGN: Nutritional status, energy intake, resting energy expenditure, and fasting glucose, insulin, and leptin were assessed in 31 patients with cirrhosis. Postprandial glucose, insulin, C-peptide, leptin, and ghrelin responses were studied in a subgroup of patients after a standard meal. Ten healthy subjects served as controls. RESULTS: Patients with cirrhosis had a lower energy intake (P < 0.05), higher resting energy expenditure (P < 0.05), higher fasting leptin (P < 0.05), and higher insulin resistance (P < 0.001) than did the healthy control subjects. In the patients with cirrhosis, fasting leptin was negatively correlated with resting energy expenditure (r = -0.38, P < 0.05) but not with energy intake. In control subjects, leptin was negatively correlated with energy intake (r = -0.72, P < 0.05) but not with resting energy expenditure. The patients with cirrhosis had higher postprandial glucose (P < 0.001) and lower ghrelin (P < 0.05) concentrations at 4 h postprandially than did the control subjects. The increase in ghrelin from its minimal postmeal value to 4 h postmeal was negatively correlated (r = -0.66, P = 0.014) with weight loss in the patients with cirrhosis. Energy intake was negatively correlated (r = -0.42, P < 0.01) with the postprandial increase in glucose. CONCLUSIONS: In cirrhosis, altered postprandial glucose and ghrelin are associated with reduced energy intake and weight loss, respectively, and the effects of leptin on energy intake and expenditure seem to be altered. Insulin resistance might be involved in these altered postprandial responses.     

Substrate efficacy in early nutrition support of critically ill multiple trauma victims.

The metabolic consequences of excessive nutrition support in patients have been increasingly recognized in recent years. Time-dependent optimal nutrition support is desired for an early and uncomplicated recovery after severe injury or illness. Metabolic effects of adding balanced amino acids to glucose infusion during total parenteral nutrition were investigated in 18 patients after major trauma (injury severity score 32 +/- 2). Two studies were conducted on each subject, one in the early "flow" phase of injury (40-60 hours postinjury) in the basal state without any dietary intake and then after 4 to 6 days of intravenous nutrition provided solely as glucose (24 +/- 2 kcal/kg per day, 80% resting energy expenditure, n = 8) or isocaloric glucose (28 +/- 3 kcal/kg per day) with amino acids (275 +/- 28 mg of nitrogen per kilogram per day, n = 10). Whole-body fuel substrate kinetics were studied for energy metabolism (indirect calorimetry), protein kinetics (primed-constant infusion of 15N glycine), and lipid mobilization (two-stage infusion of 10% glycerol). Injury-induced hypoaminoacidemia was equally modulated whether the glucose-based nutrition had amino acids or not. The negative nitrogen balance is reduced similarly in both groups. Protein breakdown rate is significantly (p = .025) decreased in both groups and it is more so (30% vs 18%) in patients receiving total parenteral nutrition. Intravenous nutrition could not stimulate protein synthesis. Whole-body lipolysis rate as well as net fat oxidation rate are suppressed more when glucose alone is given, and this also results in less reesterification. Provision of intravenous glucose alone, not to exceed the resting energy expenditure, seems to be superior to isocaloric glucose with amino acids during this early catabolic flow phase of injury because the injured body could not assimilate this exogenous amino acid.     

Amino acid kinetics in patients with sepsis

BACKGROUND: In patients with sepsis and systemic inflammatory response syndrome, amino acid extraction by the liver is enhanced, resulting in decreased plasma amino acid concentrations. Systematic investigations of the elimination of intravenously infused amino acids have not been performed. OBJECTIVE: The objective of this study was to compare the elimination of 17 amino acids in patients with sepsis and in healthy control subjects. DESIGN: Elimination of amino acids was evaluated in 9 patients with sepsis and in 8 healthy control subjects by using a combined loading and maintenance infusion of 375 mg amino acids/kg body wt for 60 min. Pharmacokinetic variables were analyzed from plasma curves. RESULTS: With the exception of lysine, methionine, glutamate, ornithine, phenylalanine, and tyrosine, plasma concentrations of amino acids were lower in the patients with sepsis than in the control subjects; phenylalanine was the only amino acid whose plasma concentration increased (P < 0.001). In patients with sepsis, whole-body clearance (Cl(tot)) of total amino acids was 74% higher than in control subjects (x +/- SEM: 13,161 +/- 1659 and 7566 +/- 91 mL/min, respectively; P < 0.01), the Cl(tot) of essential amino acids was 64% higher (P < 0.02), that of nonessential amino acids was 82% higher (P < 0.01), and that of both branched-chain amino acids and glucogenic amino acids was 97% higher (P < 0.001). With the exception of phenylalanine, ornithine, proline, and glutamate, the Cl(tot) of all amino acids was elevated. The Cl(tot) of phenylalanine and ornithine decreased slightly (NS). CONCLUSIONS: In patients with sepsis, plasma concentrations of most amino acids are greatly decreased and the elimination of amino acids from the intravascular space during intravenous infusion is greatly enhanced.     

