Metabolic Disorders In Patients Research Articles

Impaired glucose metabolism and other metabolic disorders in patients with primary hyperparathyroidism

The clinical picture of primary hyperparathyroidism (PHPT) which caused by parathyroid neoplasms often includes metabolic syndrome leading to the development of cardiovascular diseases. According to clinical studies, an increased incidence of diabetes mellitus, insulin resistance, obesity, dyslipidemia, hyperuricemia and other disorders that signifi tly affect the life span and quality are observed in patients with PHPT regardless of the form and the severity of the underlying disease. Basic research shows the potential nonclassical effects of high levels of parathyroid hormone and calcium on adipose tissue, pancreas, gastrointestinal tract and kidneys. However, the pathogenetic mechanisms of impaired carbohydrate and other types of metabolism in patients with parathyroid hyperfunction remain unclear because of the lack of relevant experimental models and the heterogeneity of patient groups. Besides, the effect of surgery on metabolic abnormalities is also controversial. Nowadays a deeper understanding of this issue is required, which can subsequently help in the creation of optimal approach to diagnosis and treatment of patients. This review covers different aspects of metabolic disorders in patients with PHPT, as well as potential key factors of their development.

Prevalence and correlates of metabolic syndrome and its components in adults with psychotic disorders in Eldoret, Kenya.

A high prevalence of metabolic syndrome and its components in patients with psychotic disorders may increase the risk for cardiovascular diseases. Unfortunately, relatively little work in this field has emerged from low-resourced contexts. This study investigated the prevalence, correlates, and treatment patterns of metabolic disorders in patients with psychotic disorders in Western Kenya. 300 patients with psychosis and 300 controls were recruited at Moi Teaching and Referral Hospital in Eldoret, Kenya. Data on demographic characteristics, weight, height, abdominal circumference, blood pressure, blood glucose, lipid profile, and treatments were collected. Categorical and continuous data were compared between the patient and control groups using Pearson's chi-squared tests and t-tests, respectively. Variables found to be significantly different between these groups were included in logistic regression models to determine potential predictors of metabolic syndrome. Compared to controls, patients with psychosis were found to have a higher mean random blood glucose [5.23 vs 4.79, p = 0.003], higher body mass index [5.23 vs 4.79, p = 0.001], higher triglycerides [1.98 vs 1.56, p<0.001], larger waist circumference [89.23 vs 86.39, p = 0.009] and lower high density lipoprotein [1.22 vs 1.32, p<0.001]. The odds of developing metabolic syndrome were increased with age [OR = 1.05, CI: 1.02-1.07] and presence of a psychotic disorder [OR = 2.09 [CI 1.23-3.55]; and were reduced with female gender [OR 0.41, CI 0.25-0.67], among those who were never married [OR 0.52, CI 0.28-0.94] and among the widowed/separated/ divorced marital status [OR 0.38, CI 0.17-0.81]. While the majority of patients received treatment with olanzapine, there was no association between olanzapine use and metabolic syndrome and its components. More than half of the patients in this study sample were not receiving treatment for the various components of metabolic syndrome. In the study setting of Eldoret, metabolic syndrome and its components were more prevalent among patients with psychotic disorders than in controls; and a clear treatment gap for these disorders was evident. There is a need for efforts to ensure adequate screening and treatment for these physical disorders in resource-limited settings.

Structural and functional condition of the myocardium and the relationship of metabolic disorders in patients with chronic kidney disease

