The increasing use of industrial chemicals has raised concerns regarding exposure to endocrine-disrupting chemicals (EDCs), which interfere with developmental, reproductive and metabolic processes. Of particular concern is their interaction with adipose tissue, a vital component of the endocrine system regulating metabolic and hormonal functions. The SGBS (Simpson Golabi Behmel Syndrome) cell line, a well-established human-relevant model for adipocyte research, closely mimics native adipocytes' properties. It responds to hormonal stimuli, undergoes adipogenesis and has been successfully used to study the impact of EDCs on adipose biology. In this study, we screened human exposure-relevant doses of various EDCs on the SGBS cell line to investigate their effects on viability, lipid accumulation and adipogenesis-related protein expression. Submicromolar doses were generally well tolerated; however, at higher doses, EDCs compromised cell viability, with cadmium chloride (CdCl2) showing the most pronounced effects. Intracellular lipid levels remained unaffected by EDCs, except for tributyltin (TBT), used as a positive control, which induced a significant increase. Analysis of adipogenesis-related protein expression revealed several effects, including downregulation of fatty acid-binding protein 4 (FABP4) by dibutyl phthalate, upregulation by CdCl2 and downregulation of perilipin 1 and FABP4 by perfluorooctanoic acid. Additionally, TBT induced dose-dependent upregulation of C/EBPα, perilipin 1 and FABP4 protein expression. These findings underscore the importance of employing appropriate models to study EDC-adipocyte interactions. Conclusions from this research could guide strategies to reduce the negative impacts of EDC exposure on adipose tissue.

• MeSH
• adipogeneze * účinky léků   MeSH
• buněčné linie MeSH
• endokrinní disruptory * toxicita   MeSH
• fluorokarbony toxicita   MeSH
• kapryláty toxicita   MeSH
• lidé MeSH
• metabolismus lipidů účinky léků   MeSH
• proteiny vázající mastné kyseliny * metabolismus   genetika   MeSH
• trialkylcínové sloučeniny toxicita   MeSH
• tuková tkáň účinky léků   metabolismus   MeSH
• tukové buňky účinky léků   metabolismus   MeSH
• viabilita buněk * účinky léků   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Allelic and genotypic distribution of polymorphisms in diacylglycerol acyltransferase 1 (DGAT1), fatty acid binding protein 4 (FABP4), fatty acid synthase (FASN), and peroxisome proliferator-activated receptor-γ coactivator-1α (PPARGC1A) genes were assessed in 679 Fleckvieh bulls. Single-locus genotype effects and the combined effect of the two polymorphisms within the FASN gene were evaluated for association with the intramuscular fat content and fatty acid profile determined in muscle and subcutaneous fat. The FASN (g.16024G>A) and FASN (g.17924A>G) polymorphisms were significantly associated mainly with C14:0, C16:0, and C18:1 n-9 concentrations as well as with the atherogenic index. The proportion of explained phenotypic variation markedly increased when the effect of a combination of the two polymorphisms within the FASN gene was tested, with the highest values of 8.6% and 14.8%, respectively, observed for C14:0 in muscle and subcutaneous fat. With a focus on improving the fatty acid composition of beef, the results of this study provide valuable information about the markers applicable in marker-assisted selection.

• MeSH
• alely MeSH
• ateroskleróza MeSH
• diacylglycerol-O-acyltransferasa genetika   metabolismus   MeSH
• druhová specificita MeSH
• fenotyp * MeSH
• genotyp * MeSH
• jednonukleotidový polymorfismus MeSH
• lidé MeSH
• maso analýza   MeSH
• mastné kyseliny metabolismus   MeSH
• podkožní tuk metabolismus   MeSH
• polymorfismus genetický * MeSH
• proteiny vázající mastné kyseliny genetika   metabolismus   MeSH
• skot MeSH
• svaly metabolismus   MeSH
• syntázy mastných kyselin genetika   metabolismus   MeSH
• transkripční faktory genetika   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• skot MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

In-vitro investigation of the effects of hypoxia is limited by physical laws of gas diffusion and cellular O2 consumption, making prolonged exposures to stable O2 concentrations impossible. Using a gas-permeable cultureware, chronic effects of mild and severe hypoxia on triglyceride accumulation, lipid droplet size distribution, spontaneous lipolysis and gene expression of adipocyte-specific markers were assessed. 3T3-L1 cells were differentiated under 20%, 4% or 1% O2 using a gas-permeable cultureware. Triglyceride accumulation, expression of genes characteristic for advanced adipocyte differentiation and involvement of key lipogenesis enzymes were assessed after exposures. Lipogenesis increased by 375% under mild hypoxia, but dropped by 43% in severe hypoxia. Mild, but not severe, hypoxia increased formation of large lipid droplets 6.4 fold and strongly induced gene expression of adipocyte-specific markers. Spontaneous lipolysis increased by 488% in mild, but only by 135% in severe hypoxia. Inhibition of ATP-dependent citrate lyase suppressed hypoxia-induced lipogenesis by 81% and 85%. Activation of HIF inhibited lipogenesis by 59%. Mild, but not severe, hypoxia stimulates lipolysis and promotes adipocyte differentiation, probably through excess of acetyl-CoA originating from tricarboxylic acid cycle independently of HIF activation.