Differential effects of amino acid and ketoacid on protein metabolism in humans

We examined the effects of insulin, amino acid (AA), and branched-chain ketoacid (KA) availability on leucine kinetics in eight healthy volunteers (age = 22 +/- 2 y, body mass index = 24 +/- 1 kg) by using the euglycemic insulin clamp and [1-14C] leucine turnover techniques. Four experimental conditions were studied: study I, hyperinsulinemia; study II, hyperinsulinemia with maintenance of basal plasma AA and branched-chain KA concentrations; study III, hyperinsulinemia with hyperaminoacidemia and basal plasma branched-chain KA concentrations; and study IV, hyperinsulinemia plus basal plasma AA concentrations and elevated branched-chain KA levels. Basal endogenous leucine flux (ELF) averaged 1.20 +/- 0.05 (mumol.kg-1.min-1, mean +/- SE); basal leucine oxidation (LOX) was 0.25 +/- 0.01; and basal non-oxidative leucine disposal (NOLD) was 0.95 +/- 0.04. ELF significantly decreased in study I (0.77 +/- 0.06 mumol.kg-1.min-1, P < 0.01 versus basal). When plasma AA and branched-chain KA were either maintained at their basal levels (study II) or increased above baseline values (studies III and IV), ELF declined further (0.64 +/- 0.05, 0.66 +/- 0.02, and 0.66 +/- 0.03 mumol.kg-1.min-1, respectively; all Ps < 0.01 versus basal and P < 0.01 versus study I). LOX declined in study I (0.12 +/- 0.02 mumol.kg-1.min-1, P < 0.01 versus basal) but increased significantly in studies II, III, and IV (0.31 +/- 0.04, 0.37 +/- 0.03, and 0.40 +/- 0.03 mumol.kg-1.min-1, respectively, all Ps < 0.01 versus basal, P < 0.05 study IV versus study II, and P < 0.05 study III versus study II). NOLD declined in study I (0.65 +/- 0.05 mumol/kg.min, P < 0.01 versus basal), whereas neither the maintenance of basal plasma AA/branched-chain KA levels (study II; 0.89 +/- 0.2 mumol.kg-1.min-1) nor the elevation of plasma branched-chain KA concentration (study IV; 0.96 +/- 0.1 mumol.kg-1.min-1) increased NOLD above baseline level. A stimulation of NOLD was observed only when plasma AA levels were increased (study III; 1.23 +/- 0.03 mumol/kg.min, P < 0.01 versus basal). In conclusion, the present data do not support the concept of a direct anabolic action of ketoanalogs but do provide additional evidence for the pivotal role of AA availability in the stimulation of whole-body protein synthesis.     

Hypermetabolism in clinically stable patients with liver cirrhosis.

BACKGROUND: Hypermetabolism has a negative effect on prognosis in patients with liver cirrhosis. Its exact prevalence and associations with clinical data, the nutritional state, and beta-adrenergic activity are unclear. OBJECTIVE: We investigated resting energy expenditure (REE) in 473 patients with biopsy-proven liver cirrhosis. DESIGN: This was a cross-sectional study with a controlled intervention (beta-blockade) in a subgroup of patients. RESULTS: Mean REE was 7.12 +/- 1.34 MJ/d and correlated closely with predicted values (r = 0.70, P < 0.0001). Hypermetabolism was seen in 160 patients with cirrhosis (33.8% of the study population). REE was > 30% above the predicted value in 41% of the hypermetabolic patients with cirrhosis. Hypermetabolism had no association with clinical or biochemical data on liver function. REE correlated with total body potassium content (TBP; r = 0.49, P < 0.0001). Hypermetabolic patients had lower than normal body weight and TBP (P < 0.05). About 47% of the variance in REE could be explained by body composition whereas clinical state could maximally explain 3%. Plasma epinephrine and norepinephrine concentrations were elevated in hypermetabolic cirrhotic patients (by 56% and 41%, respectively; P < 0.001 and 0.01). Differences in REE from predicted values were positively correlated with epinephrine concentration (r = 0.462, P < 0.001). Propranolol infusion resulted in a decrease in energy expenditure (by 5 +/- 3%; P < 0.05), heart rate (by 13 +/- 4%; P < 0.01), and plasma lactate concentrations (by 32 +/- 12%; P < 0.01); these effects were more pronounced in hypermetabolic patients (by 50%, 33%, and 68%, respectively; each P < 0.05). CONCLUSIONS: Hypermetabolism has no association with clinical data and thus is an extrahepatic manifestation of liver disease. Increased beta-adrenergic activity may explain approximately 25% of hypermetabolism.     

