[Disorders of copper metabolism and dysfunction of the immune system in children with a nephrotic form of chronic glomerulonephritis].
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Adolescent↗
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Results for “Metabolic dysfunction”
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Tubular dysfunction in metabolic acidosis. First step to acute renal failure.
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Acidosis↗
[Thyroid gland dysfunction and metabolic abnormalities, with special reference to abnormal lipid and glucose metabolism].
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Adolescent↗
Pathogenesis of cardiac dysfunction during metabolic acidosis: therapeutic implications.
Based on work performed in many laboratories including our own, we suggest the following schematic shown in Figure 4 to explain metabolic acidosis and the effects of alkalinization therapy. Metabolic acidosis induces prompt and substantial decreases in cardiac functional performance. This is mediated by an intracellular acidosis which impairs cardiac function directly as well as leads to an impairment of cardiac energy metabolism which further impairs cardiac function. Attempts to alkalinize the cell with sodium bicarbonate therapy lead to a paradoxical intracellular acidosis and further impairment of cardiac function, whereas Carbicarb may correct the intracellular acidosis and improve physiological function. However, at the time which this paper was written, Carbicarb was not available for clinical use in the United States.
Acidosis↗
Prevalence of obesity, glucose homeostasis disorders and metabolic syndrome in psychiatric patients taking typical or atypical antipsychotic drugs: a cross-sectional study.
AIMS/HYPOTHESIS: Atypical antipsychotic drugs may be associated with obesity and other components of the metabolic syndrome, but this relationship is controversial. We investigated the hypothesis that atypical antipsychotics are associated with a greater degree of metabolic dysfunction than typical agents. METHODS: Metabolic parameters were measured in 103 diagnostically heterogeneous psychiatric out-patients. Patients had been taking typical or atypical antipsychotic drugs for a minimum of six months. RESULTS: Sixty-nine patients were taking atypical agents, 20 typical agents and 14 a combination. Mean values (+/-SD) for the whole group were: age 43.8 years (11.4); BMI 29.1 kg/m(2) (5.1); W:H ratio 0.88 (0.09). Metabolic parameters, including beta cell function and insulin sensitivity, measured by HOMA, did not differ with regard to the prescribed antipsychotic drug. Six patients had undiagnosed diabetes, six patients had impaired fasting glucose, and eight fulfilled criteria for the metabolic syndrome, all of whom were taking atypical agents (p=0.07 vs typical agents). Subgroup analyses of those taking atypical agents revealed differences in BMI (mean, +/-SD) between olanzapine (27.3 kg/m(2)+/-5.1) and quetiapine (31.9 kg/m(2)+/-5.1), p=0.01, and HbA(1c) (olanzapine, 5.1%+/-0.6 vs quetiapine, 5.6%+/-0.6; p=0.03). Other atypical agents were intermediate with regard to these parameters. CONCLUSIONS: Obesity, dyslipidaemia and abnormalities of glucose homeostasis are prevalent in this group. Patients taking atypical agents showed a trend towards abnormalities of glucose homeostasis. Prospective studies are needed to explore the precise relationship between antipsychotic drugs, glucose homeostasis, obesity and the metabolic syndrome.
Adult↗
[Diabetic cardiopathy. Pathophysiologic concepts and therapeutic approaches].
Epidemiological data reviewed suggest that diabetes itself increases the cardiac risk of diabetics (types I and II), independently from the development of coronary heart disease and in addition to other risk factors (hypertension, hypercholesterolemia, hypertriglyceridemia, smoking and others), presumably by a specific myocardial disease called "diabetic cardiopathy", or according to the recommendations of the WHO, "diabetic heart muscle disease." Disturbances of the left and right ventricular function as well as the autonomic function of the heart can be understood as signs of this specific cardiopathy. The pathophysiological mechanisms underlying this disease are not yet fully known; however, recent evidence is presented that diabetes leads to a facet of metabolic dysfunctions regarding glucose and energy metabolism, calcium homeostasis and the expression of specific proteins that diminish the ability of the heart to respond to increased workload and increase the vulnerability of the heart in diabetes. Since preliminary experimental data indicate that inhibitors of the angiotensin-converting enzyme can protect the heart in diabetes, it is intriguing to suggest that increased release of angiotensin II plays a significant role in the change from reduced adaptability to irreversible damage of the heart in diabetes.