• MeSH
• acetylkoenzym A metabolismus   MeSH
• adipogeneze účinky léků   genetika   MeSH
• ATP-citrát-(pro-S)-lyasa genetika   metabolismus   MeSH
• buněčná diferenciace účinky léků   MeSH
• buňky 3T3-L1 MeSH
• citrátový cyklus účinky léků   genetika   MeSH
• diacylglycerol-O-acyltransferasa genetika   metabolismus   MeSH
• faktor 1 indukovatelný hypoxií - podjednotka alfa genetika   metabolismus   MeSH
• hypoxie buňky MeSH
• kyslík farmakologie   MeSH
• lipidová tělíska chemie   účinky léků   MeSH
• lipogeneze účinky léků   genetika   MeSH
• lipolýza účinky léků   genetika   MeSH
• myši MeSH
• perilipin 1 genetika   metabolismus   MeSH
• proteiny vázající mastné kyseliny genetika   metabolismus   MeSH
• regulace genové exprese účinky léků   MeSH
• signální transdukce MeSH
• sterolesterasa genetika   metabolismus   MeSH
• triglyceridy metabolismus   MeSH
• tukové buňky cytologie   účinky léků   metabolismus   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

Metabolický syndrom, který výrazně zvyšuje kardiovaskulární morbiditu, mortalitu ariziko rozvoje diabetes mellitus 2. typu, vsoučasné době dosahuje epidemických proporcí. Tato komplexní porucha vyžaduje urgentní vývoj nových farmakoterapeutických řešení. Patofyziologické mechanismy vedoucí k rozvoji tohoto syndromu nejsou dosud plně objasněny, nicméně se zdá zřejmé, že k jeho rozvoji přispívá řada metabolických dysregulací. Za potenciálně slibný cíl pro vývoj nových léčiv se považuje dysregulace endokrinních aparakrinních funkcí tukové tkáně. Specifické adipokiny, což jsou proteiny secernované tukovou tkání s jistými pleiotropními účinky, jsou silně asociovány s regulací energetického metabolismu, chuti k jídlu, inzulinové signální dráhy, senzitivity periferních tkání k inzulinu aprozánětlivému stavu spojenému smetabolickým syndromem. Cílem této práce je poskytnout stručný přehled endokrinních aparakrinních funkcí tukové tkáně ve spojitosti s rozvojem metabolického syndromu, jeho patofyziologických podkladů apoukázat na některé adipokiny jako potenciální cíle pro vývoj nových farmakoterapeutických přístupů.

Metabolic syndrome, acondition increasing cardiovascular morbidity, mortality and risk for diabetes mellitus type 2, is currently worldwide reaching epidemic proportions. This complex disorder represents an urgent challenge for new pharmacotherapeutic strategies formulation. Pathophysiological mechanisms underlying metabolic syndrome are not completely understood, nevertheless growing evidence is supporting the hypothesis that multiple metabolic dysregulations do contribute to its development. Apotential target for pharmacological intervention is considered to be dysregulation of adipose tissue endocrine/paracrine function. Specific adipokines, proteins secreted by the adipose tissue, with some pleiotropic effects, have been identified with strong association to regulation of energy metabolism, appetite, insulin signaling, tissue insulin sensitivity and the proinflammatory state related to metabolic syndrome. The aim of this paper is to provide abrief overview of endocrine/paracrine functions of the adipose tissue with regard to metabolic syndrome development and pathophysiology and particular adipokines as potential targets for innovative pharmacotherapeutic approaches.

• Klíčová slova
• omentin, vaspin,
• MeSH
• adipokiny * metabolismus   MeSH
• adiponektin metabolismus   MeSH
• cytokiny metabolismus   MeSH
• GPI-vázané proteiny metabolismus   MeSH
• inzulinová rezistence MeSH
• lektiny metabolismus   MeSH
• leptin metabolismus   MeSH
• lidé MeSH
• metabolický syndrom * etiologie   metabolismus   patofyziologie   MeSH
• nikotinamidfosforibosyltransferasa metabolismus   MeSH
• proteiny vázající mastné kyseliny metabolismus   MeSH
• resistin metabolismus   MeSH
• serpiny metabolismus   MeSH
• tuková tkáň * metabolismus   patofyziologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• práce podpořená grantem MeSH
• přehledy MeSH

