Energy Metabolism In Patients Research Articles

The Untargeted Metabolomics Reveals Differences in Energy Metabolism in Patients with Different Subtypes of Ischemic Stroke.

Ischemic stroke (IS) is the most common subtype of stroke. The risk factors and pathogenesis of IS are complex and varied due to different subtypes. Therefore, we used metabolomics technology to investigate the biomarkers and potential pathophysiological mechanisms of different subtypes of IS. We included 126 IS patients and divided them into two groups based on the TOAST classification: large-artery atherosclerosis (LAA) group (n = 87) and small-vessel occlusion (SVO) group (n = 39). Plasma metabolomics analysis was performed using liquid chromatography-high-resolution mass spectrometry (LC-HRMS) to identify metabolic profiles in LAA and SVO subtype IS patients and to determine metabolic differences between patients with the two subtypes of IS. We identified 26 differential metabolites between LAA and SVO subtype IS. A multiple prediction model based on the plasm metabolites had good predictive ability for IS subtyping (AUC = 0.822, accuracy = 77.8%), with 12,13-DHOME being the most important differential metabolite in the model. The differential metabolic pathways between the two subtypes of IS patients included tricarboxylic acid (TCA) cycle, alanine, aspartate and glutamate metabolism, and pyruvate metabolism, mainly focused on energy metabolism. 12,13-DHOME emerged as the primary discriminatory metabolite between LAA and SVO subtypes of IS. In LAA subtype IS patients, energy metabolism, encompassing pyruvate metabolism and the TCA cycle, exhibited lower activity levels when compared to patients with the SVO subtype IS. The utilization of targeted metabolomics holds the potential to improve diagnostic accuracy for distinguishing stroke subtypes.

Brain Regional Energy Metabolism in Patients with Traumatic Brain Injury: A Cerebral Microdialysis Guided Study.

In traumatic brain injuries (TBI), cerebral microdialysis (CMD)-derived parameters, especially the lactate to pyruvate ratio (LP ratio), have been utilized for cerebral perfusion optimization. The objectives were to identify cerebral ischemia as measured by CMD in TBI patients requiring decompressive craniectomy and to observe the correlation between cerebral perfusion pressure (CPP), intracranial pressure (ICP), and CMD variables in these patients. Our secondary aim was to observe the effect of CPP augmentation on ischemia biomarkers. After the Institute Ethics Committee approvals, seven adult patients requiring decompressive craniectomy following TBI were enrolled and CMD data were obtained prospectively for 72 h. CPP was augmented by 20% with noradrenaline infusion if LP ratio >40. Correlations were done with bootstrapping (n = 500) to obtain the confidence intervals (CI) due to the small sample size. One patient had cerebral ischemia (median LP ratio of 265.5 and median pyruvate of 38 μmol/L), while another patient had non-ischemic mitochondrial dysfunction (median LP ratio 40.7 and median pyruvate 278.5). The coefficients of correlation between the LP ratio with CPP and ICP were r = -0.05 (CI = -0.14-0.03) and r = 0.09 (CI = -0.03-0.24), respectively. The coefficient of correlation between cerebral and blood glucose was r = 0.38, (CI - 0.35-0.14). Only two patients needed CPP augmentation, however, postaugmentation cerebral biochemistry did not change appreciably. CMD can identify cerebral ischemia, however, no correlations were observed between the LP ratio and CPP or ICP. CPP augmentation did not improve cerebral biochemistry. More studies are required to understand and treat cerebral metabolism in TBI.

Abstract 12273: Circulating Monocyte Mitochondrial Function Reflects Myocardial Oxidative Metabolism in Humans With Heart Failure

