BACKGROUND: There is a growing interest in metabolic alterations in patients with psychiatric disorders due to their increased risk for metabolic syndrome (MetS) development. Inflammation is known to underlie the pathophysiology of schizophrenia and depression as well as MetS. Vulnerability factors for schizophrenia/depression and MetS hence appear to be shared. METHODS AND RESULTS: Based on a Web of Science search, this review examines current evidence for MetS pathophysiology involving dysregulation of adipose tissue signaling - adipokines and pro-inflammatory cytokine, both also known to be aberrant in schizophrenia/depression. Further, gender differences in the incidence and course of schizophrenia/depression were reported. The disturbances linked to the MetS are also described. Therefore, this review further maps the gender differences in the psychiatric-metabolic comorbidities. CONCLUSION: There is evidence supporting a pathological predisposition to MetS in both schizophrenia and depression in both humans and animal models. This predisposition is dramatically enhanced by antipsychotic medication. Further, there are gender differences from clinical findings suggesting women with schizophrenia/depression are more vulnerable to MetS development. This has not yet been assessed in animal studies. We suggest further validation of existing schizophrenia and depression animal models for the assessment of metabolic disturbances to provide tools for developing new antipsychotics and antidepressants with "metabolically inert" profile or improving the metabolic status in schizophrenic/depressed patients.
- Klíčová slova
- AFABP, adipokines, adiponectin, depression, leptin, metabolic syndrome, resistin, schizophrenia, sex/gender differences,
- MeSH
- cytokiny fyziologie MeSH
- depresivní poruchy komplikace MeSH
- lidé MeSH
- metabolický syndrom psychologie MeSH
- modely nemocí na zvířatech MeSH
- pohlavní dimorfismus MeSH
- resistin fyziologie MeSH
- schizofrenie komplikace MeSH
- zánět patofyziologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- cytokiny MeSH
- resistin MeSH
Both immune and non-immune mechanisms are involved in muscle damage and dysfunction occurring in idiopathic inflammatory myopathies (IIMs). Crosstalk among inflammatory cells, muscle and endothelial cells is essential in the pathogenesis of IIMs. Resistin, originally described as an adipokine linking obesity and insulin resistance in rodents, has been shown a pro-inflammatory molecule in humans. Besides its direct effect on production of several inflammatory mediators, resistin influences chemotaxis, migration, proliferation, cell survival, endothelial dysfunction and metabolism--all aspects implicated in the pathogenesis of IIMs. Up-regulation of resistin in muscle tissue and elevated serum resistin levels have been recently demonstrated in patients with IIMs. In addition, serum levels of resistin reflected global disease activity, including extramuscular organ involvement, in patients with this disease. However, there are currently not sufficient data to distinguish the features of resistin that cause injury of muscle tissue from those that promote muscle regeneration and repair. The aim of this review is therefore to summarize current knowledge about potential implication of resistin in idiopathic inflammatory myopathies.
- MeSH
- biologické markery metabolismus MeSH
- cévní endotel metabolismus patologie MeSH
- chemotaxe fyziologie MeSH
- cytokiny metabolismus MeSH
- endoteliální buňky metabolismus patologie MeSH
- lidé MeSH
- myozitida krev etiologie patologie MeSH
- pohyb buněk fyziologie MeSH
- proliferace buněk MeSH
- resistin fyziologie MeSH
- upregulace MeSH
- viabilita buněk fyziologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- biologické markery MeSH
- cytokiny MeSH
- resistin MeSH
- RETN protein, human MeSH Prohlížeč
Resistin was originally described as an adipocyte-secreted peptide that induced insulin resistance in rodents. Increasing evidence indicates its important regulatory roles in various biological processes, including several inflammatory diseases. Further studies have shown that resistin in humans, in contrast to its production by adipocytes in mice, is synthesized predominantly by mononuclear cells both within and outside adipose tissue. Possible roles for resistin in obesity-related subclinical inflammation, atherosclerosis and cardiovascular disease, non-alcoholic fatty liver disease, rheumatic diseases, malignant tumors, asthma, inflammatory bowel disease, and chronic kidney disease have already been demonstrated. In addition, resistin can modulate several molecular pathways involved in metabolic, inflammatory, and autoimmune diseases. In this review, current knowledge about the functions and pathophysiological implications of resistin in different human pathologies is summarized, although there is a significant lack of firm evidence regarding the specific role resistin plays in the "orchestra" of the numerous mediators of inflammation.
- MeSH
- lidé MeSH
- nádory metabolismus MeSH
- obezita komplikace metabolismus MeSH
- resistin chemie fyziologie MeSH
- zánět metabolismus MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- resistin MeSH
OBJECTIVE: To investigate the mechanism by which fat-specific transgenic expression of resistin affects fatty acid metabolism in the spontaneously hypertensive rat (SHR). DESIGN: Basal- and adrenaline-stimulated lipolysis, basal- and insulin-stimulated lipogenesis as well as the site (glycerol versus acyl moiety) of glucose incorporated into triglycerides were determined in adipose tissue isolated from SHR-Resistin transgenic and SHR control rats. RESULTS: A moderate expression of transgenic resistin in adipose tissue was associated with significant increase in the FFA/glycerol ratio during adrenaline-stimulated lipolysis in the SHR-Resistin transgenic rats (3.27+/-0.26) compared to SHR controls (2.11+/-0.10, P=0.0005). Transgenic SHR also exhibited a significant decrease in FFA re-esterification in adipose tissue (approximately by 23%). CONCLUSION: These findings raise the possibility that the prodiabetic effects of transgenic resistin may be partly mediated by increased FFA release from adipose tissue due to impaired FFA re-esterification in adipocytes.
- MeSH
- adrenalin farmakologie MeSH
- esterifikace MeSH
- geneticky modifikovaná zvířata MeSH
- glukosa metabolismus MeSH
- glycerol metabolismus MeSH
- krysa rodu Rattus MeSH
- kyseliny mastné neesterifikované metabolismus MeSH
- lipolýza účinky léků fyziologie MeSH
- potkani inbrední SHR MeSH
- resistin genetika metabolismus fyziologie MeSH
- tuková tkáň metabolismus MeSH
- tukové buňky metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
- Názvy látek
- adrenalin MeSH
- glukosa MeSH
- glycerol MeSH
- kyseliny mastné neesterifikované MeSH
- resistin MeSH
Resistin is a 12.5-kDa polypeptide hormone produced by adipocytes and immunocompetent cells. It was originally proposed as a link between obesity and insulin resistance/diabetes. Later, studies revealed that substantial inter-species differences exist between the major sites of resistin production in rodents (adipocytes) and humans (immunocompetent cells). While in rodents resistin appears to have an important role in the development of liver insulin resistance, its role in humans is less clear, and it is probably involved in the regulation of inflammatory processes rather than in insulin sensitivity. Current experimental and clinical data concerning resistin physiology and pathophysiology, and its possible role in the development of insulin resistance and atherosclerosis are detailed in this review.
- MeSH
- ateroskleróza etiologie MeSH
- inzulinová rezistence * MeSH
- lidé MeSH
- mezibuněčné signální peptidy a proteiny MeSH
- modely nemocí na zvířatech MeSH
- nervový růstový faktor fyziologie MeSH
- obezita metabolismus MeSH
- PPAR gama agonisté MeSH
- proteiny fyziologie MeSH
- resistin fyziologie MeSH
- zánět etiologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- mezibuněčné signální peptidy a proteiny MeSH
- nervový růstový faktor MeSH
- PPAR gama MeSH
- proteiny MeSH
- resistin MeSH
- Retnla protein, mouse MeSH Prohlížeč
