PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Metabolic dysfunction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 973 records · Page 54Linked to original sources
PubMed1985

Cellular function in liver and muscle during hemorrhagic shock in primates.

The results of this study demonstrated that muscle ATP levels were sustained in hemorrhagic shock despite marked deterioration of muscle function as indicated by a decline in PD. This indicated that energy depletion was not the primary basis of the cellular dysfunction in hemorrhagic shock. Cellular dysfunction and metabolic abnormalities in the liver occurred earlier during the course of hemorrhagic shock than in muscle. Other studies were cited in which it was suggested that inhibition of the membrane bound sodium and potassium active transport mechanism is the likely cause of tissue electrolyte and fluid shifts observed during prolonged periods of hemorrhagic shock.

Adenosine Triphosphate↗
PubMed1984

Reye's syndrome.

Reye's syndrome (encephalopathy with fatty infiltration of the viscera) is an acute illness of childhood that produces hepatic dysfunction and metabolic encephalopathy. The disease is fatal in as many as 40% of cases. The cause is unknown. Several environmental agents, particularly salicylates and aflatoxin, have been implicated as possible toxins in this disorder. Treatment is directed at controlling intracranial pressure, reversing metabolic abnormalities and providing intensive supportive care. Normal neurologic function returns in most survivors.

Adolescent↗
PubMed1982

Calcification of the basal ganglia on computed tomography.

A review of computed tomograms (CT) of 7,120 patients demonstrated bilateral basal ganglia calcifications in 17. Skull roentgenograms were normal in all patients. Seven patients (41%) were older than 50 years of age with no basal ganglia dysfunction and metabolic abnormalities. Therefore it was thought that they may represent the senescent calcification. The second largest group was idiopathic hypoparathyroidism. These five patients (29%) were 16 to 32 years of age, had convulsive seizures and widespread calcifications. The other five patients had various symptomatology. Hypoparathyroidism should be investigated in young patients, if they have convulsive seizures and widespread basal ganglia calcifications on CT.

Adolescent↗
PubMed1978

[Copper and zinc in cerebrospinal fluid of children with neurological diseases (author's transl)].

We examined CSF copper and zinc concentrations in 30 children with acute febrile illness and meningism (control group) and in 37 patients with shortlasting seizures, febrile or not, and acute viral meningitis. The trace elements were quantitatively measured by means of atomic absorption spectrophotometry. 1. It was shown that the concentrations of copper and zinc in CSF remain constant during childhood.--2. No increase could be found in the concentrations of copper and zinc in CSF caused by the neurological diseases of our patients. These data suggest that permanent cerebral lesions as a consequence of shortlasting seizures and viral meningitis would be very unlikely and that a transient dysfunction of metabolism does not liberate copper- and zinc-metallo-proteins in CSF. 3. There was no correlation between the protein concentration in CSF and copper and zinc concentrations in CSF.

Adolescent↗
PubMed1993

Hemodynamic and regional blood flow responses of neonatal and adult dogs to endotoxin challenge.

Our recent studies showed developmental differences in the functional responses of the myocardium to isoproterenol and exogenous calcium, suggesting that decreased cardiovascular reserves in the immature heart contribute to the greater morbidity/mortality reported in neonatal compared to adult endotoxin shock. In this study, hemodynamic, hormonal and regional blood flow responses to Escherichia coli endotoxin challenge (1 mg/kg, 055:35 B lipopolysaccharide) were compared in adult (N = 12) and neonatal (19-21 days of age, N = 38) dogs. Compared to neonates, adult dogs had higher baseline mean arterial pressures (78 +/- 3 vs. 127 +/- 7 mmHg, P = 0.01), while values were lower for cardiac output (635 +/- 30 vs. 130 +/- 7 ml/kg, P = 0.01), left ventricular +dP/dt max (4,500 +/- 200 vs. 2,700 +/- 190 mmHg/sec, P = 0.02), heart rate (138 +/- 3 vs. 86 +/- 6 beats/min, P = 0.02), coronary flow (3.46 +/- 0.18 vs. 1.19 +/- 0.15 ml/min/g, P = 0.01), serum glucose (136 +/- 6 vs. 113 +/- 4 mg%, P = 0.01), insulin (20 +/- 3 vs. 15 +/- 2 mU/ml, P = 0.05), and glucagon (518 +/- 98 vs. 172 +/- 27 pg/ml, P = 0.01). Endotoxin caused progressive cardiocirculatory dysfunction and metabolic acidosis, regardless of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1993

[Anomalies of lipoprotein metabolism in chronic renal insufficiency].

