Relationship of resting energy expenditure with liver function and nutritional status in patients with alcoholic cirrhosis.

Resting energy expenditures (REEs) were measured in 40 alcoholic cirrhotic (AC) patients by indirect calorimetry and corrected for 24-h urinary creatinine and excretion. These REEs were compared according to the stage of severity of the cirrhosis, the nutritional status, and the presence or absence of alcoholic hepatitis (AH). Mean REE was not significantly different between the Child class A, B, and C patients, even when corrected for 24-h urinary creatinine. Mean REE was significantly less in malnourished AC than in well-nourished patients (1308 +/- 285 vs. 1531 +/- 255 kcal, p less than 0.02). However, when measured energy expenditure was corrected for 24-h urinary creatinine, the difference between the two groups of patients disappeared (1800 +/- 540 kcal/g creatinine in malnourished patients vs. 1890 +/- 780 kcal/g creatinine in well-nourished patients). Finally, there was no significant difference between the REE, corrected or not, for the 24-h urinary creatinine in AC with or without AH. Thus, when REE is normalized to lean body mass, represented by 24-h urinary creatinine, the metabolic activity in AC is not dependent on the severity of the cirrhosis, nutritional status, or existence of AH.     

Resting energy expenditure and nutritional state in patients with liver cirrhosis before and after liver transplantation

Resting energy expenditure (REE), body composition, and the biochemical parameters of liver function were measured in 26 patients before and 432 days (range: 103-1022 days) after liver transplantation (LTX). PreLTX REE was variable (mean: 1638 +/- 308 kcal/day, range: 1220-2190 kcal/day or +10 +/- 11% of Harris Benedict = HB prediction, range: -19 - +33%) and was closely related to body cell mass (r = 0.66, p < 0.0003). PostLTX REE was variable (mean: 1612 +/- 358 kcal/day, range: 1010-2490 kcal/day or +5 +/- 15% of HB prediction, range: -20 - +37%) and was closely related to body cell mass (r = 0.65, p < 0.0006). When compared with preLTX values only small changes in mean REE (-71 +/- 43 kcal/day) and a close correlation between pre and postLTX REE (r = 0.82, p < 0.001) were observed. In contrast to REE, changes in body weight were highly variable (-16.5 - +32.7 kg/year). This variance was not explained by the number of postoperative complications, pre and postLTX liver function, possible graft rejection and/or hepatitis reinfection. Pre-operative hypermetabolism (i.e. REE >+20% of HB prediction) was associated with postoperative hypermetabolism and a reduced liver function before and after LTX. Hypermetabolic patients had a poorer nutritional outcome after LTX (weight change: 0 +/- 8.4 kg/year) when compared with normometabolic controls (weight change: +5.7 +/- 7.4 kg/year; p < 0.05). There was no significant association between deviations in pre and postLTX REE and changes in body weight. When corrected for changes in the nutritional state our data provide evidence for the persistence of resting energy expenditure in liver transplant patients.     

Body composition and energy expenditure in Duchenne muscular dystrophy

OBJECTIVE: To investigate the relationship between resting energy expenditure (REE) and body composition in Duchenne Muscular Dystrophy (DMD). DESIGN: An observational study. SETTING: University Research Centre. SUBJECTS: Nine Duchenne children (age range 6-12 y), mean relative weight 128%, agreed to undergo the investigation and all of them completed the study; INTERVENTIONS: Assessment of body composition (total body fat and skeletal muscle mass) by magnetic resonance imaging and resting energy expenditure by indirect calorimetry. MAIN OUTCOME MEASURES: Fat mass (FM; kg and percentage weight), fat-free mass (FFM; kg and percentage weight), muscle mass (kg and percentage weight), resting energy expenditure (kJ/kg body weight and kJ/kg fat-free mass). RESULTS:: In Duchenne children fat mass averages 32% and total skeletal muscle mass 20% of body weight. Resting energy expenditure per kg of body weight falls within the normal range for children of the same age range, while when expressed per kg of FFM is significantly higher than reference values. No relationship was found between REE and total skeletal muscle mass. CONCLUSIONS: Our results do not demonstrate a low REE in DMD boys; on the contrary REE per kg of FFM is higher than normal, probably due to the altered FFM composition. We suggest that the development of obesity in DMD children is not primarily due to a low REE but to other causes such as a reduction in physical activity and or overfeeding.     