Purpose. Study of the structural and functional characteristics of the heart in patients receiving long term hemodialysis (HD) treatment, and the identification of links with bone mineral, lipid disorders and anemia.Material and methods. A total of 160 patients with chronic kidney disease (CKD) of the 5th dialysis (5D) stage (70 men, 90 women) who were treated in the hemodialysis departments of Izhevsk were examined. The average age of patients is 52.9 ± 2.0 years old (31 to 78 years old). The procedures were performed 3 times a week for 4–4.5 hours. The inclusion criteria were the duration of dialysis therapy for at least one year and the availability of informed consent. The adequacy index Kt / V amounted to1.56 ± 0.2. Echocardiographic examination assessed the structural and functional parameters, calculated Left Ventricular Mass, LVM index, relative thickness index, “inner membrane”, fractional-shortening of the middle fibers. A study of general clinical indicators of mineral-bone disorders, Lipemic index, erythrocytes was carried out.Results. Violation of left ventricular (LV) geometry was found in 140 (87.5%) patients with 5D CKD stage. Concentric and eccentric hypertrophy prevailed. No significant dependence on patient’s sex was revealed. Patients with eccentric hypertrophy showed high rates of inter-dialysis weight gain (p &lt; 0.05) and ultrafiltration (p &lt; 0.05). In patients with concentric hypertrophy, high indicators of calcium-phosphorus metabolism (p &lt; 0.05), pre-dialysis systolic pressure (p &lt; 0.05) and pulsatility (p &lt; 0.05) were obtained. They also tended to have higher triglyceride indices and more pronounced anemia. The correlation of the structural and functional state of the myocardium with the level of phosphorus, calcium, calcium-phosphorus ratio and pulsatility was established.Conclusions. In most patients with stage 5D CKD, LV remodeling with the prevalence of concentric and eccentric hypertrophy is observed. No significant gender differences were found. In patients with hypervolemia requiring more intense ultrafiltration during dialysis, eccentric LV hypertrophy was detected. High values of pre-dialysis and pulsatility, as well as levels of calcium and phosphorus, are observed with the concentric remodeling type. Correlations of structural changes in the myocardium with calcium-phosphorus metabolism were revealed. The data obtained may open new ways of influencing the regression of LV hypertrophy and improve the cardiovascular prognosis in patients receiving programmed hemodialysis treatment.

Correction of metabolic disorders in patients with aneurysmal intracranial hemorrhages

The article presents data assessment of the severity of the clinical condition and a number of biochemical parameters in 51 patients with aneurysmal intracranial hemorrhage on the 10th day, on average, after the rupture of the arterial aneurysm and after treatment with the additional use of magnesium sulfate to standard therapy in the postoperative period. It is shown, that at the time of hospitalization, 75 % of patients in the control group and 50 % of patients in the main group had cerebral vascular spasm according to transcranial dopplerography; activation of lipid peroxidation processes, a decrease in superoxide dismutase activity, an increase in the content of vascular endothelial growth factor and highly sensitive C-reactive protein (CRP) with a decrease in the level of stable nitrogen monoxide exchange products were detected. A statistically significant improvement in the clinical condition of patients on the Hunt-Hess scale, the modified Fisher scale, and an increase in the score on the Glasgow coma scale with normalization of pro- and antioxidant status of the blood were revealed in the main group after neurosurgical treatment and course use of magnesium sulfate. At the same time, high levels of highly sensitive CRP and low levels of nitrates/nitrites in the patients blood of both groups are maintained. Consequently, the additional use of magnesium sulfate improves the clinical condition of patients with intracranial hemorrhage and increases the antioxidant potential of the blood in the postoperative period.

A Study of Platelet Indices in Patients with Metabolic Syndrome and Type 2 Diabetes Mellitus

Altered platelets have been reported in patients with diabetes mellitus and MS has been considered asa ‘prothrombotic state’ with enhanced platelet reactivity. They have been associated with increased riskof vascular complications in these patients. Platelet indices correlate with functional status of plateletsand is an emerging risk factor of vascular complications in diabetes and MS. The study was undertakento know the efficacy of platelet analysis in assessing the prognosis of diabetes mellitus and MS. Resultsof our study may lay a foundation for a discovery of new approaches for prevention and treatment ofcardiovascular complications in MetS and DMT2 in early stages of metabolic disorders in patients. MetS isa proinflammatory and prothrombotic state, characterized by alteration of platelet indices. Plateletcrit wasshown to be a significant biomarker along with other parameters, including waist circumference,SBP, andserum triglyceride levels. Platelet activation causes high risk of cardiovascular complications in MetS. T2DM is associated with the changes in the intra cellular signaling systems regulating platelet functions.