Disturbances of the lipid metabolism in chronic renal failure (CRF) are characterized by an accumulation of serum VLDL, IDL, and remnants and also by a decrease of the HDL pool, especially for HDL2. CRF is also associated with a decrease of apolipoproteins (apo) AI and AII in relation to a preferential decrease of lipoparticles (Lp) AI-AII by comparison with the anti-atherogenic Lp AI containing no AII. It is furthermore characterized by a marked increase of apo CIII, which is disproportionate with respect to the increase of apo CII and the variation of apo E, in relation with an accumulation of Lp B-CIII (and also Lp B-E and Lp B-C-E for hemodialyzed patients) in the whole spectrum of low density lipoproteins. The abnormal distribution of apo into the various classes of lipoproteins is the consequence firstly of the relative inefficacy of the lipolytic process implicated in TG-rich lipoprotein metabolism (LPL dysfunction), and secondly of the abnormal reverse cholesterol transport (anomalies of CETP and LCAT). The hormonal, nutritional, and iatrogenic factors implicated in the uremic dyslipoproteinemia are described and the implications of such abnormalities on cardiovascular disease and on the progression of renal disease are discussed.

Apolipoproteins↗
PubMedDate not supplied

[Lowe syndrome: report of one case].

The Lowe syndrome, or oculocerebrorenal syndrome, is a rare X-linked recessive hereditary disease which typically involves three major systems including ocular defects (congenital cataracts, glaucoma, searching nystagmus), central nervous system defects (generalized hypotonia with decreased or absent deep tendon reflex and severe mental retardation), and renal dysfunction (progressive renal tubular dysfunction with acidosis and hyperaminoaciduria). Less than 200 cases have been reported in the English literatures since 1952. This article presents the first case of Lowe syndrome in Taiwan. Patient was a newborn who was born with congenital cataracts, glaucoma, generalized hypotonia with areflexia. In following laboratory studies showed early manifestations of renal tubular dysfunction with metabolic acidosis, proteinuria, glycosuria, phosphaturia and generalized hyperaminoaciduria (19 types). CT of brain showed an arachnoid cyst about 4.5 x 5 cm in size below the cerebellar tentorium. Large amount of copper, about 20-30 times above normal range, was detected in the urine. To our knowledge, Lowe syndrome associated with hypercupriuria and arachnoid cyst has not been reported in the past. Whether hypercupriuria is a part of the entity of this disease or prodromal stage of Wilson's disease is obscure. Further investigation and long-term observation are necessary to draw any conclusion.

Arachnoid Cysts↗
PubMed2006

Clinical implications of mitochondrial dysfunction.

Mitochondria produce metabolic energy, serve as biosensors for oxidative stress, and eventually become effector organelles for cell death through apoptosis. The extent to which these manifold mitochondrial functions are altered by previously unrecognized actions of anesthetic agents seems to explain and link a wide variety of perioperative phenomena that are currently of interest to anesthesiologists from both a clinical and a scientific perspective. In addition, many surgical patients may be at increased perioperative risk because of inherited or acquired mitochondrial dysfunction leading to increased oxidative stress. This review summarizes the essential aspects of the bioenergetic process, presents current knowledge regarding the effects of anesthetics on mitochondrial function and the extent to which mitochondrial state determines anesthetic requirement and potential anesthetic toxicity, and considers some of the many implications that our knowledge of mitochondrial dysfunction poses for anesthetic management and perioperative medicine.

Aged↗
PubMedDate not supplied

Insulin resistance and endothelial dysfunction: the road map to cardiovascular diseases.

