Serum hepcidin/ferroportin levels in bipolar disorder and schizophrenia

Background: Despite several alternatives for cellular iron influx, the only mechanism for cellular iron efflux is ferroportin mediated active transport. In cases of ferroportin dysfunction, iron accumulates in the cell and causes ferroptosis. Hepcidin suppresses ferroportin levels and inflammatory activation increases hepcidin production. Mild inflammation in schizophrenia and bipolar disorder may alter hepcidin and ferroportin. Methods: The study included a total of 137 patients aged 18-65 years, 57 diagnosed with schizophrenia and 80 with bipolar disorder, according to the DSM-IV diagnostic criteria, and a control group (HC) of 42 healthy in-dividuals. Biochemical analyses, thyroid function tests, hemogram, serum iron level, iron-binding capacity, and ferritin levels were examined. Serum levels of hepcidin and ferroportin were measured with enzyme-linked immunosorbent assay (ELISA) method. Results: A statistically significant difference was determined between the groups in terms of the serum ferroportin levels (F = 15.69, p < 0.001). Post-hoc analyses showed that the schizophrenia group had higher ferroportin levels than in the bipolar group (p < 0.001) and HCs (p < 0.001). Hepcidin levels did not differ between the groups. Chlorpromazine equivalent doses of antipsychotics correlated with ferroportin levels (p = 0.024). Conclusion: Ferroportin levels were increased in the schizophrenia group, although iron and hepcidin levels were within normal ranges. Antipsychotics may alter the mechanisms which control ferroportin levels. Further studies are needed to examine the relationships between antipsychotics and iron metabolism for determination of causal relationship

Blood levels of agouti-related peptide (AgRP), obestatin, corticosteroid-binding globulin (CBG), and cortisol in patients with bipolar disorder (BD): a case–control study

OBJECTIVES: Bipolar disorder (BD) is a chronic psychiatric disorder with a high prevalence of obesity. There are a number of hypotheses regarding the association between obesity and BD. One involves common neurobiological abnormalities, such as dysfunction in the hypothalamic pituitary adrenal axis and changes in secretions of orexigenic and anorectic peptides. The purpose of this study was to evaluate the blood levels of agouti-related peptide (AgRP), obestatin cortisol, and corticosteroid-binding globulin (CBG) and metabolic parameters in patients with euthymic BD, and to compare these to those of healthy controls. METHODS: Twenty-nine outpatients with BD type I admitted to the psychiatric clinic were consecutively enrolled and compared with 25 sex- and body mass index (BMI)-matched controls. RESULTS: There was a significant difference in AgRP, cortisol, and CBG levels between patients and the controls (p = .005, .021, and .034, respectively). AgRP and CBG did not correlate with any parameter in BD patients, but cortisol correlated with BMI. CONCLUSIONS: We conclude that BD patients have higher levels of AgRP, cortisol, and CBG than healthy controls with similar BMIs. This may represent a new insight into the neurobiology of BD

The effects of edaravone in ketamine-induced model of mania in rats

Bipolar disorder is a chronic disease characterized by recurring episodes of mania and depression that can lead to disability. This study investigates the protective effects of edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a drug with well-known antioxidant properties, in a model of mania induced by ketamine in rats. Locomotor activity was assessed in the open-field test. Superoxide dismutase (SOD), catalase (CAT) and thiobarbituric acid reactive substances (TBARS) levels were measured in order to evaluate oxidative damage in the rat hippocampus and prefrontal cortex. Increased locomotor activity (hyperlocomotion) was observed at the open-field test with ketamine treatment (25 mg/kg, i.p., 8 days). Edaravone (18 mg/kg) treatment did not prevent hyperlocomotion in the mania model induced with ketamine in rats, but lithium chloride (47.5 mg/kg, i.p., positive control) did prevent hyperlocomotion. Edaravone and lithium chloride treatments were found to reduce the increase in SOD and CAT activity following ketamine administration in a non-significant manner but caused no change in TBARS levels