Whole-body protein metabolism in chronic heart failure: relationship to anabolic and catabolic hormones

BACKGROUND: Patients with chronic heart failure frequently experience profound wasting during the course of the disease, a condition termed cardiac cachexia. Although protein is the primary structural and functional component of most tissues, few studies have examined the effect of heart failure on protein metabolism. Moreover, no study has assessed the relationship of protein turnover to hormonal alterations thought to promote cachexia. Thus, our goal was to determine if whole-body protein metabolism is altered in heart failure patients and to assess the relationship of protein kinetics to circulating levels of anabolic and catabolic hormones. METHODS: We measured whole-body protein metabolism using 13C-leucine, body composition, and circulating anabolic and catabolic hormone levels in 10 patients with chronic heart failure and 11 elderly controls. RESULTS: No differences in leucine rate of appearance, oxidation, or nonoxidative disposal were noted between heart failure patients and controls. However, in a subgroup of patients characterized by increased resting energy expenditure for their metabolic body size (n = 4; > or = 20% above that predicted from fat-free mass), leucine rate of appearance (mean +/- SE; 146 +/- 6 micromol/min), an index of protein breakdown, tended to be higher compared with patients with normal resting energy expenditure (n = 5; 120 +/- 8 micromol/min) and controls (127 +/- 4 micromol/min; p = .06). Alterations in anabolic/catabolic hormone balance did not explain increased protein breakdown in this subgroup, and no correlations were found between hormone levels and protein breakdown in the heart failure group as a whole. In contrast, increased circulating interleukin-6 soluble receptor (r = 0.829; p < .01) and reduced insulin-like growth factor-I (r =-.751; p < .05) levels were related to greater rates of leucine oxidation in heart failure patients. CONCLUSION: Our results demonstrate that, although increased protein turnover is not a generalized feature of heart failure, there is a subgroup of patients characterized by resting hypermetabolism and increased protein breakdown. Moreover, hormonal alterations related to the heart failure syndrome were related to increased protein oxidation.     

Metabolic advantages of spreading the nutrient load: effects of increased meal frequency in non-insulin-dependent diabetes.

The acute effect of increasing meal frequency as a model of slow absorption was studied for 1 d in 11 patients with non-insulin-dependent diabetes. On 1 d they took 13 snacks (the nibbling diet) and on another day the same diet was taken as three meals and one snack (the three-meal diet). The nibbling diet reduced mean blood glucose, serum insulin, and C peptide concentrations over the 9.5 h of observation and 24-h urinary C peptide output by 12.7 +/- 3.7% (mean +/- SE) (P = 0.0062), 20.1 +/- 5.8% (P = 0.0108), 9.2 +/- 2.6% (P = 0.0073), and 20.37 +/- 8.12% (P = 0.039), respectively, compared with the three-meal diet. Serum triglyceride concentrations were lower by 8.5 +/- 3.2% (P = 0.037). Despite lower insulin concentrations on the nibbling diet, the concentrations of free fatty acids, 3-hydroxybutyrate, and the insulin-sensitive branched-chain amino acids responded similarly on both treatments. Metabolic benefits seen with increased meal frequency may explain the success of similar agents that prolong absorption, including fiber and enzyme inhibitors.     

