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PubMed2004

GTP-binding protein-independent potentiation by mastoparan of IL-1beta-induced nitric oxide release from insulin-secreting HIT-T15 cells.

Our recent data implicated small molecular weight G-proteins (e.g., H-Ras) in interleukin 1beta (IL 1beta)-induced metabolic dysfunction and apoptotic demise of the islet beta cell (Tannous et al., Biochem Pharmacol 2001; 62:1459-1468, Kowluru and Morgan, Biochem Pharmacol, 2002; 63:1027-1035, Chen et al. Biochem Pharmacol, 2003; 66:1681-1694). Recently, we have shown that mastoparan, a tetradecapeptide from wasp venom, has been shown to directly activate islet endogenous G-proteins and regulate islet function (Amin et al., Endocrinology 2003; 144: 4508-4518). Herein, we investigated potential contributory roles, if any, of mastoparan (Mas)-sensitive G-proteins in IL-induced nitric oxide (NO) release from insulin-secreting HIT-T15 cells. While, ineffective by itself, Mas significantly potentiated IL-induced NO release from HIT-T15 cells. Interestingly, Mas-17, an inactive analog of Mas, also potentiated IL-induced NO release, suggesting that the potentiating effect of Mas may not involve activation of specific G-proteins. Such potentiating effects on IL-induced NO release were also demonstrable in the presence of another polycationic compound, melittin. Together, these findings suggest that Mas-induced potentiation of IL-induced NO release may in part be due to its amphiphilic and polycationic nature. These data also warrant caution in the use of Mas to study its regulation of cellular function without the use of an appropriate negative control, such as Mas-17.

Dose-Response Relationship, Drug↗

PubMed1977

Inhibition of phagocytosis and glucose metabolism of alveolar macrophages during pulmonary tumour growth.

Alveolar macrophage (AM) phagocytic activity and glucose metabolism were evaluated during lung tumour growth in adult rats challenged i.v. with 10(5) viable Walker 256 tumour cells. Phagocytosis was estimated by the in vitro uptake of (14)C-labelled Pseudomonas aeruginosa and glucose oxidation was evaluated by (14)CO(2) production from 1-(14)C-glucose. AM were harvested by lung lavage from rats prior to and at 7 and 21 days following i.v. tumour-cell challenge. Macroscopic lung tumour nodules were not observed by 7 days after tumour challenge. However, 3 weeks after tumour challenge, tumour nodules were clearly identifiable on the surfaces of the lungs. One week after the i.v. tumour challenge a marked increase in the number of AM was evident. The in vitro phagocytosis of (14)C-labelled Pseudomonas aeruginosa was unaltered at that time, but became progressively depressed thereafter. Three weeks after tumour challenge, this decrease in phagocytic activity was evident when cells were incubated in normal serum, and was furtheri ntensified by serum obtained from tumour-bearing animals. Glucose oxidation by AM in either the resting condition or during bacterial phagocytosis was clearly decreased at both 1 and 3 weeks following i.v. tumour challenge. These findings indicate that the growth of pulmonary metastases is associated with a depression of alveolar macrophage bacterial phagocytic capacity, perturbations in serum opsonic activity and distinct alterations in macrophage energy metabolism. The metabolic dysfunction may impair pulmonary macrophage host defences against lung tumour growth.

Animals↗

PubMed2004

Effects of Trolox on the activity and gene expression of cytochrome P450 in hepatic ischemia/reperfusion.

1. The aim of this study was to investigate the effect of Trolox on hepatic microsomal cytochrome P450 (CYP) activity and gene expression during ischemia and reperfusion (I/R). 2. Rats were subjected to 60 min of hepatic ischemia, and 5 h (acute phase) and 24 h (subacute phase) of reperfusion. Rats were treated intravenously with Trolox (2.5 mg kg(-1)) or vehicle, 5 min before reperfusion. 3. The serum alanine aminotransferase level and lipid peroxidation were increased as a result of I/R. These increases were attenuated by Trolox. Reduced glutathione concentration decreased in I/R group, and this decrease was inhibited by Trolox. 4. Both total hepatic CYP content and NADPH-cytochrome P450 reductase activity decreased after I/R, which were restored by Trolox. 5. CYP1A1 activity and its protein level decreased 24 h after reperfusion; decreases which were prevented by Trolox. Both the activity and mRNA expression of CYP1A2 decreased 24 h after reperfusion. The decrease in CYP1A2 mRNA was prevented by Trolox. CYP2B1 activity and mRNA expression decreased 5 h after reperfusion. The decrease in CYP2B1 activity was prevented by Trolox. In contrast, the CYP2E1 activity and its protein level increased 5 h after reperfusion and this increase was prevented by Trolox. 6. The expression of TNF-alpha and iNOS mRNAs increased after I/R. Trolox inhibited increase in iNOS mRNA expression. 7. Trolox ameliorates hepatic drug-metabolizing dysfunction, as indicated by abnormalities in CYP isoforms during I/R, and this protection is likely due to the scavenging of reactive oxygen species.

