Alzheimerova nemoc je progresivní neurodegenerativní onemocnění charakterizované ukládáním β-amyloidu a hyperfosforylací τ-proteinu v postiženém mozku. Jedná se o multifaktoriální onemocnění, na jehož patologii se podílejí jak faktory genetické, tak faktory vnějšího prostředí. Kromě genetického pozadí Alzheimerovy nemoci se stále častěji diskutuje o pozadí biochemickém. Mezi jedny z biochemických markerů, které mohou ovlivňovat Alzheimerovu nemoc, patří adipokiny. Adipokiny jsou bílkoviny produkované tukovou tkání, které po vyplavení do krevního řečiště ovlivňují řadu procesů. Vliv adipokinů na rozvoj Alzheimerovy nemoci je patrný, avšak ne zcela jednoznačný. Tento přehled popisuje roli vybraných adipokinů při vzniku a rozvoji Alzheimerovy nemoci.

Alzheimer's disease is a progressive neurodegenerative disorder characterized by the deposition of β-amyloid and hyperphosphorylation of τ-protein in a brain. The pathology of this multifactorial disease is influenced by genetic as well as environmental factors. In addition to the genetic background of Alzheimer's disease, there are increasingly discussed biochemical background. Among some of the biochemical markers that can affect the Alzheimer's disease are adipokines. Adipokines are proteins secreted by adipose tissue, which after flooding to the bloodstream affect a variety of processes. The influence of adipokines in development of Alzheimer's disease is evident, however not entirely clear. This review describes the role of selected adipokines in the creation and development of Alzheimer's disease.

• MeSH
• adipokiny * fyziologie   MeSH
• adiponektin fyziologie   MeSH
• Alzheimerova nemoc * etiologie   metabolismus   patologie   MeSH
• energetický metabolismus fyziologie   MeSH
• komplement - faktor D fyziologie   MeSH
• leptin fyziologie   MeSH
• lidé MeSH
• mitochondrie fyziologie   metabolismus   MeSH
• nikotinamidfosforibosyltransferasa fyziologie   MeSH
• resistin fyziologie   MeSH
• tuková tkáň metabolismus   MeSH
• zánět metabolismus   MeSH
• Check Tag
• lidé MeSH

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.

• 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

• Klíčová slova
• visfatin, vaspin, omentin,
• MeSH
• adipokiny * MeSH
• adiponektin farmakologie   fyziologie   imunologie   metabolismus   nedostatek   sekrece   MeSH
• bariatrická chirurgie * využití   MeSH
• buněčné proteiny vázající retinol farmakologie   fyziologie   krev   metabolismus   škodlivé účinky   MeSH
• cytokiny farmakologie   škodlivé účinky   MeSH
• diabetes mellitus 2. typu * diagnóza   epidemiologie   etiologie   patofyziologie   prevence a kontrola   terapie   MeSH
• fyziologie výživy MeSH
• hmotnostní úbytek MeSH
• inzulinová rezistence * MeSH
• leptin farmakologie   imunologie   metabolismus   škodlivé účinky   terapeutické užití   MeSH
• lidé MeSH
• mikrobiota * MeSH
• mitochondrie patologie   MeSH
• obezita * diagnóza   epidemiologie   chirurgie   komplikace   metabolismus   prevence a kontrola   terapie   MeSH
• pioglitazon MeSH
• pohybová aktivita MeSH
• resistin farmakologie   fyziologie   chemická syntéza   imunologie   metabolismus   škodlivé účinky   MeSH
• thiazolidindiony aplikace a dávkování   farmakologie   kontraindikace   škodlivé účinky   terapeutické užití   MeSH
• tuková tkáň * fyziologie   imunologie   metabolismus   patofyziologie   účinky léků   MeSH
• výzkum MeSH
• zánět * diagnóza   chemicky indukované   terapie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• přehledy 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

• MeSH
• adipokiny klasifikace   metabolismus   MeSH
• adiponektin fyziologie   metabolismus   MeSH
• bariatrická chirurgie MeSH
• endokrinní systém patofyziologie   MeSH
• glukagonu podobný peptid 1 terapeutické užití   MeSH
• inkretiny terapeutické užití   MeSH
• leptin fyziologie   metabolismus   MeSH
• lidé MeSH
• obezita komplikace   metabolismus   MeSH
• resistin fyziologie   metabolismus   MeSH
• tuková tkáň fyziologie   patofyziologie   MeSH
• žaludeční inhibiční polypeptid terapeutické užití   MeSH
• Check Tag
• lidé MeSH

• Klíčová slova
• visfatin, TNF-?, interleukin 6,
• MeSH
• adipokiny fyziologie   metabolismus   MeSH
• adiponektin fyziologie   metabolismus   MeSH
• interleukiny fyziologie   metabolismus   MeSH
• leptin fyziologie   metabolismus   MeSH
• lidé MeSH
• nikotinamidfosforibosyltransferasa fyziologie   metabolismus   MeSH
• resistin fyziologie   metabolismus   MeSH
• Check Tag
• lidé MeSH

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 fyziologie   chemie   MeSH
• zánět metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• práce podpořená grantem MeSH
• přehledy 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 fyziologie   účinky léků   MeSH
• potkani inbrední SHR MeSH
• resistin fyziologie   genetika   metabolismus   MeSH
• tuková tkáň * metabolismus   MeSH
• tukové buňky metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• zvířata MeSH
• Publikační typ
• práce podpořená grantem MeSH
• Research Support, N.I.H., Extramural 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
• financování organizované MeSH
• inzulinová rezistence MeSH
• lidé MeSH
• mezibuněčné signální peptidy a proteiny MeSH
• modely nemocí na zvířatech MeSH
• neurotrofní faktory 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

• Klíčová slova
• acylation stimulating, protein (ASP),
• MeSH
• adiponektin fyziologie   metabolismus   MeSH
• diabetes mellitus 2. typu metabolismus   MeSH
• hormony fyziologie   metabolismus   MeSH
• inhibitor aktivátoru plazminogenu 1 fyziologie   metabolismus   MeSH
• inzulinová rezistence fyziologie   imunologie   MeSH
• klinické zkoušky kontrolované jako téma MeSH
• kohortové studie MeSH
• komplikace diabetu MeSH
• leptin farmakologie   metabolismus   nedostatek   MeSH
• lidé MeSH
• proteiny fyziologie   chemie   metabolismus   MeSH
• resistin fyziologie   metabolismus   MeSH
• TNF-alfa fyziologie   metabolismus   MeSH
• tuková tkáň fyziologie   chemie   metabolismus   MeSH
• Check Tag
• lidé MeSH