Higher prevalence of metabolic disorders in patients with bilateral primary aldosteronism than unilateral primary aldosteronism.

Metabolic syndrome (MetS) is a frequent clinical condition in hypertension patients and is more frequently reported in primary aldosteronism (PA). This study is aimed at investigating the prevalence of MetS and its components in the two major types of patients with adrenal venous sampling (AVS)-confirmed unilateral PA and bilateral PA. This was a retrospective cross-section study. We analysed metabolic parameters from 169 PA patients subtyped by AVS, including 85 unilateral PA patients and 84 bilateral PA patients, and we also included 169 non-PA patients matched for age and sex. Patients with unilateral PA had higher concentrations of aldosterone and lower serum potassium than patients with bilateral PA. However, patients with bilateral PA had higher prevalence of MetS (79.8% vs 64.7%, P=.029), obesity (40.5% vs 24.7%, P=.029), dyslipidemia (72.6% vs 55.3%, P=.019) and hyperglycaemia (29.8% vs 16.5%, P=.040) than those with unilateral PA. Meanwhile, bilateral PA had higher BMI (27.55±4.58 vs 25.57±3.28kg/m2 , P=.001), waist circumference (98.54±11.44 vs 93.32±10.64cm, P=.003) and fasting plasma glucose (4.98±1.16 vs 4.64±0.93mmol/L, P=.034). The logistic regression analysis also showed that bilateral PA was associated with the presence of MetS after adjustment for age, sex and duration of hypertension. Patients with bilateral PA have a higher prevalence of MetS than those with unilateral PA, despite unilateral PA patients exhibiting higher concentrations of aldosterone and lower serum potassium, suggesting that unilateral PA and bilateral PA may have differing mechanisms of MetS.

Evaluation of body composition, resting metabolic rate and frequency of metabolic disorders in adolescents with Klinefelter syndrome

Kleinfelter syndrome (KS) is a common genetic disease characterized by hypergonadotropic hypogonadism. The high risk of developing of metabolic disorders in patients with KS is be explained by the presence of androgen deficiency, which leads to a decrease in the amount of lean soft mass and an increase of the adipose tissue content. The basal metabolic rate (BMR) is determined by the amount of lean soft mass, and its reduction can contribute to weight gain and the progression of metabolic disorders in KS. Body composition, assessment of basal metabolism and metabolic profile in adolescents with KS. The study included 28 adolescents with KS, comparable in age and stage of sexual maturation. All patients were divided into two groups depending on the presence of clinical laboratory signs of hypogonadism. Patients passed through the evaluation of metabolic profile, bioelectrical impedance analysis for the body composition and chamber-based indirect calorimetry for the evaluation of BMR. Normal indicants of body composition were determined in 20 (71.4%) adolescents, excess of adipose mass &ndash; in 6 (21.4%) patients, and deficit of adipose mass &ndash; in 7.2% of cases. Among 6 patients with excess of adipose mass, three were obese or overweight, while the rest had normal SDS body mass index (BMI). 64.3% of adolescents showed normal indicants of energy exchange at rest, 6 (21.4%) &ndash; a decrease of BMR, 4 (14.3%) - an increase of BMR. A comparative analysis of patient groups did not reveal statistically significant differences in BMR adjusted to a lean soft mass (OO/TM) (p=0.36). Insulin resistance was detected in 11 patients (39.3%), and the incidence of dyslipidemia was 3.6%. The groups did not significantly differ in terms of glycemia levels in the fasted state and lipid profile indicants. Most adolescents with KS have normal indicants of body composition and basal metabolism, as well as a low frequency of metabolic disorders, regardless of the level of total testosterone in blood. In some patients with normal SDS BMI, excess of adipose mass is detected. The lack of correlation between the level of testosterone and the intensity of BMR may indicate a slight effect of androgen deficiency on energy exchange at rest in adolescents with KS.