The aim of our study was to characterize resistance to ischemia/reperfusion (I/R) injury in Langendorff-perfused rat hearts and effectivity of ischemic preconditioning (PC) under condition of simulated acute hyperglycemia (SAHG) by perfusion of the hearts with Krebs-Henseleit (KH) solution with elevated glucose concentration (22 mmol/l). I/R injury was induced by 30-min coronary occlusion followed by 120-min reperfusion and PC by two cycles of 5-min occlusion/5-min reperfusion, prior to I/R. The severity of I/R injury was characterized by determination of the size of infarction (IS, expressed in % of area at risk size) and the amount of heart-type fatty acid binding protein (h-FABP, a marker of cell injury) released from the hearts to the effluent. Significantly smaller IS (8.8+/-1 %) and lower total amount of released h-FABP (1808+/-660 pmol) in PC group compared with IS 17.1+/-1.2 % (p<0.01) and amount of h-FABP (8803+/-2415 pmol, p<0.05) in the non-PC control hearts perfused with standard KH solution (glucose 11 mmol/l) confirmed protective effects of PC. In contrast, in SAHG groups, PC enhanced IS (21.4+/-2.2 vs. 14.3+/-1.3 %, p<0.05) and increased total amount of h-FABP (5541+/-229 vs. 3458+/-283 pmol, p<0.05) compared with respective non-PC controls. Results suggest that PC has negative effect on resistance of the hearts to I/R injury under conditions of elevated glucose in vitro.

• MeSH
• časové faktory MeSH
• funkce levé komory srdeční MeSH
• glukosa metabolismus   MeSH
• hyperglykemie komplikace   metabolismus   MeSH
• infarkt myokardu etiologie   metabolismus   patologie   patofyziologie   prevence a kontrola   MeSH
• ischemické přivykání * MeSH
• komorový tlak (srdce) MeSH
• modely nemocí na zvířatech MeSH
• myokard metabolismus   patologie   MeSH
• potkani Wistar MeSH
• proteiny vázající mastné kyseliny metabolismus   MeSH
• reperfuzní poškození myokardu etiologie   metabolismus   patologie   patofyziologie   prevence a kontrola   MeSH
• stupeň závažnosti nemoci MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

OBJECTIVES: Adiponectin, adipocyte fatty acid-binding protein (AFABP), and leptin have been shown to be present in human breast milk (BM). We determined intraindividual changes of BM levels of these proteins during 12 months of lactation. SUBJECTS AND METHODS: Proteins were measured using a high-sensitivity enzyme-linked immunosorbent assay method in 72 healthy mothers after delivery (day 0, D0) and after 1, 3, 6, and 12 months of lactation. RESULTS: Adiponectin levels in BM on D0 were 22.8 ± 0.8 (mean ± standard error of the mean), in 1 month (M1) 22.0 ± 0.6, in 3 months (M3) 20.5 ± 0.6, in 6 months (M6) 21.4 ± 0.8, and in 12 months (M12) 25.7 ± 1.4 ng/mL. AFABP levels were 12.3 ± 2.0, 6.2 ± 1.3, 1.3 ± 0.2, 2.5 ± 1.0, and 4.6 ± 1.9 ng/mL, respectively. Leptin levels were 0.3 ± 0.04, 0.2 ± 0.03, 0.1 ± 0.01, 0.1 ± 0.02, and 0.2 ± 0.04 ng/mL, respectively. We found significantly higher levels of adiponectin in M12 in comparison to M3 and M6 (P = 0.0026), higher levels of AFABP in D0 and M1 when compared with M3, M6, and M12 (P < 0.0001), and higher levels of leptin on D0 than in M1, M3, M6, and M12 (P < 0.0001). AFABP levels correlated negatively with infants' body weight in M1, but there was no correlation throughout the lactation period between body weight and other proteins. We found positive correlation between adiponectin, AFABP, and leptin throughout the lactation. CONCLUSIONS: All of the hormones were detectable in BM up to 12 months of lactation, with decreasing trend until M3 and subsequent increase till M12. We speculate that higher levels in M6 and M12 may be caused by longer intervals between breast-feeding due to the introduction of complementary food.