Animals↗

PubMed1990

Spatially resolved changes in diabetic rat skeletal muscle metabolism in vivo studied by 31P-n.m.r. spectroscopy.

Phase-modulated rotating-frame imaging (p.m.r.f.i.), a localization technique for 31P-n.m.r. spectroscopy, has been applied to obtain information on the heterogeneity of phosphorus-containing metabolites and pH in the skeletal muscle of control and streptozotocin-diabetic rats. Using this method, the metabolic changes in four spatially resolved longitudinal slices (where slice I is superficial and slice IV is deep muscle) through the ankle flexor muscles have been investigated at rest and during steady-state isometric twitch-contraction at 2 Hz. At rest, intracellular pH was lower, and phosphocreatine (PCr)/ATP was higher, throughout the muscle mass in diabetic compared with control animals. The change in PCr/ATP in diabetic muscle correlated with a decrease in the chemically determined ATP concentration. During the muscle stimulation period, the decrease in pH observed in diabetic muscle at rest was maintained, but not exacerbated, by the contractile stimulus. Stimulation of muscle contraction caused more marked changes in PCr/(PCr + Pi), PCr/ATP and Pi/ATP in the diabetic group. These changes were most evident in slice III, which contains the greatest proportion of fast glycolytic-oxidative (type IIa) fibres, in which statistically significant differences were observed for all metabolite ratios. The results presented suggest that some degree of heterogeneity occurs in diabetic skeletal muscle in vivo with respect to the extent of metabolic dysfunction caused by the diabetic insult and that regions of the muscle containing high proportions of type IIa fibres appear to be most severely affected.

Adenosine Triphosphate↗

PubMed2000

Exercise training and peripheral vascular disease.

BACKGROUND: Conservative management is advocated as a treatment of choice for patients with intermittent claudication. This is a review of the mechanisms behind the improvement following an exercise rehabilitation programme. METHODS: All Medline articles from the National Library of Medicine, USA containing the text words 'claudication' or 'peripheral vascular disease' and 'exercise' were reviewed. Cross-referencing from relevant articles was carried out. RESULTS AND CONCLUSION: The poor physical status of a patient with intermittent claudication is not solely due to a reduction in blood flow to the lower limbs; associated factors, such as metabolic inefficiency, poor cardiorespiratory reserve and exercise-induced inflammation contribute. An exercise programme frequently improves both the physical aspect and quality of life, and the success of such exercise is multifactorial. An increase in the blood flow to the lower extremity is uncommon. Other factors, such as a redistribution of blood flow, changes in oxidative capacity of the skeletal muscles and greater utilization of oxygen, occur and the associated metabolic dysfunction of the skeletal muscles is rectified. Following exercise training, blood rheology improves and exercise-induced inflammation is ameliorated; cardiorespiratory status also benefits and the oxygen cost of exercise decreases.

Biomechanical Phenomena↗

PubMed2001

Histological changes in the hypofunctional pituitary gland following conventional radiotherapy for adenoma.