Cavin1 Deficiency Causes Disorder of Hepatic Glycogen Metabolism and Neonatal Death by Impacting Fenestrations in Liver Sinusoidal Endothelial Cells.

It has been reported that Cavin1 deficiency causes lipodystrophy in both humans and mice by affecting lipid metabolism. The ablation of Cavin1 in rodents also causes a significant deviation from Mendelian ratio at weaning in a background‐dependent manner, suggesting the presence of undiscovered functions of Cavin1. In the current study, the results show that Cavin1 deficiency causes neonatal death in C57BL/6J mice by dampening the storage and mobilization of glycogen in the liver, which leads to lethal neonatal hypoglycemia. Further investigation by electron microscopy reveals that Cavin1 deficiency impairs the fenestration in liver sinusoidal endothelial cells (LSECs) and impacts the permeability of endothelial barrier in the liver. Mechanistically, Cavin1 deficiency inhibits the RhoA‐Rho‐associated protein kinase 2‐LIM domain kinase‐Cofilin signaling pathway and suppresses the dynamics of the cytoskeleton, and eventually causes the reduction of fenestrae in LSECs. In addition, the defect of fenestration in LSECs caused by Cavin1 deficiency can be rescued by treatment with the F‐actin depolymerization reagent latrunculin A. In summary, the current study reveals a novel function of Cavin1 on fenestrae formation in LSECs and liver glycogen metabolism, which provide an explanation for the neonatal death of Cavin1 null mice and a potential mechanism for metabolic disorders in patients with Cavin1 mutation.

Current Knowledge Regarding the Interaction Between Oral Bone Metabolic Disorders and Diabetes Mellitus

Diabetes mellitus, a major chronic disease affecting human health, has been increasing in prevalence in recent years. Diabetes mellitus can cause bone metabolic disorders in patients, leading to osteoporosis, a higher risk of traumatic fracture, and other bone diseases. Bone metabolic disorders in the oral cavity principally manifest as periodontitis, loss of alveolar bone, and failure of implant osseointegration. In recent years, numerous studies have shown that there is a complex interaction between bone metabolic disorders and diabetes mellitus. This paper reviews the adverse effects of diabetes on oral bone metabolism disorders such as alveolar osteoporosis and bone loss in patients with periodontitis, discusses the potential mechanisms of diabetic bone loss, and suggests potential ways to prevent and treat oral bone loss in patients with diabetes mellitus.

Impact of the adherence to medical treatment on the main urinary metabolic disorders in patients with kidney stones

ObjectiveTo assess the effect of the adherence to medical treatment on urinary parameters in the 24-h metabolic study of patients with kidney stones. MethodsA retrospective, longitudinal, descriptive, and observational study was carried out by reviewing the hospital electronic medical record from 2014 to 2018. The adherence to drug treatment was measured 6 months after its initiation, and the numerical values of the metabolic studies were compared. Wilcoxon tests were performed to compare the difference before and after treatment. ResultsNinety patients were evaluated, with 73.3% of adherence. The 180-day overall adherence rate was 61.2% in patients treated with a single drug and 85.4% in patients treated with multiple drugs. There is a statistically significant increase in citrate levels in patients with good adherence in comparison with non-adherent patients (p=0.031 vs.p=0.528). ConclusionsMedical treatment and dietary measures in patients with kidney stones have an initial impact at 6 months on the values of the main urinary metabolic alterations that predispose to calculi formation; the most significant is seen in those patients with adherence to medical treatment for hypocitraturia.

Inherited Metabolic Disorders Presenting with Ataxia.