Introduction: We previously showed that mitochondrial function in circulating monocytes is abnormal in humans with heart failure (HF) compared to normal controls, and that it correlates to cardiomyocyte mitochondrial function in dogs with HF. But, there is no data in humans supporting a relationship between monocyte mitochondrial function and cardiac energy metabolism. Hypothesis: To test the association of circulating monocyte mitochondrial function metrics with myocardial energy metabolism in patients with HF and reduced left ventricular (LV) ejection fraction (HFrEF) quantified using C 11 acetate PET imaging. Methods: We studied 10 patients with stable HFrEF that underwent the PET imaging. Region of interest analysis was used to yield time-activity curves that represent multiple LV myocardial regions. The early phase of tracer washout curves were fitted mono-exponentially to obtain the constant Kmono (a measure of oxidative metabolism). Peripheral blood monocytes were isolated and mitochondrial function was quantified using SEAHORSE. We tested the correlation of mitochondrial metrics with Kmono, adjusted for mechanical energetic output of the heart (calculated as stroke volume index*mean BP*heartrate). Results: Among the 10 patients (aged 57-74), 3 were women, 4 self-identified as Black, and 4 had ischemic etiology. Mean EF was 35% (range 18-45%), mean systolic BP was 126 (range 100-147), and mean Kmono was 0.054 (range 0.038-0.102). Results are summarized in the table. After accounting for variation in mechanical cardiac work, we found significant positive correlations of each mitochondrial metric with Kmono. Conclusions: We find that mitochondrial function in circulating blood monocytes may be a biomarker of cardiac oxidative metabolism and cardiomyocyte mitochondrial function. If validated as a non-invasive measure of cardiac energetics, this could accelerate research in cardiac energy deprivation and its relationship to HF progression.

Magnetic Resonance Spectroscopy Studies of Brain Energy Metabolism in Schizophrenia: Progression from Prodrome to Chronic Psychosis.

Schizophrenia (SZ) is a debilitating mental illness; existing treatments are partially effective and associated with significant side effect burden, largely due to our limited understanding of disease mechanisms and the trajectory of disease progression. Accumulating evidence suggests that metabolic changes associated with glucose metabolism, mitochondrial dysfunction, and redox imbalance play an important role in the pathophysiology of schizophrenia. However, the molecular mechanisms associated with these abnormalities in the brains of schizophrenia patients and the ways in which they change over time remain unclear. This paper aims to review the current literature on molecular mechanisms and in vivo magnetic resonance spectroscopy (MRS) studies of impaired energy metabolism in patients at clinical high risk for psychosis, with first-episode SZ, and with chronic SZ. Our review covers research related to high-energy phosphate metabolism, lactate, intracellular pH, redox ratio, and the antioxidant glutathione. Both first-episode and chronic SZ patients display a significant reduction in creatine kinase reaction activity and redox (NAD + /NADH) ratio in the prefrontal cortex. Chronic, but not first-episode, SZ patients also show a trend toward increased lactate levels and decreased pH value. These findings suggest a progressive shift from oxidative phosphorylation to glycolysis for energy production over the course of SZ, which is associated with redox imbalance and mitochondrial dysfunction. Accumulating evidence indicates that aberrant brain energy metabolism associated with mitochondrial dysfunction and redox imbalance plays a critical role in SZ and will be a promising target for future treatments.

Chronic Kidney Disease is Associated With Attenuated Plasma Metabolome Response to Oral Glucose Tolerance Testing

Chronic kidney disease (CKD) is associated with decreased anabolic response to insulin contributing to protein-energy wasting. Targeted metabolic profiling of oral glucose tolerance testing (OGTT) may help identify metabolic pathways contributing to disruptions to insulin response in CKD. Using targeted metabolic profiling, we studied the plasma metabolome response in 41 moderate-to-severe nondiabetic CKD patients and 20 healthy controls at fasting and 2hours after an oral glucose load. We used linear mixed modeling with random intercepts, adjusting for age, gender, race/ethnicity, body weight, and batch to assess heterogeneity in response to OGTT by CKD status. Mean estimated glomerular filtration rate among CKD participants was 38.9±12.7mL/min per 1.73m2 compared to 87.2±17.7mL/min per 1.73m2 among controls. Glucose ingestion induced an anabolic response resulting in increased glycolysis products and a reduction in a wide range of metabolites including amino acids, tricarboxylic acid cycle intermediates, and purine nucleotides compared to fasting. Participants with CKD demonstrated a blunted anabolic response to OGTT evidenced by significant changes in 13 metabolites compared to controls. The attenuated metabolome response predominant involved mitochondrial energy metabolism, vitamin B family, and purine nucleotides. Compared to controls, CKD participants had elevated lactate:pyruvate (L:P) ratio and decreased guanosine diphosphate:guanosine triphosphate ratio during OGTT. Metabolic profiling of OGTT response suggests a broad disruption of mitochondrial energy metabolism in CKD patients. These findings motivate further investigation into the impact of insulin sensitizers and mitochondrial targeted therapeutics on energy metabolism in patients with nondiabetic CKD.