AIMS: Although delayed hypopituitarism is a common complication of conventional radiotherapy of sellar tumours, histological changes that may account for it have been rarely reported. To elucidate the changes, hypofunctional pituitary glands following irradiation were studied. METHODS AND RESULTS: Two pituitary glands obtained at autopsy from patients who had been irradiated for adenoma and exhibited hypopituitarism were examined. In both cases diffuse fibrosis was observed in the adenohypophysis, whereas the neurohypophysis remained unchanged. Immunohistochemistry showed that stellate-shaped S100 protein-positive cells were increased in number and distributed among the endocrine cells. Some irradiated endocrine cells showed dense granular immunoreactivity for mitochondrial protein, cytochrome oxidase and manganese-superoxide dismutase. In addition to faint reactivity with anti-cytokeratin 8, 18 antibody, many cells were densely positive with anti-cytokeratin 1, 5, 10, 14 antibody. CONCLUSIONS: These results indicate that radiation- induced fibrosis is associated with an increased number of folliculo-stellate cells and the presence of metabolic dysfunctional mitochondria resembling mitochondria in oncocytes. Squamous metaplasia in the irradiated endocrine cells was also noted. Various intracellular changes may participate in delayed pituitary hypofunction following radiotherapy.

Adenoma↗

PubMed2001

Increased levels of tPA antigen and tPA/PAI-1 complex in myotonic dystrophy.

OBJECTIVE: To assess the fibrinolytic system in myotonic dystrophy (DM1), a disease connected to features of the metabolic syndrome, including a prominent insulin resistance, increased body fat mass, and hypertriglyceridaemia. We hypothesized that abnormalities in the fibrinolytic system are linked to metabolic dysfunction in DM1. DESIGN: Circulating morning levels of tissue plasminogen activator (tPA) and plasminogen activator inhibitor type 1 (PAI-1) antigens, tPA/PAI-1 complex, lipids and insulin were determined. Genetic analyses, including calculation of allele size, were performed in all patients. Body fat mass was estimated with bioelectrical impedance analysis. SETTING: Out-patient clinic in collaboration with Umeå University Hospital. SUBJECTS: A total of 42 otherwise healthy patients with DM1 (22 men, 20 women; median age 41.5 years) and 50 controls (27 men, 23 women; median age 42.0 years). MAIN OUTCOME MEASURES: The tPA and PAI-1 antigens, tPA/PAI-1 complex, blood lipids and body fat mass. RESULTS: The tPA antigen and tPA/PAI-1 complex levels were significantly increased in DM1 patients (P < 0.001 and P < 0.05, respectively) whilst levels of PAI-1 did not differ from controls. Triglyceride levels were increased (P < 0.001) whereas HDL cholesterol levels were lower in DM1 patients (P < 0.05). Body fat mass was increased in DM1 patients (P < 0.001). CONCLUSIONS: The fibrinolytic system is disturbed in DM1 patients, with increased levels of tPA and tPA/PAI-1 complex but paradoxically unaltered levels of PAI-1, in spite of a severely increased body fat mass. This may imply an abnormal function of adipose tissue in DM1, and calls for further studies of the fibrinolytic system in this disease.bstra

Adult↗

PubMed1985

Classic migraine attack complicated by confusional state: EEG and CT study.

We report electroencephalographic and clinical observations in one attack of classic migraine, accompanied by a confusional state. The ictal EEG showed slow waves over the left hemisphere, the abnormality gradually clearing up during the four days following the attack. A brain CT scan was normal during the attack and also a few days later. A possible relationship between impairment of consciousness during the attack and left hemispheric metabolic dysfunction is discussed.

Adolescent↗

PubMed1994

Enhanced phosphodiestric breakdown of phosphatidylinositol bisphosphate after experimental brain injury.

Regional levels of lactate and inositol 1,4,5-trisphosphate (IP3), a cellular second messenger of the excitatory neurotransmitter system, were measured after lateral fluid percussion (FP) brain injury in rats. At 5 min postinjury, tissue lactate concentrations were significantly elevated in the cortices and hippocampi of both the ipsilateral and contralateral hemispheres. By 20 min postinjury, lactate concentrations were elevated only in the cortices and hippocampus of the ipsilateral hemisphere. Whereas the IP3 concentrations were elevated in the hippocampi of the ipsilateral and contralateral hemisphere and in the cortex of ipsilateral hemisphere at 5 min postinjury, no elevation in these sites was found at 20 min postinjury. Histologic analysis revealed neuronal damage in the cortex and CA3 regions of hippocampus ipsilateral to the injury at 24 h postinjury. The present results suggest activation of the phosphoinositide signal transduction pathway at the onset of injury and of a possible requirement of early persistent metabolic dysfunction (> 20 min) such as the lactate accumulation in the delayed neuronal damage.