Angiotensin-Converting Enzyme Inhibitors↗
Magnetic resonance spectroscopic imaging in temporal lobe epilepsy: neuronal dysfunction or cell loss?
BACKGROUND: Magnetic resonance spectroscopy (MRS) has demonstrated consistent metabolic abnormalities in temporal lobe epilepsy. The reason for decreases in N-acetylated compounds are thought to be related to neuronal hippocampal cell loss as observed in hippocampal sclerosis. However, mounting evidence suggest that the N-acetylated compound decreases may be functional and reversible. OBJECTIVE: To establish whether the metabolic changes measured by MRS correlate to hippocampal cell loss in temporal lobe epilepsy. SUBJECTS AND METHODS: We prospectively performed quantitative hippocampal MR imaging volumetry and MRS imaging in 33 patients with intractable mesial temporal lobe epilepsy who were undergoing surgery. A neuronal-glial ratio of cornu ammonis and fascia dentata was obtained and correlated while validating the pathologic analysis by comparisons with specimens of age-matched autopsy control-case hippocampus (n = 14). RESULTS: The neuronal-glial ratio of the patient group was statistically significantly lower than in the control group for the cornu ammonis region (P<.001). Correlations of hippocampal volumes with cornu ammonis and neuronal-glial ratios revealed a significant interdependence (P<.01). However, correlations of the resected hippocampal creatine-N-acetylated compound ratio with the cornu ammonis or fascia dentata neuronal-glial ratios showed no significant interdependence (P>.8). CONCLUSIONS: Our findings support the concept that the metabolic dysfunction measured by MRS imaging and the hippocampal volume loss detected by MR imaging volumetry do not have the same neuropathologic basis. These findings suggest that the MRS imaging metabolic measures reflect neuronal and glial dysfunction rather than neuronal cell loss as previously assumed.
Adolescent↗
Mitochondrial amyloid-beta peptide: pathogenesis or late-phase development?
Mitochondrial and metabolic dysfunction have been linked to Alzheimer's disease for some time. Key questions regarding this association concern the nature and mechanisms of mitochondrial dysfunction, and whether such changes in metabolic properties are pathogenic or secondary, with respect to neuronal degeneration. In terms of mitochondria and Alzheimer's, altered function could reflect intrinsic properties of this organelle, potentially due to mutations in mitochondrial DNA, or extrinsic changes secondary to signal transduction mechanisms activated in the cytosol. This review presents data relevant to these questions, and considers the implication of recent findings demonstrating the presence of amyloid-beta peptide in mitochondria, as well as intra-mitochondrial molecular targets with which it can interact. Regardless of the underlying mechanism(s), it is likely that mitochondrial dysfunction contributes to oxidant stress which is commonly observed in brains of patients with Alzheimer's and transgenic models of Alzheimer's-like pathology.
Alzheimer Disease↗
Mechanisms of endothelial dysfunction in the metabolic syndrome.
Cardiovascular disease is a leading cause of death and disability in patients with diabetes or metabolic syndrome (MS). The available data suggest that many patients with diabetes or MS already have vascular abnormalities by the time they are diagnosed with their metabolic disorder. Endothelial dysfunction (ED), which is one of the initial steps in the process of vascular disease, is often present in patients with diabetes or MS. Although the precise mechanism(s) by which diabetes or MS causes ED remains to be elucidated, several possibilities exist. Hyperglycemia, hyperinsulinemia, increased oxidative stress, and diabetic dyslipidemia can all contribute to ED individually or in concert with one another. ED in the setting of diabetes or MS can subsequently result in the activation of a variety of pathways that alter vascular function and participate in the process of vascular remodeling and atherosclerosis. Because insulin resistance is the predominant mechanism responsible for various perturbations seen in MS or diabetes, it is essential to develop a therapeutic strategy that can improve insulin sensitivity with the hope that such interventions would reduce the risk of future cardiovascular events.