Analysis of Resting Energy Consumption and Its Influencing Factors in Stroke Patients with Severe Neurological Diseases: A Retrospective Clinical Study

Background: This study aimed to observe the changes of resting energy metabolism in patients with severe neurological diseases, and to explore the effects of tracheostomy status, stroke severity, and complications on resting energy expenditure (REE) and respiratory quotient (RQ). Methods: A retrospective study was conducted in 105 patients with neurological rehabilitation who were hospitalized in the Rehabilitation Department of the Affiliated Jiangning Hospital of Nanjing Medical University from August 2018 to October 2021. REE was measured by Italian Cosmed k4b² indirectly, and white blood cell count and C-reactive protein (CRP) were collected. Results: Among the 105 patients, there were 18 cases of mild stroke, 45 cases of moderate stroke, and 42 cases of severe stroke. The difference between predicted REE and actual REE among different degrees of stroke patients was statistically significant (p < 0.05); there was no significant difference in RQ values among different degrees of stroke patients (p > 0.05). Hemoglobin, albumin, and body mass index were significantly and positively correlated with predicted REE and actual REE, while CRP was significantly negatively correlated with predicted REE and actual REE. There was no significant difference in predicted REE, actual REE, and RQ between renal insufficiency, type 2 diabetes mellitus, and chronic obstructive pulmonary disease (p > 0.05). The CRP level could affect the REE of stroke patients. Conclusion: Metabolic vehicle assay has a certain clinical value in accurately evaluating the metabolic needs and feeding level of patients.

Зміни показників енергетичного та ліпідного обміну в пацієнтів на гострий інфаркт міокарда та цукровий діабет 2 типу

The purpose of the study was to examine the indicators of lipid and energy metabolism in patients with acute myocardial infarction in the presence or absence of type 2 diabetes mellitus. Materials and methods. A total of 134 patients with acute ST-segment elevation myocardial infarction in the presence or absence of type 2 diabetes mellitus aged 58.97 ± 7.92 years were examined on the basis of the Intensive Care Department at the Government Institution “L. T. Malaya Therapy National Institute of the National Academy of Medical Sciences of Ukraine” and the Kharkiv Railway Clinical Hospital No. 1 of the branch “Center of Healthcare” of Public Joint Stock Company “Ukrainian Railway”. Group 1 consisted of 74 patients with acute myocardial infarction and type 2 diabetes mellitus aged 59.42 ± 7.66 years. Group 2 (comparison group) included 60 patients with acute myocardial infarction without type 2 diabetes mellitus aged 58.42 ± 8.25 years. The control group comprised of 20 healthy individuals. All the patients of groups 1 and 2 underwent percutaneous coronary intervention. The study was conducted from September 1, 2018 to December 31, 2020. Serum concentration of adropin and irisin in patients was determined by enzyme-linked immunosorbent assay. Total cholesterol and high-density lipoprotein cholesterol in serum were measured by peroxidase enzymatic method. Triglyceride levels were analyzed by enzymatic colorimetric method. The atherogenic index was calculated by A. M. Klimov formula. Very low-density lipoprotein cholesterol and low-density lipoprotein cholesterol levels were estimated by the Friedewald formula. Results and discussion. Group 1 patients were found to have higher serum triglyceride levels compared with group 2 patients (p&lt;0.05). In groups 1 and 2, total cholesterol and low-density lipoprotein cholesterol levels presented an upward tendency (p˃0.05), and very low-density lipoprotein cholesterol levels were significantly by 4.04 and 2.92 times increased, respectively, as compared to the control group (p&lt;0.05). The serum adropin levels were significantly lower in patients with acute myocardial infarction and type 2 diabetes mellitus in comparison to those in patients with acute myocardial infarction without type 2 diabetes mellitus (p&lt;0.05). There was a significant decrease in the concentrations of adropin and irisin in both groups compared with the control group (p&lt;0.05). Conclusion. Characteristics of changes in adropin and irisin levels suggest an energy homeostasis imbalance in acute myocardial infarction in the presence or absence of type 2 diabetes mellitus that may significantly increase the risk of cardiovascular complications of acute myocardial infarction in this category of patients. The relationship between adropin, irisin and lipid profile may indicate the influence of these markers on lipid metabolism

Metabolic profiling analysis for clinical urine of colorectal cancer.