Response of muscle protein and glutamine kinetics to branched-chain-enriched amino acids in intensive care patients after radical cancer surgery

OBJECTIVE: Patients with cancer are characterized by decreased muscle protein synthesis and glutamine availability that contribute to an impaired immune response. These abnormalities worsen after surgical stress. We tested the hypothesis that pharmacologic doses of branched-chain amino acids would improve the early metabolic response after major cancer surgery. METHODS: By using a crossover experimental design, we compared the metabolic effects of isonitrogenous solutions of balanced and branched-chain-enriched amino acid mixtures infused at the rate of 82 mg x h(-1) x kg(-1) for 3 h in patients with colorectal or cervical cancer on the first and second days after radical surgery combined with intraoperative radiation therapy. The ratios of leucine to total amino acid (grams) in the two mixtures were 0.09 and 0.22, respectively. Muscle protein and glutamine kinetics were determined by using stable isotope of amino acids and the leg arteriovenous balance technique. Glucose and insulin were continuously infused throughout the 2-d study to maintain near euglycemia. RESULTS: Rates of muscle protein synthesis and degradation were not significantly affected by the balanced amino acid infusion. In contrast, the isonitrogenous, branched-chain-enriched amino acid mixture accelerated muscle protein turnover by stimulating (P 相似文献   

Energy metabolism and substrate oxidation in patients with Crohn's disease

Weight loss and malnutrition are common features in patients with Crohn's disease. This study was designed to evaluate diet-induced thermogenesis and substrate oxidation in patients with Crohn's disease. Twenty-three patients (17 women, 6 men; age 34 +/- 2 y) and 17 healthy control subjects (13 women, 4 men; age 36 +/- 3 y) were studied. Resting energy expenditure and fasting substrate oxidation were measured by indirect calorimetry in the morning after an overnight fast. After a standard homogenized test meal (10 kcal/kg), indirect calorimetry was performed every 30 min for 3 h to measure the diet-induced thermogenesis and the postprandial substrate oxidation. In the fasting state, resting energy expenditure was significantly higher in patients than in control subjects (1433 +/- 43 versus 1279 +/- 53 kcal/24 h). Lipid oxidation was higher in patients with Crohn's disease than in control subjects (1.17 +/- 0. 07 versus 0.61 +/- 0.11 mg. kg(-1). min(-1), P < 0.01). Postprandially, diet-induced thermogenesis was significantly lower in patients with Crohn's disease than in control subjects (4.6% +/- 0.5 versus 6.3% +/- 0.5 of energy intake, P < 0.01). Lipid oxidation was significantly higher in patients with Crohn's disease than in control subjects (0.78 +/- 0.05 versus 0.56 +/- 0.08 mg. kg(-1). min(-1), P < 0.05), and glucose oxidation was lower in patients with Crohn's disease than in control subjects. In patients with Crohn's disease, lipid oxidation positively correlates with the disease activity evaluated by the Crohn's Disease Activity Index (r = 0.48, P150), fasting and postprandial lipid oxidation was significantly higher than in patients with inactive Crohn's disease (P < 0.05). In conclusion, patients with Crohn's disease have increased fat oxidation, which correlates with disease activity and this may explain the reduced fat stores in patients with Crohn's disease.     

Resting metabolic rate in chronic renal failure.

OBJECTIVE: A decrease in resting metabolic rate (RMR) in patients with chronic renal failure was assumed to occur because of the decreasing oxygen consumption of the kidneys, which in healthy subjects, accounts for 7.2% of RMR. Contrary to this assumption, RMR per body weight in end-stage renal disease was increased. DESIGN AND METHODS: To test the impact of chronic renal failure on the RMR, direct bedside calorimetry was performed on 51 outpatients (age, 53.2 +/- 13.9 y; creatinine clearance, 6.9 to 52 mL/min). Twenty two of 51 patients were examined repeatedly (at the start of the study, after 3 months, and after 6 months) during declining kidney function. RESULTS: In the total group, RMR per body weight (RMR/BW) was 100.0 +/- 4.96 kJ/kg/day and RMR per body surface area (RMR/BSA) was 4.582 +/- 0.181 kJ/min/1.73m(2). RMR/BW and RMR/BSA correlated significantly with creatinine clearance (n = 51, r = -.763, P <.001; n = 51, r = -.557, P <.001). In the follow-up group, creatinine clearance decreased from 27.5 +/- 9.5 mL/min initially, to 19.4 +/- 6.25 mL/min at 3 months, to 13.0 +/- 3.8 mL/min at 6 months (P <.001), while RMR/BW and RMR/BSA increased from 98.28 +/- 6.3, to 101.64 +/- 5.46, to 105.42 +/- 6.3 kJ/kg BW/d (P <.005), respectively, and 4.41 +/- 0.126, to 4.578 +/- 0.168, to 4.704 +/- 0.168 kJ/min/1.73 m(2) (P <.05), respectively. CONCLUSION: Taking into account the reduced oxygen consumption of the shrinking kidneys, the normal RMR suggests an increased energy expenditure per body cell mass. The raising RMR in deteriorating excretory kidney function reflects the increasing energy expenditure in progressive chronic renal failure.     