Diabetes Complications↗
Pathophysiology of shock.
Shock is an acute widespread reduction in effective tissue perfusion that invokes an imbalance of oxygen supply and demand, anaerobic metabolism, lactic acidosis, cellular and organ dysfunction, metabolic abnormalities, and, if prolonged, irreversible damage and death. The pathophysiologic events in the various types of shock are different and complex with hemodynamic and oxygenation changes, alterations in the composition of the fluid compartments, and various mediators. Shock results from a change in one or a combination of the following: intravascular volume, myocardial function, systemic vascular resistance, or distribution of blood flow. The clinical types of shock include hypovolemic, cardiogenic, distributive (septic), and obstructive. An understanding of the pathophysiologic changes, rapid diagnosis, appropriate monitoring, and appropriate therapy can reduce the high morbidity and mortality in shock states.
Humans↗
Metabolic syndrome, endothelial dysfunction, and erectile dysfunction: association and management.
The metabolic syndrome, the criteria for which include glucose intolerance, obesity, hypertension, and dyslipidemia, has rapidly become understood to have a major association with erectile dysfunction (ED). On a mechanistic level, their common grounds may involve endothelial dysfunction, although the conditions of oxidative stress understood to be a pathologic element of the syndrome also may affect various components of the vascular biology of the penis. The foremost importance of recognizing the association between ED and the metabolic syndrome is that addressing ED presentations may afford opportunities to identify and improve a major adverse health profile and thereby promote health maintenance objectives for patients.
Endothelium, Vascular↗
Mitochondrial damage and dysfunction in traumatic brain injury.
The enduring cognitive deficits and histopathology associated with traumatic brain injury (TBI) may arise from damage to mitochondrial populations, which initiates the metabolic dysfunction observed in clinical and experimental TBI. The anecdotal evidence for in vivo structural damage to mitochondria corroborates metabolic and physiologic dysfunction, which depletes substrates and promotes free radical generation. Excessive calcium pathology differentially disrupts the heterogeneous mitochondrial population, such that calcium sensitivity increases after TBI. The ongoing pathology may escalate to include protein and DNA oxidation that impacts mitochondrial function and promotes cell death. Thus, in vivo TBI damages, if not eliminates, mitochondrial populations depending on injury severity, with the remaining population left to provide metabolic support for survival or repair in the wake of cellular pathology. With a considerable understanding of post-injury mitochondrial populations, therapeutic interventions targeted to the mitochondria may delay or prevent secondary cascades that lead to long-term cell death and neurobehavioral disability.
Journal Article↗
The effects of ischemia and reperfusion on mucosal respiratory function, adenosine triphosphate, electrolyte, and water content in the ascending colon of ponies.
OBJECTIVE: The purpose of this study was to examine the effects of ischemia and reperfusion on the biochemical integrity of equine colonic mucosa to assess the relative roles of ischemic- and reperfusion-induced damage. STUDY DESIGN: Two hours of no-flow ischemia experimentally induced by 720 degrees counterclockwise ascending colon volvulus followed by 2 hours reperfusion after derotation. ANIMALS: Ten ponies. METHODS: Ascending colon biopsies were obtained every hour for measurement of mucosal adenosine triphosphate (ATP), water, sodium, and potassium content. Additional samples were homogenized for assay of mitochondrial respiratory function. RESULTS: ATP content diminished 92% after ischemia and recovered to only 44% of control levels (P < .001 versus controls) after 2 hours reperfusion. Reperfusion increased mucosal water and decreased sodium and potassium content for the duration of the experiment. Both NADH-(pyruvate) and FADH-linked (succinate) respiration decreased after ischemia and did not recover during reperfusion indicating electron transport chain dysfunction. CONCLUSIONS: Two hours ischemia induced severe metabolic dysfunction in equine colon mucosa which persisted throughout reperfusion. Unequivocal evidence of injury specific to reperfusion was not observed in this study suggesting that much of the damage observed during reperfusion may be a continuation of injury induced during the ischemic period and not specific to reperfusion per se. CLINICAL RELEVANCE: This study suggests that greater efforts to metabolically support ischemically injured mucosa may be an important aspect of obtaining improved survival of horses affected by ascending colon volvulus (ACV).