To demonstrate the little-known metabolic changes and pathways in patients with colorectal cancer (CRC). We used gas chromatography time-of-flight mass spectrometry (GC-TOF/MS) to perform metabolic profiling of urine samples from 163 consecutive patients with CRC and 111 healthy controls without history of gastrointestinal tumors. The metabolic profiles were assayed using multivariate statistical analysis and one-way analysis of variance, and further analyzed to identify potential marker metabolites related to CRC. The GC-TOF/MS-derived models showed clear discriminations in metabolic profiles between the CRC group and healthy control group. We demonstrated that 15 metabolites contributed to the differences. Among them, eleven metabolites were significantly upregulated, while other four metabolites were downregulated in the urine samples of CRC patients compared with healthy controls. Pathway analysis revealed changes in energy metabolism of patients with CRC, which are reflected in the upregulation of glycolysis and amino acid metabolism and the downregulation of lipid metabolism. Our study revealed the metabolic profile of urine from CRC patients and indicated that GC-TOF/MS-based methods can distinguish CRC from healthy controls. GC-TOF/MS-based metabolomics has the potential to be developed into a novel, non-invasive, and painless clinical tool for CRC diagnosis, and may contribute to an improved understanding of disease mechanisms.

Effects of the SGLT2 Inhibitor Dapagliflozin on Energy Metabolism in Patients With Type 2 Diabetes: A Randomized, Double-Blind Crossover Trial.

SGTL2 inhibitors increase urinary glucose excretion and have beneficial effects on cardiovascular and renal outcomes. The underlying mechanism may involve caloric restriction-like metabolic effects due to urinary glucose loss. We investigated the effects of dapagliflozin on 24-h energy metabolism and insulin sensitivity in patients with type 2 diabetes. There were 26 patients with type 2 diabetes randomized to a 5-week double-blind, crossover study with a 6- to 8-week washout. Indirect calorimetry was used to measure 24-h energy metabolism and the respiratory exchange ratio (RER), both by whole-room calorimetry and by ventilated hood during a two-step euglycemic-hyperinsulinemic clamp. Results are presented as the differences in least squares mean (95% CI) between treatments. Evaluable patients (n = 24) had a mean (SD) age of 64.2 (4.6) years, BMI of 28.1 (2.4) kg/m2, and HbA1c of 6.9% (0.7) (51.7 [6.8] mmol/mol). Rate of glucose disappearance was unaffected by dapagliflozin, whereas fasting endogenous glucose production (EGP) increased by dapagliflozin (+2.27 [1.39, 3.14] μmol/kg/min, P < 0.0001). Insulin-induced suppression of EGP (-1.71 [-2.75, -0.63] μmol/kg/min, P = 0.0036) and plasma free fatty acids (-21.93% [-39.31, -4.54], P = 0.016) was greater with dapagliflozin. Twenty-four-hour energy expenditure (-0.11 [-0.24, 0.03] MJ/day) remained unaffected by dapagliflozin, but dapagliflozin reduced the RER during daytime and nighttime, resulting in an increased day-to-nighttime difference in the RER (-0.010 [-0.017, -0.002], P = 0.016). Dapagliflozin treatment resulted in a negative 24-h energy and fat balance (-20.51 [-27.90, -13.12] g/day). Dapagliflozin treatment for 5 weeks resulted in major adjustments of metabolism mimicking caloric restriction, increased fat oxidation, improved hepatic and adipose insulin sensitivity, and improved 24-h energy metabolism.

Dysfunctional energy metabolisms in fibromyalgia compared with healthy subjects.

This study aimed to investigate the levels of creatine (Cr) metabolites in the anterior cingulate cortex (ACC), thalamus, and insula of patients with fibromyalgia (FM) using proton magnetic resonance spectroscopy (MRS). The levels of Cr and phosphocreatine (PCr) relative to total Cr (tCr), which includes Cr and PCr, in the ACC, thalamus, and insula were determined using MRS in 12 patients with FM and in 13 healthy controls. The FM group had lower levels of PCr/tCr in the ACC and right insula compared to healthy controls. There was a negative correlation between Cr/tCr in the ACC and total pain levels (McGill Pain Questionnaire-Total; r = −0.579, p = 0.049) and between Cr/tCr in the left insula and affective pain levels (McGill Pain Questionnaire-Affective; r = −0.638, p = 0.047) in patients with FM. In addition, there were negative correlations between stress levels (Stress Response Inventory) and Cr/tCr in the right (r = −0.780, p = 0.005) and left thalamus (r = −0.740, p = 0.006), as well as in the right insula (r = −0.631, p = 0.028) in patients with FM. There were negative correlations between symptom levels of post-traumatic stress disorder (PTSD; PTSD checklist) and Cr/tCr in the right (r = −0.783, p = 0.004) and left thalamus (r = −0.642, p = 0.024) of patients with FM. These findings are paramount to understanding the decisive pathologies related to brain energy metabolism in patients with FM.