Cardiovascular disease affects approximately 60% of the adult population over the age of 65 and represents the number one cause of death in the United States. Coronary atherosclerosis is responsible for the vast majority of the cardiovascular events, and a number of cardiovascular risk factors have been identified. In recent years, it has become clear that insulin resistance and endothelial dysfunction play a central role in the pathogenesis of atherosclerosis. Much evidence supports the presence of insulin resistance as the fundamental pathophysiologic disturbance responsible for the cluster of metabolic and cardiovascular disorders, known collectively as the metabolic syndrome. Endothelial dysfunction is an important component of the metabolic or insulin resistance syndrome and this is demonstrated by inadequate vasodilation and/or paradoxical vasoconstriction in coronary and peripheral arteries in response to stimuli that release nitric oxide (NO). Deficiency of endothelial-derived NO is believed to be the primary defect that links insulin resistance and endothelial dysfunction. NO deficiency results from decreased synthesis and/or release, in combination with exaggerated consumption in tissues by high levels of reactive oxygen (ROS) and nitrogen (RNS) species, which are produced by cellular disturbances in glucose and lipid metabolism. Endothelial dysfunction contributes to impaired insulin action, by altering the transcapillary passage of insulin to target tissues. Reduced expansion of the capillary network, with attenuation of microcirculatory blood flow to metabolically active tissues, contributes to the impairment of insulin-stimulated glucose and lipid metabolism. This establishes a reverberating negative feedback cycle in which progressive endothelial dysfunction and disturbances in glucose and lipid metabolism develop secondary to the insulin resistance. Vascular damage, which results from lipid deposition and oxidative stress to the vessel wall, triggers an inflammatory reaction, and the release of chemoattractants and cytokines worsens the insulin resistance and endothelial dysfunction.From the clinical standpoint, much experimental evidence supports the concept that therapies that improve insulin resistance and endothelial dysfunction reduce cardiovascular morbidity and mortality. Moreover, interventional strategies that reduce insulin resistance ameliorate endothelial dysfunction, while interventions that improve tissue sensitivity to insulin enhance vascular endothelial function. There is general agreement that aggressive therapy aimed simultaneously at improving insulin-mediated glucose/lipid metabolism and endothelial dysfunction represents an important strategy in preventing/delaying the appearance of atherosclerosis. Interventions that 1 correct carbohydrate and lipid metabolism, 2 improve insulin resistance, 3 reduce blood pressure and restore vascular reactivity, and 4 attenuate procoagulant and inflammatory responses in adults with a high risk of developing cardiovascular disease reduce cardiovascular morbidity and mortality. Whether these benefits hold when the same prevention strategies are applied to younger, high-risk individuals remains to be determined.

Aged↗
PubMed2002

Gene expression profiling reveals alterations of specific metabolic pathways in schizophrenia.

Dysfunction of the dorsal prefrontal cortex (PFC) in schizophrenia may be associated with alterations in the regulation of brain metabolism. To determine whether abnormal expression of genes encoding proteins involved in cellular metabolism contributes to this dysfunction, we used cDNA microarrays to perform gene expression profiling of all major metabolic pathways in postmortem samples of PFC area 9 from 10 subjects with schizophrenia and 10 matched control subjects. Genes comprising 71 metabolic pathways were assessed in each pair, and only five pathways showed consistent changes (decreases) in subjects with schizophrenia. Reductions in expression were identified for genes involved in the regulation of ornithine and polyamine metabolism, the mitochondrial malate shuttle system, the transcarboxylic acid cycle, aspartate and alanine metabolism, and ubiquitin metabolism. Interestingly, although most of the metabolic genes that were consistently decreased across subjects with schizophrenia were not similarly decreased in haloperidol-treated monkeys, the transcript encoding the cytosolic form of malate dehydrogenase displayed prominent drug-associated increases in expression compared with untreated animals. These molecular analyses implicate a highly specific pattern of metabolic alterations in the PFC of subjects with schizophrenia and raise the possibility that antipsychotic medications may exert a therapeutic effect, in part, by normalizing some of these changes.

Adult↗
PubMed2026

Quantitative proteomic profiling of neural cells-specific metabolic reprogramming in response to mitochondrial dysfunction using iMPAQT2.

Age-related mitochondrial dysfunction is increasingly recognized as a key contributor to neurodegenerative disease pathogenesis. In the central nervous system, neurons, oligodendrocytes, and astrocytes which derived from neural stem cells, fulfill distinct metabolic and functional roles. However, the specific vulnerabilities of these cell types to mitochondrial impairment remain unclear. In this study, we employed the iMPAQT2 proteomics platform to systematically compare the metabolic profiles of neurons, oligodendrocytes, and astrocytes, and to elucidate the molecular consequences of mitochondrial dysfunction induced by chloramphenicol and oligomycin. Our findings indicate that neurons and oligodendrocytes primarily rely on oxidative phosphorylation (OXPHOS) for ATP production, whereas astrocytes predominantly utilize glycolysis. It is noteworthy that oligodendrocytes exhibited enriched pathways for cholesterol synthesis, fatty acid degradation, and heme catabolism-processes that are critical for myelin maintenance. Treatment with the mitochondrial function inhibitors chloramphenicol or oligomycin reduced the expression of OXPHOS enzymes in all cell types. This reduction was particularly pronounced in oligodendrocytes for glycolysis, cholesterol synthesis, heme degradation, and fatty acid degradation. These results suggest that oligodendrocytes are particularly vulnerable to mitochondrial dysfunction, which may play a pivotal role in the pathogenesis of age-related neurodegenerative disorders.