Adenosine Triphosphate↗
Erectile dysfunction: interrelationship with the metabolic syndrome.
Erectile dysfunction (ED) is more commonly seen in men with various components of the metabolic syndrome (a constellation of various cardiovascular and diabetes risk factors). ED can be considered as a risk marker of the metabolic syndrome and its associated conditions. The patient with ED should be thoroughly evaluated for coexisting vascular disease. Any cardiovascular risk factors should be modified or treated (ie, smoking, diabetes, hypertension, and hyperlipidemia). Endothelial dysfunction is a major unifying etiology for many of the aspects of the metabolic syndrome, especially diabetes and cardiovascular disease. It also plays a major role in ED. The multifactorial etiology of ED, especially in patients with the metabolic syndrome, increases the complexity of managing this problem so clinicians need to be aware of the underlying pathophysiology to ensure the best possible outcomes in management.
Biomarkers↗
Construction and Analysis of a Mitochondrial Metabolism-Related Prognostic Model for Breast Cancer to Evaluate Survival and Immunotherapy.
As one of the most prevalent malignancies among women, breast cancer (BC) is tightly linked to metabolic dysfunction. However, the correlation between mitochondrial metabolism-related genes (MMRGs) and BC remains unclear. The training and validation datasets for BC were obtained from The Cancer Genome Atlas and Gene Expression Omnibus databases, respectively. MMRG-related data were obtained from the Molecular Signatures Database. A risk score prognostic model incorporating MMRGs was established based on univariate, LASSO, and multivariate Cox regression analyses. Independent factors affecting BC prognosis were identified through regression analysis and presented in a nomogram. Single-sample gene set enrichment analysis was employed to assess the immune levels of high-risk (HR) and low-risk (LR) groups. The sensitivity of BC patients in the two groups to common anti-tumor drugs was evaluated by utilizing the Genomics of Drug Sensitivity in Cancer database. 12 MMRGs significantly associated with survival were selected from 1234 MMRGs. A 12-gene risk score prognostic model was built. In the multivariate regression analysis incorporating classical clinical factors, the MMRG-related risk score remained an independent prognostic factor. As revealed by tumor immune microenvironment analysis, the LR group with higher survival rates had elevated immune levels. The drug sensitivity results unmasked that the LR group demonstrated higher sensitivity to Irinotecan, Nilotinib, and Oxaliplatin, while the HR group demonstrated higher sensitivity to Lapatinib. The development of MMRG characteristics provides a comprehensive understanding of mitochondrial metabolism in BC, aiding in the prediction of prognosis and tumor microenvironment, and offering promising therapeutic choices for BC patients with different MMRG risk scores.
Humans↗
Endocrine and metabolic programming during intrauterine development.
In humans, low birth weight is associated with an increased risk of metabolic dysfunction in adult life. Many of these metabolic disorders have an endocrine origin and are accompanied by abnormal hormone concentrations. This has led to the hypothesis that adult metabolic disease arises in utero as a result of programming of key endocrine systems during suboptimal intrauterine conditions associated with fetal growth retardation. This review examines the experimental evidence for prenatal endocrine programming with particular emphasis on endocrine axes involved in growth and metabolism, namely, the hypothalamic-pituitary-adrenal axis, the endocrine pancreas and the somatotrophic axis. It also considers how changes in these endocrine systems contribute to the programming of metabolism in later life.