Distinct effects of carbohydrate ingestion timing on glucose fluctuation and energy metabolism in patients with type 2 diabetes: a randomized controlled study.

This randomized, open-label, and parallel-group study aimed to investigate the effects of altering the timing of carbohydrate intake at breakfast or dinner on blood glucose fluctuations and energy metabolism. A total of 43 participants with type 2 diabetes were assigned to either the breakfast or dinner group. Participants were provided an isocaloric carbohydrate-restricted diet constituting 10% carbohydrate only at breakfast or dinner for 2 days during the study. Glucose fluctuations were compared using a continuous glucose monitoring system (iPro2) and body composition, energy expenditure, blood biochemistry, and endocrine function changes. The carbohydrate restriction either at breakfast or dinner significantly decreased postprandial glucose excursion and mean 24-h blood glucose levels. The incremental blood glucose area under the curve (AUC) for 2 h (iAUC0-2h) at lunch significantly increased in the breakfast group, whereas no significant differences were observed in the iAUC0-2h between breakfast and lunch in the dinner group. Carbohydrate restriction reduced diet-induced thermogenesis at breakfast (intragroup comparison; 223 ± 117 to 109 ± 104 kcal, p = 0.002) but did not affect diet-induced thermogenesis at dinner. However, fasting plasma free fatty acids were comparable in both groups, prelunch free fatty acids increased significantly only in the breakfast group (0.20 ± 0.09 to 0.63 ± 0.19 mEq/L, p < 0.001). Carbohydrate restriction in the diet once daily decreases mean 24-h blood glucose levels and exerts unique metabolic effects depending on the timing.

Role of Mitochondrial Dysfunction in the Pathology of Amyloid-β.

Mitochondrial dysfunction has been widely reported in several neurodegenerative disorders, including in the brains of patients with Alzheimer's disease (AD), Parkinson's disease, and Huntington disease. An increasing number of studies have implicated altered glucose and energy metabolism in patients with AD. There is compelling evidence of abnormalities in some of the key mitochondrial enzymes involved in glucose metabolism, including the pyruvate dehydrogenase and α-ketoglutarate dehydrogenase complexes, which play a great significance role in the pathogenesis of AD. Changes in some of the enzyme activities of the mitochondria found in AD have been linked with the pathology of amyloid-β (Aβ). This review highlights the role of mitochondrial function in the production and clearance of Aβ and how the pathology of Aβ leads to a decrease in energy metabolism by affecting mitochondrial function.

Evaluation of glucagon-like peptide-1, adropin, and desnutrin levels, and related factors in patients with bipolar disorder

Objective: It is known that impaired energy metabolism contributes to the neuropathology of bipolar disorder (BD). Our aim in this study was to compare the levels of glucagon-like peptide-1 (GLP-1), adropin and desnutrin, which have many metabolic functions after the regulation of energy metabolism in patients with bipolar disorder and those in healthy controls, and to investigate the related factors. Methods: To the study group of the research, 73 age- and sex-matched people were included. Of them, 35 were patients diagnosed with BD, and 38 were healthy individuals. In the blood samples, in addition to routine biochemistry lipid parameters, the levels of adropin, desnutrin and GLP-1 were determined. Results: Adropin, desnutrin and GLP-1 levels were significantly lower in the patients with bipolar disorder than were those in the healthy controls. On the other hand, Body mass index, total cholesterol, triglyceride, low density lipoprotein values were significantly higher in the patients with BD than were those in the healthy controls (p

Iron overload alters the energy metabolism in patients with myelodysplastic syndromes: results from the multicenter FISM BIOFER study