Total energy expenditure, body fatness, and physical activity in children aged 6-9 y

BACKGROUND: The recent worldwide increase in the prevalence of childhood obesity may be due in part to a decrease in children's physical activity levels. OBJECTIVE: The current study of children in the years just before puberty aimed to 1) measure total energy expenditure (TEE) by use of the doubly labeled water (DLW) method, 2) determine the proportion of TEE related to physical activity, 3) investigate the relations between measures of physical activity and body fatness, and 4) investigate possible sex differences in these relations. DESIGN: The DLW technique was used to measure TEE over 10 d in 106 healthy children (52 boys) aged 7.8 +/- 0.9 y (x +/- SD). Fat-free mass, and hence fat mass, was derived from the (18)O dilution space. Resting energy expenditure (REE) was calculated with use of the Schofield equations. Physical activity level was calculated as TEE/REE. RESULTS: Mean TEE in both boys (7871 +/- 1135 kJ/d) and girls (7512 +/- 1195 kJ/d) was significantly different (P < 0.0001) from FAO/WHO/UNU recommendations (13% and 9% lower, respectively). There was no significant difference in physical activity level between boys (1.69 +/- 0.22) and girls (1.71 +/- 0.23). In boys but not girls, physical activity level was inversely correlated with BMI (r = -0.37, P < 0.01), fat mass (r = -0.46, P < 0.005), and percentage of body fat (r = -0.50, P < 0.0001). CONCLUSIONS: In boys but not girls, percentage of body fat is inversely associated with physical activity level. Physical activity is one factor contributing to body fatness in boys, but additional factors may influence the size of the fat stores in girls.     

Radionuclide ventriculography in severely underweight anorexia nervosa patients before and during refeeding therapy

Congestive heart failure is a well-recognized complication of refeeding therapy in underweight patients with anorexia nervosa but there are few data describing cardiac function during the critical refeeding period. This prospective study examined left ventricular function with conventional electrocardiographic-gated radionuclide ventriculography (RVG) in severely underweight anorexia nervosa patients both before and during refeeding therapy. Eight patients underwent rest and exercise RVG at admission and after regaining approximately 5% to 10% of their ideal body weight. With the admission study serving as a control, the left ventricular ejection fraction and regional wall motion analysis were analyzed before and after refeeding and weight gain. Resting left ventricular ejection fractions were not significantly different between the first and second RVGs (64 +/- 11% vs. 62 +/- 8%, respectively; P greater than .05). Likewise, the left ventricular ejection fraction with maximal exercise did not significantly differ when comparing the first or the second RVG (74 +/- 10% vs. 72 +/- 8%, P greater than .05). During the baseline RVG, the left ventricular ejection fraction increased from 64 +/- 11% (rest) to 74 +/- 10% (maximal exercise) (P less than .001). During the second RVG, the ejection fraction increased from 62 +/- 8% (rest) to 72 +/- 8% (maximal exercise) (P = .003). However, the left ventricular exercise ejection fraction in the second RVG in one patient increased only by one absolute percentage point. Four of the eight patients had regional wall motion abnormalities detected during resting and/or exercise RVG. Abnormal cardiac function occurs in asymptomatic patients with anorexia nervosa undergoing refeeding therapy.     

Total daily energy expenditure in wasted chronic obstructive pulmonary disease patients

OBJECTIVES: To investigate total daily energy expenditure in chronic obstructive pulmonary disease (COPD) patients during a rehabilitation programme. DESIGN: Observational study involving a case and a control group. SUBJECTS: Ten COPD patients (six with body mass index (BMI) <18.5 kg/m(2) and four with BMI >18.5 kg/m(2)) were evaluated for their energy expenditure profile. Four additional healthy age-matched volunteers were also included for methodology evaluation. INTERVENTIONS: Measurements of total daily energy expenditure (TEE), resting energy expenditure (REE) and diet-induced thermogenesis (DIT) and energy intake were undertaken by indirect calorimetry and bicarbonate-urea methods and dietary records. RESULTS: REE in COPD patients was not significantly different from that predicted by the Harris-Benedict equation. Before the exercise day the mean TEE was 1508 kcal/day and physical activity level (PAL as calculated by TEE/REE) was 1.52. On the exercise day the TEE increased to 1568 kcal/day and PAL was 1.60, but neither of these changes were significant. The energy cost of increased physical activity during rehabilitation exercise was estimated to be 191 kcal/day. No significant change was found in DIT between the two patient groups. However, overall energy balances were found to be negative (-363 kcal/day). CONCLUSION: The rehabilitation programme did not cause a significant energy demand in COPD patients. TEE in COPD patients was not greater than in free-living healthy subjects. Patients, who were underweight, did not have a higher TEE than patients with normal weight. This suggested that malnutrition in COPD patients was not due to an increased energy expenditure. On the other hand, a significant negative energy balance due to insufficient energy intake was found in seven out of 10 patients.     