Animals↗

PubMed2000

Clinical relevance of cytokine production in hemodialysis.

Blood-dialyzer interaction in hemodialysis has the potential to activate mononuclear cells leading to the production of inflammatory cytokines. The extent of activation is dependent on the dialyzer material used and is considered an index of biocompatibility. Cytokines, such as interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and IL-6, may induce an inflammatory state and are believed to play a significant role in dialysis-related morbidity. The interleukin hypothesis suggests that the release of proinflammatory cytokines acts as an underlying pathophysiologic event in hemodialysis-related acute manifestations, such as fever and hypotension. Nevertheless, a cytokine overproduction may alter sleep pattern in chronic hemodialyzed patients, thus explaining the presence of sleep disorders in these patients. A potential role of cytokines in chronic-related morbidity has also been suggested. High levels of some inflammatory cytokines are often associated with anemia caused by hyporesponsiveness to erythropoietin. Cytokine production may also play a relevant role in bone remodeling by regulating osteoblast/osteoclast cell functions and parathyroid hormone (PTH). Finally, cytokine release may have a long-term deleterious effect on mortality of uremic patients by altering immune response and increasing susceptibility to infections. Bioincompatibility of dialytic membranes may also contribute to malnutrition in dialysis patients by increasing the monocyte release of catabolic cytokines such as TNF-alpha and IL-6. Bioincompatible dialytic treatment may induce an inappropriate monocyte activation and cytokine production, which, in turn, may mediate some of the immune and metabolic dysfunction associated with hemodialysis. The use of biocompatible dialytic membranes appears to reduce the monocyte activation and to improve the survival of hemodialysis patients.

Biocompatible Materials↗

PubMed2001

Time course of postoperative recovery of N-acetyl-aspartate in temporal lobe epilepsy.

PURPOSE: To assess the time course of increases in N-acetyl-aspartate/creatine (NAA/Cr), which can be measured using proton MR spectroscopic imaging (1H-MRSI), in patients with intractable nonlesional temporal lobe epilepsy (TLE) after successful epilepsy surgery. METHODS: We performed pre- and postoperative 1H-MRSI in 16 seizure-free (SF) patients and 16 not seizure-free (NSF) TLE patients. We calculated a mixed-design analysis of variance (ANOVA) between SF and NSF groups, ipsi- and contralateral to the side of operation, and pre- and postoperative NAA/Cr measurements. We applied nonlinear regression between pre- and postoperative NAA/Cr differences and the time interval between 1H-MRSI scans to fit a negative exponential model to NAA recovery. RESULTS: Mixed-design ANOVA revealed that (a) postoperative NAA/Cr was significantly higher in SF than in NSF patients (p = 0.02) and that (b) in the SF group, postoperative NAA/Cr values were significantly higher than preoperative values (p < 0.05) and returned to the normal range in most patients. According to our nonlinear regression model, in SF patients, there was a 50% increase relative to preoperative NAA/Cr values after 5.8 months, whereas an improvement of 95% was reached after 25 months. CONCLUSIONS: Our results extend preliminary observations of postoperative NAA recovery of SF patients by characterizing the time course of recovery as an exponential function with a half-time of approximately 6 months. The reversal of neuronal metabolic dysfunction remote from the epileptic focus may underlie the clinical observation of improvement of cognitive dysfunction after successful epilepsy surgery.

Adolescent↗

PubMed1988

EEG changes in untreated hyperthyroidism and under the conditions of thyreostatic treatment.

20 patients with hyperthyroidism were observed with repeated EEG measurements before and during treatment (ObsidanR; MethimazolR). 17 patients, before starting antithyroid therapy, had slight to moderate EEG abnormalities. A prevalence for moderate disturbances occurred for patients with a higher degree of hyperthyroidism. The dominant EEG frequency was higher than in euthyroid controls, but no exact correlation to T3-values could be observed. 16 patients showed abnormal reactivity to photic stimulation. One-week therapy by propranolol produced only a slight synchronizing effect in EEG's, where T3-values decreased. After 4 weeks selective therapy by MethimazolR all patients were euthyroid, but some EEG abnormalities persisted in 12 patients in a lower degree. The dominant EEG frequency decreased to control-group ranges and abnormal photic reactivity was reduced. After 6 months some EEG disturbances re-increased tentiatively, in 3 relapses excessively. These observations confirm the prognostic value of EEG measurements for the recognition of occurrence and persistence of cerebral disturbances in severe metabolic dysfunctions.