Myelodysplastic syndromes (MDS) are hematological malignancies characterized by ineffective hematopoiesis and increased apoptosis in the bone marrow, which cause peripheral cytopenia. Mitochondria are key regulators of apoptosis and a site of iron accumulation that favors reactive oxygen species (ROS) production with detrimental effects on cell survival. Although the energy metabolism could represent an attractive therapeutic target, it was poorly investigated in MDS. The purpose of the study was to analyze how the presence of myelodysplastic hematopoiesis, iron overload and chelation impact on mitochondrial metabolism. We compared energy balance, OxPhos activity and efficiency, lactic dehydrogenase activity and lipid peroxidation in mononuclear cells (MNCs), isolated from 38 MDS patients and 79 healthy controls. Our data show that ATP/AMP ratio is reduced during aging and even more in MDS due to a decreased OxPhos activity associated with an increment of lipid peroxidation. Moreover, the lactate fermentation enhancement was observed in MDS and elderly subjects, probably as an attempt to restore the energy balance. The biochemical alterations of MNCs from MDS patients have been partially restored by the in vitro iron chelation, while only slight effects were observed in the age-matched control samples. By contrast, the addition of iron chelators on MNCs from young healthy subjects determined a decrement in the OxPhos efficiency and an increment of lactate fermentation and lipid peroxidation. In summary, MDS-MNCs display an altered energy metabolism associated with increased oxidative stress, due to iron accumulation. This condition could be partially restored by iron chelation.

Inflammatory cytokines, appetite-regulating hormones, and energy metabolism in patients with gastrointestinal cancer.

This study investigated energy metabolism and its association with inflammatory cytokines and appetite- regulating hormones in patients with gastrointestinal cancer. Subjects were inpatients scheduled to undergo therapeutic intervention for diagnosed gastrointestinal cancer. Nutritional status on admission was assessed based on anthropometric measurements, nutrition screening results, food intake rate (energy intake/energy provided in hospital food), and biochemical test results. Fat-free mass (FFM) was measured using the bioelectrical impedance analysis. Resting energy expenditure (REE) and respiratory quotient were measured with indirect calorimetry, and basal energy expenditure (BEE) was calculated using the Harris-Benedict equation. A total 51 patients with gastrointestinal cancer were enrolled (17 with esophageal cancer, 15 with gastric cancer, and 19 with colorectal cancer); 16 had stage I disease, 11 had stage II, 13 had stage III, and 11 had stage IV. The levels of inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α increased significantly with cancer stage progression (P<0.001; Jonckheere-Terpstra trend test). The REE/body weight and the REE/FFM tended to increase with cancer stage progression (P=0.064 and P=0.053, respectively; Jonckheere-Terpstra trend test). FFM showed a significant negative correlation with the level of TNF-α (P=0.008; Spearman's correlation coefficient). Also, food intake rate showed a significant negative correlation with levels of IL-6 and TNF-α (P<0.001). The level of active ghrelin was positively correlated with that of IL-6 and energy metabolism (P=0.004 and 0.016, respectively) and negatively correlated with food intake rate (P=0.035), which suggests a state of ghrelin resistance. In conclusion, this study confirmed increases in the levels of inflammatory cytokines with the progression of gastrointestinal cancer and suggested the possible association of such increases with decreased FFM and the increased energy metabolism. However, the increased levels of active ghrelin failed to compensate for cachexia in cancer patients.

Shenmai Injection Improves Energy Metabolism in Patients With Heart Failure: A Randomized Controlled Trial.

BackgroundIn recent years, the application of Shenmai (SM) injection, a traditional Chinese medicine (TCM), to treat heart failure (HF) has been gradually accepted in China. However, whether SM improves energy metabolism in patients with HF has not been determined due to the lack of high-quality studies. We aimed to investigate the influence of SM on energy metabolism in patients with HF.MethodsThis single-blind, controlled study randomly assigned 120 eligible patients equally into three groups receiving SM, trimetazidine (TMZ), or control in addition to standard medical treatment for HF for 7 days. The primary endpoints were changes in free fatty acids (FFAs), glucose, lactic acid (LA), pyroracemic acid (pyruvate, PA) and branched chain amino acids (BCAAs) in serum. The secondary outcomes included the New York Heart Association (NYHA) functional classification, TCM syndrome score (TCM-s), left ventricular injection fraction (LVEF), left ventricular internal diastolic diameter (LVIDd), left ventricular internal dimension systole (LVIDs), and B-type natriuretic peptide (BNP).ResultsAfter treatment for 1 week, the NYHA functional classification, TCM-s, and BNP level gradually decreased in the patients in all three groups, but these metrics were significantly increased in the patients in the SM group compared with those in the patients in the TMZ and control groups (P < 0.05). Moreover, energy metabolism was improved in the NYHA III–IV patients in the SM group compared with those in the patients in the TMZ and control groups as evidenced by changes in the serum levels of FFA, LA, PA, and BCAA.ConclusionsIntegrative treatment with SM in addition to standard medical treatment for HF was associated with improved cardiac function compared to standard medical treatment alone. The benefit of SM in HF may be related to an improvement in energy metabolism, which seems to be more remarkable than that following treatment with TMZ.