Assessment of energy expenditure by indirect calorimetry in healthy subjects and patients with liver cirrhosis

The reliability of resting energy expenditure (REE) measurements by indirect calorimetry with a ventilated hood was investigated in 50 healthy controls and 10 patients with liver cirrhosis. In each subject basal energy expenditure (BEE) was determined once and REE three times (morning REE1, noon REE2, afternoon REE3). In controls and patients the first 5-minute BEE and first 5-minute REE (controls also second 5-minute REE) were higher than in the remainder of the 30-minute recording. Only the last 20 minutes of recordings were used to calculate BEE (1645 +/- 315, mean +/- SD, in kilocalories per day), REE1 (1880 +/- 365), REE2 (1782 +/- 384), and REE3 (1775 +/- 316) in controls, and in cirrhotics: BEE (1530 +/- 235), REE1 (1714 +/- 267), REE2 (1715 +/- 238), and REE3 (1779 +/- 275). REE was higher than BEE in controls and cirrhotics (p less than 0.05). The REE variation coefficient was 5 +/- 3% in controls and 5 +/- 2% in cirrhotics. No systematic difference between REE1, REE2, and REE3 was found. Energy expenditure predicted by the Harris-Benedict equation differed up to 21% from measured BEE in individual controls; group mean BEE, however, was correctly predicted. In cirrhotics differences between measured and predicted BEE up to 26% occurred, while measured BEE was higher than predicted BEE (p = 0.06). It is concluded that REE can be reliably assessed by indirect calorimetry with a ventilated hood system in controls and patients at any time of the day, when values obtained in the first 10 minutes are deleted.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Resting energy expenditure in diabetic and nondiabetic patients with liver cirrhosis: relation with insulin sensitivity and effect of liver transplantation and immunosuppressive therapy

BACKGROUND: Hypermetabolism, insulin resistance, and diabetes are common in patients with liver cirrhosis. OBJECTIVE: We assessed whether diabetes and insulin resistance influence postabsorptive energy homeostasis in these patients and whether liver transplantation (LTx) and immunosuppressive drugs affect these relations. DESIGN: Twenty-six patients with liver cirrhosis (16 with and 10 without diabetes) were studied with an insulin clamp and indirect calorimetry. Eleven of these subjects were studied 9 mo after LTx to longitudinally assess its effects. To cross-sectionally explore a longer follow-up period, we studied 65 patients 6, 14, and 32 mo after LTx. Seven patients with chronic uveitis (receiving immunosuppressive therapy) and 20 healthy subjects served as control subjects. RESULTS: Diabetic and nondiabetic patients with cirrhosis had insulin resistance (S(I(clamp)); P < 0.03) and higher measured resting energy expenditure (REE) as a percentage of predicted REE than did healthy subjects (107.6 +/- 1.8% compared with 97.4 +/- 2.3%; P < 0.03), and these 2 alterations were associated (R(2) = 0.119, P = 0.0002). The longitudinal study showed an improvement in the 2 variables after LTx, but full restoration was not achieved. The cross-sectional analysis confirmed this observation in patients studied 6 mo (n = 28) after LTx. In patients studied 14 (n = 21) and 32 mo (n = 16) after LTx, S(I(clamp)) and measured REE as a percentage of predicted REE were not significantly different from those in control subjects. CONCLUSIONS: In patients with liver cirrhosis, higher-than-normal postabsorptive REE was associated with insulin resistance regardless of diabetes. This abnormality persisted in patients studied 6-9 mo after LTx but improved simultaneously with the improvement in insulin sensitivity thereafter.     