Adult↗

PubMed2005

[Psychosocial factors in coronary heart disease -- scientific evidence and recommendations for clinical practice].

Psychosocial risk factors like low socio-economic status, lack of social support and social isolation, chronic work or family stress, as well as negative emotions, e. g. depression and hostility, contribute significantly to the development and adverse outcome of coronary heart disease (CHD). Negative effects of psychosocial risk factors are conveyed via behavioural pathways including unhealthy lifestyle, e. g. food choice, smoking, sedentary life, inadequate utilisation of medical resources, and psychobiological mechanisms like disturbed autonomic and hormonal regulation: all these factors contribute to metabolic dysfunction and inflammatory and haemostatic processes, which are directly involved in the pathogenesis of CHD. Interventions to improve pychosocial factors are available and have demonstrated positive effects on risk factors and - at least in part - on CHD morbidity and mortality. The prevention of CHD should therefore include screening for psychosocial risk factors and adequate interventions. Recommedations for the screening of risk factors, behavioural change and further management of psychosocial risk factors in clinical practice are pointed out.

Coronary Disease↗

PubMedDate not supplied

[Embryopathy and diabetic fetopathy in a premature stillborn infant. Case report and review of the disease picture].

The diabetic embryopathy syndrome comprises a number of developmental anomalies among fetuses of diabetic mothers. Fetopathia diabetica, on the other hand, is characterized by typical, hormonal, and metabolic dysfunctions and their morphological sequelae in fetuses and offsprings of diabetic mothers. We observed the combination of both these conditions in an immature stillborn fetus. The 34 year-old diabetic mother, who had been treated by insulin since age 16, was first seen at 27 weeks of gestation. Sonography revealed severe congenital malformations of the fetus, and a late abortion was induced. The stillborn female revealed the typical congenital malformations of the diabetic embryopathy syndrome, such as abnormalities of face and skull, skeletal malformations of the thorax, spine, and lower extremities, and malformations of the heart, great vessels and the genitourinary system. We, too, found the characteristic features of fetopathia diabetica, i.e. obesity, macrosomia, increased weight and size of the internal organs, polynesia and macronesia of the pancreas, increased extramedullary hematopoiesis and cellular depletion of lymphoid tissues. A review of the literature revealed various hypotheses about the etiology and pathogenesis of both conditions.

Abnormalities, Multiple↗

PubMedDate not supplied

[Etiology and pathogenesis of epiphyseal necrosis in childhood as exemplified with the hip].

In many cases the etiology of juvenile necrosis of the femoral head has not been unequivocally explained. Essentially, however, it is due to reduced arterial blood flow, although venous congestion also has to be considered. Epiphyseal necrosis is frequently a result of known underlying diseases. These include, for example, both specific and nonspecific forms of coxitis and rheumatic coxitis, hormonal dysfunctions, metabolic disorders such as mucopolysaccharidosis, blood diseases (e.g. hemophilia, sickle cell anemia), leukosis, and tumors and necrosis following cortisone and cytostatic therapy. The following four factors may directly or indirectly cause arterial vascular damage and thus necrosis: 1) primarily exogenous and 2) primarily endogenous factors, 3) genetic, and 4) skeletal maturation factors. These etiological factors are described in detail and discussed. Epiphyseal deformation occurs in a strict sequence of five phases, which are described. It should be emphasized that while necrotic bone tissue is being gradually resorbed, deposits of new bone matrix are already accumulating on dead trabecula and will subsequently form new bone fibre. In other word, a gradual substitution takes place. Two important clinical facts derive from this. First, epiphyseal crash is not due to the load of the body's weight. Since active resorption takes place, there is no justification for weight-relieving therapy in the basic therapeutic concept for Perthes' disease. Second, in light of our studies, surgical containment therapy appears to be the most suitable form of treatment if performed at the right time, i.e. in the golden period of remodelling, depending on the patient's age, the extent of necrosis and the degree of dislocation. Where stringent criteria are fulfilled we perform a three-dimensional intertrochanteric osteotomy, i.e. an extension-derotation reduction osteotomy.