机械通气的外科危重症患者静息能量消耗评价

目的比较机械通气的外科危重症患者测定的静息能耗(MREE)与校正Harris-Benedict公式计算的静息能耗(CREE)之间的差异,评估静息能耗与疾病严重程度的相关性.方法选取2008年8月至2010年2月符合入选标准的外科危重症患者21例.收集患者相关数据,计算急性生理与既往健康状况评分(APACHEⅡ评分)和器官功能不全评分(Marshall评分).采用美国MedGraphics CCM/D系统间接能耗测量仪测定MREE,采用校正Harris-Benedict公式计算CREE.结果营养支持1周内,21例患者的平均CREE明显高于平均MREE[(8305.09±1392.76)kJ比(6544.84±2079.65) kJ,P=0.000].营养支持当日和第1、2(P均=0.000)、4天(P =0.003)的CREE明显高于MREE.CREE与MREE之间无相关性(r=0.064,P=0.408),MREE与APACHEⅡ评分也无相关性(r=-0.045,P=0.563).MREE与Marshall评分有相关性(P =0.001),但相关系数较低(r=0.263).结论基于病情校正的Harris-Benedict公式明显高估了外科危重症患者的能耗水平,间接能耗仪测定的静息能耗更为准确.     

Resting and total energy expenditure in patients with inflammatory bowel disease

Patients with inflammatory bowel disease often present with weight loss. Among possible causes, an elevated energy expenditure has frequently been suggested but is the least documented. In this study resting metabolic rate (RMR) and total daily energy expenditure (TDEE) were measured in 15 outpatients with inflammatory bowel diseases and in eight healthy control subjects. Measured RMR as a percentage of that predicted from fat-free mass was not significantly different for control subjects (102 +/- 9.8%, mean +/- SD) and patients (100 +/- 13.3%). TDEE, expressed as a multiple of RMR, was 1.70 +/- 0.31 for control subjects and 1.78 +/- 0.24 for patients. When patients were subgrouped as greater than or equal to 90% or less than 90% desirable body weight, a mean increase over RMR predicted from fat-free mass was seen in the underweight patients (106 +/- 9.3%) but not in normal-weight patients (99.0 +/- 15.6%). Mean TDEE/RMR values for the patient subgroups were 1.70 +/- 0.30 and 1.88 +/- 0.08, respectively. We conclude that stable outpatients with inflammatory bowel disease have only a minimal increase in energy needs.     

Circulating ghrelin in patients with chronic obstructive pulmonary disease

OBJECTIVE: Unexplained weight loss is common in patients with chronic obstructive pulmonary disease (COPD). Because ghrelin plays an important role in energy homeostasis, this study investigated the plasma level of ghrelin in COPD. METHODS: Plasma ghrelin levels and levels of leptin, tumor necrosis factor-alpha, and C-reactive protein were measured in 29 patients with COPD and 17 healthy controls. Body composition was assessed with bioelectrical impedance analysis. RESULTS: Body mass index and percentage of body fat were lower in patients who had COPD than in healthy controls. Plasma ghrelin and leptin concentrations were significantly lower in patients who had COPD than in healthy controls (ghrelin: 0.25+/-0.22 ng/mL versus 0.43+/-0.24 ng/mL, P=0.013; leptin: 1.77+/-0.70 ng/mL versus 2.85+/-0.96 ng/mL, P=0.000). In contrast, tumor necrosis factor-alpha and C-reactive protein were significantly higher in those with COPD than in controls. Plasma ghrelin (log transformed) was positively correlated with body mass index and percentage of body fat in patients with COPD but negatively correlated in control subjects. Plasma ghrelin was negatively correlated with tumor necrosis factor-alpha and C-reactive protein in COPD. CONCLUSION: Plasma ghrelin level was decreased in COPD and this is different from other weight-loss diseases. These data suggest that decreased ghrelin and other factors may contribute to alterations in metabolic status during inflammatory stress in this disease.