Metabolic Hormones in Schizophrenia Patients with Antipsychotic-Induced Metabolic Syndrome

Boiko, Anastasiia S.; Mednova, Irina A.; Kornetova, E.; Goncharova, A. A.; Semke, A.; Бохан, Н. А.; Ivanova, Svetlana A.

doi:10.3390/jpm12101655

Cited by 4 publications

(1 citation statement)

References 48 publications

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“…MetS is a predisposing factor for cardiovascular pathologies and is regarded as a mortality risk factor in patients with mental disorders. Information on the pathogenesis of MetS can be obtained by studying hormones regulating metabolism and their genes, which in turn can also be considered potential biomarkers of the susceptibility to MetS and to lipid metabolism disorders [ 8 , 9 ]. Currently, aside from the generally accepted signs of MetS (central obesity, hyperglycemia, dyslipidemia, and blood pressure elevation), an important role is attributed to other and newer signs of MetS, such as microalbuminuria, cytokines, prothrombotic and fibrinolytic factors, and oxidative stress [ 10 , 11 , 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Cell Adhesion Molecules in Schizophrenia Patients with Metabolic Syndrome

et al. 2023

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Metabolic syndrome (MetS) is a common comorbidity of schizophrenia and significantly shortens life expectancy of the patients. Intercellular (ICAM), vascular (VCAM), and neural (NCAM) cell adhesion molecules (CAMs) mediate neuroinflammatory processes, and their soluble forms (e.g., sICAM) in plasma are present in parallel with their cell-bound forms. In this study, their serum levels were examined in 211 white Siberian patients with paranoid schizophrenia (82 patients with and 129 without MetS according to the 2005 International Diabetes Federation criteria). Serum levels of CAMs were determined with Magpix and Luminex 200 (Luminex, Austin, TX, USA) using xMAP Technology. The level of sICAM-1 was significantly higher and that of sVCAM-1 significantly lower in patients with MetS compared to patients without MetS. Levels of NCAM did not differ between the groups. More pronounced Spearman’s correlations between CAMs, age, duration of schizophrenia, and body–mass index were observed among patients without MetS than among patients with MetS. Our results are consistent with MetS’s being associated with endothelial dysfunction along with other components of inflammation. Through these endothelial components of peripheral inflammatory processes, MetS might induce intracerebral neuroinflammatory changes, but further investigation is needed to confirm this.

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Section: Introductionmentioning

confidence: 99%

Cell Adhesion Molecules in Schizophrenia Patients with Metabolic Syndrome

et al. 2023

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Pilot Study of the DRD3, GHRL, FTO, LEPR, INSIG2, GSTP1, and ABCB1 Gene Expression in Peripheral Blood Leukocytes in Schizophrenic Patients with Metabolic Syndrome

Boiko,

Paderina,

Mikhalitskaya

et al. 2024

Neurochem. J.

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Abstract—Many individuals with schizophrenia also suffer from metabolic syndrome (MetS), which is a major risk factor for the development of cardiovascular disroders associated with a heavy burden of disease, as well as with premature death of patients. This study investigated the expression of 7 genes potentially important for the development of metabolic syndrome. QuantiGene Plex 2.0 technology was used to measure how 7 studied genes (DRD3, GHRL, FTO, LEPR, INSIG2, GSTP1, and ABCB1 (MDR1)) were expressed in leukocytes in 60 recently admitted patients with schizophrenia who had been on treatment with antipsychotic drugs. The preliminary results of our study show a change in the expression of the FTO gene in schizophrenic males with metabolic disorders, however, further studies are needed to determine the role of disturbances in the expression of this gene in the development of the metabolic syndrome in patients with schizophrenia.

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The Pathologic Roles and Therapeutic Implications of Ghrelin/GHSR System in Mental Disorders

Mao,

Wang,

Yang

et al. 2024

Depression and Anxiety

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Ghrelin is a hormone consisting of 28 amino acids. Growth hormone secretagogue receptor (GHSR) is a receptor for ghrelin, which is expressed in the brain, pituitary gland, and adrenal glands, especially in the hypothalamus. The binding of ghrelin to the receptor 1a subtype mediates most of the biological effects of ghrelin. Ghrelin has a close relationship with the onset of psychosis. Ghrelin can affect the onset of psychosis by regulating neurotransmitters such as dopamine, γ‐aminobutyric acid (GABA), and 5‐hydroxytryptamine (5‐HT) through the hypothalamus–pituitary–adrenal (HPA) axis, brain–gut axis, the mesolimbic dopamine system, and other ways. Ghrelin activates neuropeptide Y (NPY) in the hypothalamic arcuate nucleus (ARC) through the GHSR. Ghrelin binds to neurons in the ventral tegmental area (VTA), where it promotes the activity of dopamine neurons in the nucleus accumbens (NAcs) in a GHSR–dependent way, increasing dopamine levels and the reward system. This article summarized the recent research progress of ghrelin in depression, anxiety, schizophrenia, anorexia nervosa (AN), and bulimia nervosa (BN), and emphasized its potential application for psychiatric disorders treatment.

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Metabolic Hormones in Schizophrenia Patients with Antipsychotic-Induced Metabolic Syndrome

Cited by 4 publications

References 48 publications

Cell Adhesion Molecules in Schizophrenia Patients with Metabolic Syndrome

Cell Adhesion Molecules in Schizophrenia Patients with Metabolic Syndrome

Pilot Study of the DRD3, GHRL, FTO, LEPR, INSIG2, GSTP1, and ABCB1 Gene Expression in Peripheral Blood Leukocytes in Schizophrenic Patients with Metabolic Syndrome

The Pathologic Roles and Therapeutic Implications of Ghrelin/GHSR System in Mental Disorders

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