Ataxia is a common clinical feature in inherited metabolic disorders. There are more than 150 inherited metabolic disorders in patients presenting with ataxia in addition to global developmental delay, encephalopathy episodes, a history of developmental regression, coarse facial features, seizures, and other types of movement disorders. Seizures and a history of developmental regression especially are important clinical denominators to consider an underlying inherited metabolic disorder in a patient with ataxia. Some of the inherited metabolic disorders have disease specific treatments to improve outcomes or prevent early death. Early diagnosis and treatment affect positive neurodevelopmental outcomes, so it is important to think of inherited metabolic disorders in the differential diagnosis of ataxia.

Berberine attenuates the abnormal ectopic lipid deposition in skeletal muscle

BackgroundLipid deposition in non-adipose tissue is associated with a propensity to obesity. Skeletal muscle mitochondrial dysfunction, evidenced by incomplete beta oxidation may contribute to ectopic lipid deposition during high fat diet-induced obesity. Berberine (BBR) has been proved to possess the properties of improving metabolic disorders in patients with obesity or type 2 diabetes mellitus. However, the precise mechanism remains obscure. MethodsMice were treated with berberine and metabolic profile were analyzed. Mitochondrial number and function were detected after berberine treatment in vitro and in vivo. The role of Adenosine 5‘-monophosphate-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) was verified after RNA interference or adenovirus infection. ResultsIn the current study, we investigated the influence of berberine on the lipid deposition of skeletal muscle and found that berberine could increase the mitochondrial number and function both in vivo and in vitro. Furthermore, berberine promoted the expression of PGC-1α, the crucial transcriptional coactivator related to mitochondrial biogenesis and function, through AMPK pathway. Berberine reduced the basal oxygen consumption rates (OCR) but increased the maximal OCR in C2C12 myocytes, which indicated that berberine could increase the potential function of mitochondria. ConclusionOur results proved that berberine can protect the lean body mass from excessive lipid accumulation, by promoting the mitochondrial biogenesis and improving fatty acid oxidation in an AMPK/PGC-1α dependent manner.

The effects of iron overload, insulin resistance and oxidative stress on metabolic disorders in patients with β- thalassemia major.

Serum lipids and glycemic dysregulation are the known characteristics of β- thalassemia major (β-TM). Here, we evaluated the association of these disorders with insulin resistance (IR), oxidative stress and serum ferritin values in patients with β-TM. This case-control study was performed in thalassemia unite of Darab Hospital (Darab, Fars province, Iran) from December 2016 to December 2017. Forty-eight patients with β-TM and 33 healthy individuals were enrolled. Serum fasting blood sugar (FBS), insulin, total cholesterol (TC), triglyceride (TG), high density lipoprotein (HDL), low density lipoprotein (LDL), ischemia modified albumin (IMA), and ferritin were measured. The values of HOMA-IR, LDL: TG ratio, atherogenic index (AI), atherogenic index of plasma (AIP), and coronary risk index (CRI) were calculated. The level of serum ferritin, IMA, FBS, TG, AIP, LDL: TG ratio, and the prevalence of IR (HOMA-IR < 3.8) were significantly higher while TC, LDL-C, HDL-C, and AI were significantly lower in the patients compared to the control group. In patient with β-TM, serum ferritin revealed to have a positive association with serum insulin, HOMA-IR, AI, and CRI levels while serum IMA showed positive association with TG and AIP and inverse association with hypocholesterolemia. HOMA-IR had positive correlation with HDL levels. Oxidative stress and iron overload are predictors of serum glycemic and lipid dysregulation, suggesting possible beneficial effect of antioxidants and efficient iron chelating therapy in reducing the risk of metabolic disorders in β- thalassemia.

Japan's Practical Guidelines for Zinc Deficiency with a Particular Focus on Taste Disorders, Inflammatory Bowel Disease, and Liver Cirrhosis.