Child↗

PubMed1987

Perioperative morbidity associated with operative resection of craniopharyngioma: a review of ten years experience.

A ten-year review of perioperative morbidity after operative resection of craniopharyngioma is presented. From 1974 to 1983, 23 patients underwent a total of 34 operations. Patients were subdivided into 95% or greater resection and partial resection groups. Features compared between the two groups included sodium, glucose, temperature, diabetes insipidus, major complications, neurological deficits and death. Patients undergoing 95% or greater resection had significant fluctuations in sodium, temperature and glucose (p less than .01). Diabetes insipidus and major postoperative complications were also significantly elevated in the 95% or greater resection group (p less than .05). Therefore, the extent of surgical resection correlated well with the degree of metabolic dysfunction and major postoperative complications. Careful assessment of surgical morbidity is warranted in the management of patients with craniopharyngioma.

Body Temperature Regulation↗

PubMed1991

[Insulin-induced edema in adolescents with type 1 diabetes mellitus].

Two girls (aged 14 and 16 years) with type I diabetes were hospitalized with blood sugar levels of 394 and 319 mg/dl as well as HbA1 levels of 14.2 and 14.1%, respectively. In the first case it was the first sign of diabetes, in the other it was the result of a metabolic dysfunction with an injection abscess after ten years of the disease. After an initial substitution with regular insulin (subcutaneously in Case 1 [1.5-1.7 IU/kg daily for 3 days; in Case 2, continuous i.v. infusion [1.3 IU/kg daily] for 58 hours, followed by injections of appropriate mixtures of short and long-acting insulin) serum glucose levels were nearly always within normal range from the third day onward. Within 6 days of normal glucose levels being established hard pitting oedema, especially of the legs, developed in both girls, associated with a weight gain of 6.1 and 7.0 kg, respectively. Renal, hepatic and cardiovascular disease having been excluded the diagnosis of insulin-induced oedema was made. Within a further two weeks the oedema had disappeared without any specific treatment.

Adolescent↗

PubMed2001

Peroxisome proliferator-activated receptor-gamma ligands inhibit adipocyte 11beta -hydroxysteroid dehydrogenase type 1 expression and activity.

Peroxisome proliferator-activated receptor-gamma (PPARgamma) has been shown to play an important role in the regulation of expression of a subclass of adipocyte genes and to serve as the molecular target of the thiazolidinedione (TZD) and certain non-TZD antidiabetic agents. Hypercorticosteroidism leads to insulin resistance, a variety of metabolic dysfunctions typically seen in diabetes, and hypertrophy of visceral adipose tissue. In adipocytes, the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) converts inactive cortisone into the active glucocorticoid cortisol and thereby plays an important role in regulating the actions of corticosteroids in adipose tissue. Here, we show that both TZD and non-TZD PPARgamma agonists markedly reduced 11beta-HSD-1 gene expression in 3T3-L1 adipocytes. This diminution correlated with a significant decrease in the ability of the adipocytes to convert cortisone to cortisol. The half-maximal inhibition of 11beta-HSD-1 mRNA expression by the TZD, rosiglitazone, occurred at a concentration that was similar to its K(d) for binding PPARgamma and EC(50) for inducing adipocyte differentiation thereby indicating that this action was PPARgamma-dependent. The time required for the inhibitory action of the TZD was markedly greater for 11beta-HSD-1 gene expression than for leptin, suggesting that these genes may be down-regulated by different molecular mechanisms. Furthermore, whereas regulation of PPARgamma-inducible genes such as phosphoenolpyruvate carboxykinase was maintained when cellular protein synthesis was abrogated, PPARgamma agonist inhibition of 11beta-HSD-1 and leptin gene expression was ablated, thereby supporting the conclusion that PPARgamma affects the down-regulation of 11beta-HSD-1 indirectly. Finally, treatment of diabetic db/db mice with rosiglitazone inhibited expression of 11beta-HSD-1 in adipose tissue. This decrease in enzyme expression correlated with a significant decline in plasma corticosterone levels. In sum, these data indicate that some of the beneficial effects of PPARgamma antidiabetic agents may result, at least in part, from the down-regulation of 11beta-HSD-1 expression in adipose tissue.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