Endocrine System↗
[Abdominal compartment syndrome caused by ruptured abdominal aortic aneurysm in vena cava].
BACKGROUND: Abdominal compartment syndrome (ACS) is a rapid increase in intra-abdominal pressure asssociated with multi-organs dysfunction. It is caused mostly by abdominal bleeding und massive volume compensation. CASE REPORT: We reported a 76-year-old patient admitted to the hospital with aortic abdominal aneurysm, 13.7 cm in diameter, ruptured in vena cava, which caused intraabdominal hypertension, the liver and kidney dysfunction, as well as circulation, respiration and metabolic disorders. Intraabdominal pressure was measured by bladder manometry. Central venous pressure and systemic arterial pressure were monitored continuously. Clinical signs were thrill and typical abdominal bruit. Aorto-caval fistula was diagnosed by the use of contrast computerized tomography. Caval endoaneurysmatic suture and aortobiiliac bypass with 18 x 9 mm Dacron prothesis were performed. Haemodynamic changes were mostly corrected during the surgery. The complete correction of haemodynamics, liver, kidney, respiration and metabolic changes was established in the next few weeks. CONCLUSION: The ACS was caused by rupture of abdominal aortic aneurysm in vena cava followed by edema of the abdominal organs, retroperitoneum, abdominal wall and ascites. Caval endoaneurysmatic suture and aortobiiliac bypass with 18 x 9 mm Dacron prothesis solved aortocaval fistula as well as all the organs and metabolic dysfunctions caused by ACS.
Abdominal Cavity↗
Do female patients with metabolic syndrome have masked left ventricular dysfunction?
OBJECTIVE: Metabolic syndrome (MS) is a condition, which is recognized as raising the risk of cardiovascular disease. The aim of our study is to estimate the left ventricular functions by atrioventricular plane displacement (AVPD), myocardial performance index (MPI) and conventional methods in patients with MS who were diagnosed according to NCEP (ATP III) criteria. METHODS: Fifty-three female patients with MS (mean age 53.1+/-6.9 years) and 30 healthy female subjects (mean age 52.8+/-6.3 years, p>0.05) underwent complete echocardiographic assessment. All of the subjects had no heart and pulmonary diseases. The systolic mitral AVPD was recorded at 4 sites (septal, lateral, anterior, and posterior) by M-mode echocardiography and left ventricle ejection fraction (LVEF) was calculated from the AVPD-mean (EF-AVPD). The LVEF was also established by biplane Simpson's (EF-2D) and Teichholz's methods (EF-T). Left ventricular MPI was calculated as (isovolumic contraction time + isovolumic relaxation time) / aortic ejection time by Doppler echocardiography. RESULTS: Patients with MS showed mild left ventricular diastolic dysfunction (DD) in comparison to healthy subjects. The EF-2D and EF-T in patients with MS and healthy subjects were not different significantly and were within normal limits. Patients with MS showed LV global dysfunctions compared to healthy subjects (MPI: 0.56+/-0.12 and 0.46+/-0.11 respectively, p<0.01). Both the septal, anterior, lateral and posterior part of the atrioventricular plane values and also AVPD-mean during systole were statistically lower in patients with MS (12.85+/-1.76 mm) as compared with controls (14.65+/-2.19 mm, p<0.05). The EF-AVPD in patients with MS was statistically lower (65.58+/-11.95%) as compared with healthy subjects (74.45+/-11.07%, p<0.01). CONCLUSION: Female patients with MS had both left ventricular DD and a global dysfunction with an increased MPI. The EF-2D and EF-T were not different significantly between patients and controls, but patients with MS had a relatively reduced EF-AVPD. The AVPD method may indicate a systolic dysfunction with a relatively lower AVPD-mean and relatively lower EF-AVPD. The presence of global dysfunction in patients with MS may lead to heart failure.
Case-Control Studies↗