Zinc deficiency is common in Japan, yet awareness on this disorder is lacking. The Japanese Society of Clinical Nutrition recently issued the Japan’s Practical Guideline for Zinc Deficiency 2018 setting forth criteria for diagnosing zinc deficiency, i.e., (a) one or more symptoms of zinc deficiency or low serum alkaline phosphatase, (b) ruling out other diseases, (c) low serum zinc, and (d) alleviation of symptoms upon zinc administration. Serum zinc <60 μg/dL and 60–80 μg/dL indicate zinc deficiency and marginal deficiency, respectively. Zinc deficiency symptoms vary and include dermatitis and taste disorders among others. Zinc administration improves taste in 50–82% of patients suffering from taste disorders (a common symptom of zinc deficiency). Effects of zinc administration do not appear immediately, and therapy should be continued for at least three months. Zinc deficiency often accompanies various diseases and conditions. Here, we focus on inflammatory bowel diseases and liver cirrhosis. As zinc deficiency enhances intestinal inflammation via macrophage activation, we discuss the pathological mechanism for inflammation and zinc deficiency in the context of IBD. Zinc deficiency can also lead to a nitrogen metabolic disorder in patients with liver cirrhosis. Zinc supplementation can improve not only the ammonia metabolism, but also the protein metabolism. We also discuss directions for future studies of zinc deficiency.

The risks of ubiquinone and \u03b2-carotene deficiency and metabolic disorders in patients with oral cancer

BackgroundCancer development is mediated by oxidative stress and inflammation, which may correlate with metabolic disorders. The aim of this study was to evaluate antioxidant vitamins status and metabolic parameters in patients with oral cancer according to tumor-node-metastasis (TNM) stages.MethodsA total of 194 patients with oral cancer were enrolled in this study. The patients were stratified for four groups according to cancer stages and that the statistics are comparisons across these groups. The levels of antioxidant vitamins (ubiquinone, β-carotene, vitamin A and E), metabolic parameters, oxidative stress, antioxidant enzymes activity, and inflammatory markers were measured.ResultsMore than half of the subjects had high blood pressure, central obesity, hyperglycemia, and hyperlipidemia regardless of TNM stage. With regard to antioxidant vitamins status, 46 and 94% of patients had β-carotene and ubiquinone deficiency, respectively. Patients in T3 and T4 stages had significantly lower antioxidant enzyme (catalase, p = 0.03) activity and higher inflammatory markers levels (high sensitivity C-reactive protein and interleukin-6, p < 0.01) than patients in the other stages. In addition, the level of β-carotene was negatively associated with waist circumference, and ubiquinone was positively associated with the level of high-density lipoprotein cholesterol (p < 0.05). Higher β-carotene and ubiquinone levels were negatively associated with hypertriglyceridemia and the risk of metabolic syndrome (p < 0.05).ConclusionsA high proportion of patients with oral cancer had ubiquinone or β-carotene deficiency and metabolic disorders. The level of ubiquinone or β-carotene was negatively associated with the risk of central obesity, hypertriglyceridemia, and metabolic syndrome. Since patients with oral cancer suffer from high oxidative stress and inflammation (particularly in the T3 and T4 stages), supplementation with antioxidant vitamins such as ubiquinone or β-carotene could be preferentially applied.

The fibroblasts growth factor 21 study in patients with non-alcoholic fatty liver disease and hypertension comorbidities

The purpose of the study was to evaluate the fibroblast growth factor 21 levels (FGF-21) in blood plasma and the liver parenchyma state in non-alcoholic fatty liver disease (NAFLD) patients with hypertension. Materials and methods. 60 NAFLD patients aged 30 to 60 years were examined. The average age of the patients was (50.1 ± 6.9) years. The control group consisted of 20 practically healthy volunteers. All the patients were diagnosed with NAFLD, traditionally examined by clinical and laboratory methods, assessed for trophological status and lipid metabolism. The determination of FGF-21 was performed by the immune enzyme method in blood plasma using ELISA kits. Results. Evaluation of the liver parenchyma state demonstrated that in patients with NAFLD and hypertension, the F2-3 stage of fibrosis predominated in 60 % of cases. Depending on the existing stage of fibrosis, there was an increase in the liver enzymatic activity (P < 0.05, except the comparison results in patients with F0 and F1 stages), lipid profile (P < 0.001) and HOMA index (P < 0.05). An increase in the level of FGF-21 was detected in all NAFLD patients with hypertension and 3.4 times (P = 0.001) exceeded the parameters of practically healthy persons as well as its dependence on the stage of the liver fibrotic changes (P < 0.05, except the comparison results in patients with F1 and F2-3 stages). The correlations revealed confirm the pathogenetic relationship between FGF-21 and the liver inflammation development (P < 0.05). Conclusions. The FGF-21 levels in the blood plasma of NAFLD patients with hypertension exceed the parameters of the control group, are higher with increasing degree of liver fibrosis and associated with metabolic disorders in patients. The results obtained characterize the cytokine FGF-21 as a promising predictor marker for NAFLD progression.