Energy Metabolism and Nutritional Status in Hospitalized Patients with Chronic Heart Failure

Introduction: Malnutrition is a factor that defines vital prognosis in chronic heart failure. Objective: This study investigated nutritional and metabolic disorders in patients with heart failure by examining the association of severity of heart failure with inflammatory cytokines, appetite-regulating hormones, and energy metabolism. Methods: Subjects were 50 patients with heart failure. On admission, nutritional status was assessed, and biochemical blood tests were performed, including for serum tumor necrosis factor-α, interleukin-6, ghrelin, and leptin levels. Resting energy expenditure (REE) was also measured by indirect calorimetry to examine its association with severity of heart failure and levels of inflammatory cytokines and appetite-regulating hormones. Results: There were significant associations between serum brain natriuretic peptide (BNP) level and nutrition indices, indicating that nutritional status was worse when heart failure was more severe. Inflammatory cytokine levels showed significant positive correlations with BNP level. Measured REE/bodyweight was not associated with severity of heart failure, but was negatively correlated with body fat percentage and leptin levels. Conclusions: Energy metabolism was not associated with serum BNP level among patients with heart failure with New York Heart Association functional class up to III. Body fat percentage and leptin levels may be a good predictor of energy metabolism in patients with heart failure.

Influence of diabetes mellitus on energy metabolism in patients with alcoholic liver cirrhosis.

The objective was to explore the characteristics of energy metabolism in patients with alcoholic liver cirrhosis (ALC) and diabetes mellitus (DM). Thirty-four male patients with ALC and DM, 30 male patients with ALC without DM and 10 male healthy controls (HC) were enrolled in this study. Resting energy expenditure (REE), respiratory quotient (RQ) were measured by indirect calorimetry. Data were analyzed using the Student's t-test, Mann-Whitney U-test and χ2 tests between two groups. Logistic regression analysis was used to analyze the risk factors for hypermetabolism. Measured REE was significantly higher in patients with ALC and DM (1740 ± 338 kcal/d) than in patients with ALC (1400 ± 304 kcal/d, P < 0.01). Fasting blood glucose was an independent factor predicting hypermetabolism in all of the patients with ALC (P = 0.005). RQ was lower in patients with ALC and DM (0.80 ± 0.06) than in patients with ALC (0.83 ± 0.05, P = 0.027) and the HC (0.86 ± 0.03, P = 0.001). In the ALC and DM group, measured REE as percentage of predicted REE by Harris-Benedict formula was higher in patients with HbA1c ≥ 7.5% than in those with HbA1c < 7.5% (126.36 ± 15.19% vs. 109.48 ± 23.89%, P = 0.040). REE was increased and RQ was significantly decreased in patients with ALC and DM. These changes were associated with poor glucose control. HbA1c less than 7.5% may reduce the risk of hypermetabolism.

Energy metabolism in patients with diabetes and heart failure

The heart has a very high energy demand, which is mostly met by mitochondrial oxidative phosphorylation and, to a lesser extent, by glycolysis. In heart failure, there are substantial alterations in myocardial energy metabolism that lead to an “energy-deficient” state. This includes a marked reduction in overall mitochondrial oxidative phosphorylation and an uncoupling between high glycolysis rates and low glucose oxidation, which together contributes to the energy deficit and deteriorates contractile dysfunction. Cardiac ketone oxidation is also increased in heart failure, although it has yet to be determined whether this is an adaptive or maladaptive alteration. Diabetes is a major risk factor for heart failure development. It induces alterations in myocardial energy metabolism and is often associated with ventricular dysfunction. Similar to heart failure, a major change in myocardial energy metabolism in diabetic patients is a reduction in glucose oxidation, which negatively influences cardiac function. In both heart failure and diabetes, a growing body of evidence suggests that targeting myocardial energy metabolism by optimizing cardiac energy substrate preference could be a potential therapeutic approach to improve patient outcomes.

SUN-PO192: Changes in Resting Energy Metabolism in Patients on Total Parenteral Nutrition Versus Energy Supply

SUN-PO192: Changes in Resting Energy Metabolism in Patients on Total Parenteral Nutrition Versus Energy Supply