Animals↗
PubMed1988

Motor dysfunction in olivopontocerebellar atrophy is related to cerebral metabolic rate studied with positron emission tomography.

We compared the severity of motor dysfunction with local cerebral metabolic rates for glucose (lCMRGlc) and the degree of tissue atrophy in 30 patients with olivopontocerebellar atrophy (OPCA). We devised a scale to quantitate the degree of ataxia in the neurological examinations. lCMRGlc was measured with 18F-2-fluoro-2-deoxy-D-glucose and positron emission tomography (PET). Tissue atrophy was assessed by visual rating of computed tomographic scans. PET studies revealed marked hypometabolism in the cerebellar vermis, cerebellar hemispheres, and brainstem of OPCA patients compared with 30 control subjects. A significant correlation was found between severity of motor impairment and lCMRGlc within the cerebellar vermis, both cerebellar hemispheres, and the brainstem. A significant but weaker relationship was noted between the degree of tissue atrophy in these regions and clinical severity. Partial correlation analysis revealed that motor dysfunction in OPCA correlated more strongly with lCMRGlc than with the amount of tissue atrophy. These results suggest that the clinical manifestations of OPCA are more closely related to the metabolic state of the tissue than to the structural changes in the cerebellum.

Adult↗
PubMed1998

Frontal dysfunction in neurologically normal chronic alcoholic subjects: metabolic and neuropsychological findings.

BACKGROUND: Neuropsychological and imaging studies suggest that frontal dysfunction may occur in apparently normal chronic alcoholic subjects. METHODS: To investigate this issue further, we performed neuropsychological and fluorodeoxy-glucose-PET studies in 17 chronic alcoholics without patent neurological and psychiatric complications. RESULTS: Metabolic abnormalities were found in the mediofrontal and in the left dorsolateral prefrontal cortex, but not in the orbitofrontal cortex. Neuropsychological testing revealed significantly reduced verbal fluency and impaired performance on the Stroop test. The mediofrontal hypometabolism correlated with the reduction in verbal fluency and the time necessary to perform the interference condition of the Stroop test. The left dorsolateral prefrontal hypometabolism correlated with the number of errors on the Stroop test. CONCLUSION: These data indicate that circumscribed frontal dysfunctions may occur in chronic alcoholic subjects before clinically obvious neurological complications, and may account for some of the alcohol-related neuropsychological and behavioural impairments.

Adult↗
PubMed1999

Potential interactions of zinc in the neuroendocrine-endocrine disturbances of diabetes mellitus type 2.

An accumulation of evidence implicates leptin, insulin, glucocorticoids, proopiomelanocortin (POMC), and neuropeptide Y (NPY) interactions as being integral to metabolic control associated with neuroendocrine-endocrine functioning. Dysfunction of neuroendocrine-endocrine interactions contributes to the metabolic disturbances of diabetes mellitus type 2 (DM-2). Since Zn has a direct impact on the healthy functioning of hormonal and neuropeptide balance, it is possible that altered Zn status and metabolism in DM-2 are involved in some of the metabolic dysfunctions of DM-2.

Animals↗
PubMedDate not supplied

The metabolic syndrome: a cause of sexual dysfunction in women.

Female sexual dysfunction (FSD) is a significant public health problem. We assessed the prevalence of FSD in premenopausal women with the metabolic syndrome as compared to the general female population. Compared with the control group (N = 80), women with the metabolic syndrome (N = 120) had reduced mean full Female Sexual Function Index (FSFI) score (23.2+/-5.4 vs 30.1+/-4.7, P < 0.001), reduced satisfaction rate (3.5+/-1.1 vs 4.7+/-1.2, P < 0.01), and higher circulating levels of C-reactive protein (CRP: 2.2 (0.6/4.9) vs 0.8 (0.2/2.9) mg/l, median (interquartile range), P = 0.01). There was an inverse relation between CRP levels and FSFI score (r = -0.32, P=0.02). Investigation of female sexuality is suggested for patients with the metabolic syndrome.

Adult↗