Capsaicinoid nonivamide improves nonalcoholic fatty liver disease in rats fed a high-fat diet

Nonalcoholic fatty liver disease (NAFLD) is a chronic disease that causes morbidity associated with metabolic syndrome. NAFLD is a worldwide problem and represents a major cause of liver injury, which can lead to liver cell death. We investigated the effects of nonivamide (pelargonic acid vanillylamide, PAVA; 1 mg/kg) and rosuvastatin (RSV; 10 mg/kg) on hepatic steatosis induced by a high-fat diet (HFD). Male Sprague–Dawley rats were fed a HFD for 16 weeks then received PAVA or RSV for 4 additional weeks. We examined the metabolic parameters, function, fat content, histological alterations, reactive oxygen species production, and apoptotic cell death of the liver, in addition to the expression of the following important molecules: transient receptor potential cation channel subfamily V member 1 (TRPV1) phosphorylation of sterol regulatory element binding protein (pSREBP-1c/SREBP-1c), total and membrane glucose transporter 2 (GLUT2), 4-hydroxynonenal (4-HNE), and cleaved caspase-3. HFD-induced hepatic steatosis was associated with significantly increased morphological disorganization, injury markers, oxidative stress, lipid peroxidation, and apoptosis. However, metabolic dysfunction and hepatic injury were reduced by RSV and PAVA treatment. PAVA regulated lipid deposition, improved insulin resistance, and decreased oxidative stress and apoptotic cell death. Therefore, PAVA represents a promising therapeutic approach for treating metabolic disorders in patients with NAFLD.

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.

The role of selected adipokines in tumorigenesis and metabolic disorders in patients with adrenal tumors.

Recently, more and more attention has been directed to the role of adipose tissue and adipocytokines in the pathogenesis of metabolic and inflammatory disorders in humans. Excess fat tissue has also been associated with a higher risk of malignancies. Advances in the research on the role of adipokines in adrenal tumors may elucidate the relationship between various types of adipose tissue (visceral, subcutaneous, and periadrenal) and metabolic disorders observed in hormonally active adrenal tumors, as well as associations with adrenal cortex cancer. In patients with active or cured Cushing syndrome, increased leptin and resistin concentrations as well as release of pro-inflammatory cytokines can be associated with cardiovascular risk. Also, the renin-angiotensin-aldosterone system in patients with primary hyperaldosteronism may affect the metabolic activity of the adipose tissue. Elevated resistin concentrations in this group of patients are associated with morphological changes of the myocardium independently of the effects of the metabolic syndrome. Further, it has been suggested that hypoadiponectinemia comprises an additional factor in the pathogenesis of carbohydrate metabolism disorders and the risk of cardiovascular complications in pheochromocytoma patients. Understanding the mechanisms of action of adipokines may be important in developing prophylactic and therapeutic strategies in hormonally active and malignant tumors of the adrenal glands.

Functional and metabolic disorders in patients with cholelithiasis after undergone cholecystectomy

The article describes the results of a clinical observational study of patients with cholelithiasis after cholecystectomy. The article is about the metabolic disorders in patients with gallstone disease, the mechanisms of development of functional and metabolic disorders after cholecystectomy. Particular attention is paid to the genetic, hormonal mechanisms, the role of microbiota and bile acids.