Body composition and energy expenditure after weight loss following bariatric surgery

OBJECTIVES: To assess the effectiveness of biliopancreatic diversion (BPD) in the treatment of morbid obesity and to evaluate how the procedure affects body weight. SUBJECTS: Fourteen morbidly obese subjects studied before and 30 months after BPD and fifteen healthy volunteers matched for age, sex and height (controls). METHODS: Comparison of the following parameters were made in the study groups before surgery and 30 months after BPD and with those of the controls group: fat mass, fat-free mass, non-protein substrate oxidation, basal metabolic rate, plasma glucose, insulin and free fatty acid concentrations. RESULTS: Obese subjects lost 60.38+/-10.71 kg of weight during 18 months following surgery and then remained stable for another 12 months, when this study was performed. Weight loss was substantially due to a loss of fat mass (FM: 60.13+/-13.01 kg before and 19.02+/-8.61 kg after BPD; p<0.001). FM were not statistically different between post-obese subjects and controls; however, post-obese patients retained significantly more fat free mass (FFM) than controls. Subsequently, basal metabolic rates of post-obese subjects were higher than those of the control group (p<0.05). Fasting non-protein respiratory quotient (npRQ) was significantly lower before BPD than 30 months after the surgery (0.798+/-0.04 vs. 0.90+/-0.048, p<0.001), suggesting that, while obese, patients oxidized more lipids than carbohydrates. Moreover, fasting and two-hour plasma glucose and insulin concentrations decreased significantly after BPD to values comparable to those of the control group. CONCLUSION: Weight loss in obese patients after BPD is mainly due to lipid malabsorption, but increased energy expenditure associated with retaining a high FFM in physically active post-obese subjects may also play a role, enabling them to maintain long-term reduced body weights.     

Body size, body composition, and metabolic profile explain higher energy expenditure in overweight children

Lower relative rates of energy expenditure (EE), increased energetic efficiency, and altered fuel utilization purportedly associated with obesity have not been demonstrated indisputably in overweight children. We hypothesized that differences in energy metabolism between nonoverweight and overweight children are attributable to differences in body size and composition, circulating thyroid hormones, sympathetic nervous system, and adrenomedullary activity. A total of 836 Hispanic children, 5-19 y old, participated in 24-h calorimetry, anthropometric, and dual-energy X-ray absorptiometry measurements. Biochemistries were determined by standard techniques. Absolute total EE (TEE) and its components (sleep EE, basal EE, sedentary EE, cycling EE, walking EE, activity EE, nonexercising activity thermogenesis) were higher in overweight children (P = 0.001). Net mechanical energetic efficiency of cycling was lower in overweight children (P = 0.001). Adjusting for body size and composition accounted for differences in TEE, its components, and energetic efficiency. Net carbohydrate and fat utilization did not differ between groups. TEE was independently influenced by sex, Tanner stage, fat free mass, fat mass (FM), fasting serum nonesterified fatty acids (NEFA), leptin, free thyroxine, triiodothyronine, and 24-h urinary norepinephrine and epinephrine. Fat utilization was independently associated with age2, sex, FM, fasting serum NEFA, triacylglycerol, adiponectin, leptin, total thyroxine, and free triiodothyronine. Higher EE in overweight children was largely explained by differences in body size and composition, with minor contributions of thyroid and sympathoadrenal systems. Alterations in EE, energetic efficiency, and substrate utilization were not evident in the overweight children.     

Body composition as a determinant of energy expenditure: a synthetic review and a proposed general prediction equation

Differences in body composition have often been examined in conjunction with measurements of energy expenditure in men and women. Numerous studies during the past decade examined the relationship between resting energy expenditure (REE) and the components of a two-compartment model of composition, namely the fat-free mass (FFM) and the fat mass (FM). A synthetic review of these studies confirms a primary correlation between REE and FFM in adults over a broad range of body weights. A generalized prediction equation is proposed as REE = 370 +/- 21.6 x FFM. This equation explains 65-90% of the variation in REE. Several studies suggest, further, that FFM predicts total daily energy expenditure (TDEE) equally well. An independent contribution by FM to the prediction of either REE or TDEE is not supported for the general population, perhaps reflecting the relative constancy of the absolute FM in nonobese individuals. In the subset of obese women, FM may be a significant predictor.     

Serum leptin levels in alcoholic liver cirrhosis: relationship with gender, nutritional status, liver function and energy metabolism

OBJECTIVE: To determine serum leptin levels in alcoholic liver cirrhosis and the relationship with gender, nutritional status, liver function, energy metabolism, inflammatory state and refeeding. SUBJECTS: Thirty-seven hospitalized alcoholic cirrhotic patients (M/F: 24/13), 27 hospitalized patients at risk of malnutrition but with normal liver function (M/F: 15/12) as control patients, and 31 healthy control subjects (M/F: 17/14) participated. DESIGN: Liver function was assessed from Child-Pugh classification; anthropometric parameters and resting energy expenditure (REE) were measured; caloric intake was evaluated over 5 days; and serum leptin and insulin were assayed. The same protocol was performed after 1 month refeeding in 22 patients. Healthy subjects were studied as controls for anthropometric parameters and serum leptin levels. RESULTS: Serum leptin levels were higher in male cirrhotic patients than in the other two male groups (P=0.0079) and in the same range in the female groups. They were higher in female than in male subjects in the three groups. In female cirrhotic patients, logarithmically transformed serum leptin levels correlated significantly with fat mass (P=0.0043), insulin levels (P=0.0072), REE (P=0.0133), bilirubin levels (P<0.0001), prothrombin time (P=0.0003) and Pugh score (P=0.0266) in simple regression analysis and with insulin levels (P=0.0137), but not with fat mass (P=0.0761), Pugh score (P=0.4472) and REE (P=0.4576) in multiple regression analysis. In the male cirrhotic and control patients, log (leptin) levels correlated with CRP (C reactive protein) (r=0.365, P=0.0223). Log (leptin) levels did not correlate with caloric intake in any of the groups. Leptin levels (P<0.05) and fat mass (P<0.02) increased with refeeding while liver function improved (P<0.01). CONCLUSION: There is a gender difference in regulation of serum leptin level in alcoholic liver cirrhosis. Insulin level is the best determinant of leptin level in female patients while inflammatory state related to alcoholic hepatitis seems to have a greater influence in male patients. Although leptin levels positively correlated with REE in female patients, there is no evidence that leptin reduces caloric intake and fat stores in these patients.     

Resting energy expenditure in patients with end-stage liver disease and in normal population

Resting energy expenditure (REE) was measured in 10 patients with end-stage liver disease (ELD) and in 31 normal controls. Basal energy expenditure (BEE) was also predicted by the Harris-Benedict equation. In order to correlate REE to lean body mass, the 24-hr urinary creatinine was measured in patients with ELD and in normal controls and expressed as kcal/g urinary creatinine. Linear regression analysis showed a statistically significant (p less than 0.0001) correlation (r = 0.72) between the REE and the 24-hr urinary creatinine in normal controls, irrespective of age and sex. Mean BEE (1580 +/- 160 vs 1575 +/- 210) and REE (1755 +/- 215 vs 1800 +/- 330) were not significantly different between patients with ELD and controls. However, the mean REE was 1900 +/- 610 kcal/g creatinine in patients with ELD and 1180 +/- 260 (p less than 0.0001) in controls. When related to lean tissue, patients with ELD had increased energy expenditure, confirming the hypermetabolic state suggested on clinical grounds. The use of urine creatinine to estimate energy expenditure may be a simple clinical technique to predict dietary energy needs in malnourished, unstressed patients. When this estimated energy expenditure/g creatinine (EEE) is compared to measured energy expenditure/g creatinine in malnourished, stressed patients, the EEE provides an index of the extent of hypermetabolism.     

Prognostic value of energy metabolism in patients with viral liver cirrhosis

The effect of energy malnutrition on survival in patients with non-alcoholic viral liver cirrhosis has not been well defined. We characterized energy metabolism at study entrance and prospectively analyzed its effect on subsequent survival in cirrhotics. One hundred nine consecutive patients with viral liver cirrhosis and 22 healthy control subjects participated in the study. By indirect calorimetry after overnight bedrest and fasting, resting energy expenditure (REE) was measured and non-protein respiratory quotient (npRQ) was calculated. Survival of cirrhotics were followed for up to 8 y. Survival rate was estimated with the Kaplan-Meier method. REE at entrance was significantly higher than the predicted basal metabolic rate (BMR) in cirrhotics (P < 0.001). NpRQ was significantly lower in cirrhotics than in controls (P < 0.001). Survival rate was significantly lower in patients with low npRQ ( < 0.85) than in patients with scores above 0.85 (P < 0.01) and was significantly higher in normal metabolic patients (0.9 < REE/BMR < 1.1) than in hypometabolic (REE/BMR < 0.9) or hypermetabolic (1.1 < REE/BMR) patients (P < 0.05). The proportional hazards model showed that npRQ (relative risk = 0.0003, 95% confidence interval = 0.0000-0.0970), REE/BMR (0.0199, 0.0007-0.5652), prothrombin time, and ammonia were independent significant factors determining survival. Thus evaluation of energy metabolism can be used to predict survival in patients with viral liver cirrhosis.     

肝炎肝硬化患者肝功能检验结果的临床价值分析

目的分析肝炎肝硬化患者肝功能检验结果的临床价值。方法选择2014年1月—2015年2月收治的肝炎肝硬化患者37例作为研究组;选取同期健康体检者40例作为参照组。根据研究组患者肝功能分为A级7例,B级14例,C级16例。比较研究组和参照组及不同肝功能分级患者TBA、CHO、ALB、CHE水平。计量资料采用t检验及方差分析,两两比较采用LSD-t检验,P0.05为差异有统计学意义。结果研究组TBA、CHO、ALB、CHE分别为(48.55±30.45)μmol/L、(2.26±0.13)mmol/L、(30.22±3.14)g/L、(2 313.40±150.61)U/L,参照组分别为(5.11±2.13)μmol/L、(5.23±0.32)mmol/L、(47.12±4.22)g/L、(8 709.37±340.55)U/L,两组比较差异均有统计学意义(均P0.05)。肝功能A级患者TBA、CHO、ALB、CHE分别为(37.51±6.53)μmol/L、(3.23±1.12)mmol/L、(41.02±3.15)g/L、(3 141.37±1 032.55)U/L,B级分别为(41.35±20.43)μmol/L、(2.46±1.05)mmol/L、(32.12±2.54)g/L、(1 823.34±473.24)U/L,C级分别为(81.25±50.24)μmol/L、(2.11±0.13)mmol/L、(20.41±3.04)g/L、(1 343.23±231.21)U/L,三组比较差异均有统计学意义(均P0.05)。结论肝功能检验在肝炎肝硬化患者临床诊断中具有较高应用价值,值得推广使用。     

Relation between energy expenditure and body composition in man: specific energy expenditure in vivo of fat and fat-free tissue

The relationship between energy expenditure and body composition, in terms of fat and fat-free masses, has previously been described by a variety of predictive regression equations with parameters devoid of physiological content. We present here results obtained by calculating the specific energy expenditure, ie, the energy expenditure per unit of mass, of fat and fat-free tissue on the basis of measurements of the total energy expenditure (EE), the masses of fat (FM), and fat-free (FFM) tissue using the following simple model: EE = k1.FM + k2.FFM where k1 and k2 are the specific energy expenditures of fat and fat-free tissue, respectively. The results of observations on 104 women at rest yielded values for k1 and k2 of 0.31 and 1.35 watts/kg of fat and fat-free mass, respectively, with standard errors of estimate of 0.074 and 0.052 watts/kg, respectively. Analysis of several series of measurements, from other sources and on smaller samples of subjects, yielded similar values at rest but with larger standard errors of estimate. Data from subjects performing varying amounts of work in 24-h measurements showed, as expected, larger values for both tissues. The results explain to a very large extent the well-established relation between resting metabolic rate and body weight, ie, a linear relation with a non-zero intercept. The results also offer a clear-cut explanation for the well known difference in energy expenditure between men and women with the same body weight.