• MeSH
• adiponektin metabolismus   MeSH
• časové faktory MeSH
• dospělí MeSH
• kojenec MeSH
• kolostrum metabolismus   MeSH
• laktace metabolismus   MeSH
• leptin metabolismus   MeSH
• lidé MeSH
• mateřské mléko metabolismus   MeSH
• novorozenec MeSH
• porodní hmotnost MeSH
• proteiny vázající mastné kyseliny metabolismus   MeSH
• reprodukovatelnost výsledků MeSH
• těhotenství MeSH
• tělesná hmotnost MeSH
• vývoj dítěte MeSH
• Check Tag
• dospělí MeSH
• kojenec MeSH
• lidé MeSH
• mužské pohlaví MeSH
• novorozenec MeSH
• těhotenství MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Geografické názvy
• Česká republika MeSH

Background. Adipocyte fatty acid-binding protein (aFABP) has recently been identified as a potential circulating marker for metabolic syndrome. C-reactive protein (CRP), a sensitive marker of inflammation, is increased in individuals with diabetes and metabolic syndrome due to the development of subclinical inflammation. The study uses logistic regression models to analyze the relations between aFABP and CRP along with other parameters of insulin resistance. The objective was to investigate the potential use of aFABP and CRP levels as tools in the diagnosis of the metabolic syndrome. Methods and results. The following groups were studied: healthy individuals (A, n=122), obese ind1ividuals (B, n=213) and patients diagnosed with metabolic syndrome (C, n=79). Obese persons in Group B had parameters suggestive of early insulin resistance: hypertension, hyperglycaemia, QUICKI (0.305) and higher aFABP levels as compared with the healthy subjects. Group C individuals were diagnosed with metabolic syndrome, as evidenced by the QUICKI markers for insulin resistance (0.293), high aFABP levels (35.3 mg/l). CRP concentrations were lowest in Group A healthy individuals (0.67 mg/l), higher in Group B obese subjects (2.65 mg/l) and highest in Group C patients with metabolic syndrome (3.62 mg/l). Logistic regression models showed an association of aFABP and CRP with BMI (OR 1.12 and 1.39, compared Group A vs C). An association of aFABP and CRP with the QUICKI index showed OR 1.48 and 1.37 (Group A vs C); with triglyceride levels showed OR 1.68 and 1.52 (Group A vs C). An association of aFABP and CRP with glycaemia showed OR 1.48 and 1.51 (Group A vs C), with insulinaemia showed OR 1.44 and 1.38 (Group A vs C) respectively. Conclusions. AFABP levels were higher in obese individuals and highest in those with metabolic syndrome. CRP concentrations were increased in obese persons whereas individuals with metabolic syndrome were found to have high-risk CRP levels. Logistic regression models showed an association of aFABP and CRP with BMI as well as an association of aFABP and CRP with parameters of insulin resistance, namely the QUICKI index, triglyceride levels, glycaemia and insulinaemia. Both methods are of diagnostic benefit for predicting metabolic syndrome, especially in previously untreated patients.

• MeSH
• adiponektin krev   MeSH
• C-reaktivní protein analýza   MeSH
• inzulinová rezistence MeSH
• lidé středního věku MeSH
• lidé MeSH
• metabolický syndrom metabolismus   MeSH
• obezita metabolismus   MeSH
• proteiny vázající mastné kyseliny metabolismus   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• práce podpořená grantem MeSH

Tuková tkáň je dnes považována za endokrinní orgán produkující řadu hormonů. Hormony tukové tkáně se významnou měrou podílejí na regulaci energetické homeostázy, inzulínové senzitivity a řady dalších procesů včetně podílu na vzniku diabetes mellitus 2. typu. Jedním z těchto hormonů je fatty acid binding protein-4 (FABP-4). Jde o cytoplazmatický protein o molekulové hmotnosti 14,7 kDa, který se podílí na transportu, skladování a metabolizmu lipidů. Mezi další funkce FABP-4 patří modulace signálních regulačních drah a buněčných enzymatických procesů. Jde o faktor, který je primárně produkován makrofágy a adipocyty. Experimentální a klinická data svědčí pro možnost, že změny sérových koncentrací FABP-4 mohou být významným etiopatogenetickým faktorem v rozvoji inzulínové rezistence, diabetu 2. typu a aterosklerózy. Cílem tohoto článku je podat aktuální přehled o FABP-4, jeho vztahu k výše uvedeným onemocněním a perspektivách využití modulace hladin tohoto hormonu v prevenci a léčbě diabetu 2. typu a jeho komplikací.

It is now generally accepted that adipose tissue is an endocrine organ producing numerous of hormones. These hormones play an important role in the regulation of energy homeostasis, insulin sensitivity and many other processes including its possible role in the development of type 2 diabetes mellitus. Fatty acid binding protein-4 (FABP-4) is a 14,7 kDa cytoplasmic protein that plays a role in lipid transport, storage and metabolism. Other functions of FABP-4 include modulation of signalling pathways and cell enzymatic proccesses. FABP-4 is primarily produced by macrophages and adipocytes. There is a growing number of experimental and clinical evidence suggesting that fatty acid binding protein-4 is an important ethiopathogenic factor in the developement of insulin resistance, type 2 diabetes and atherosclerosis. The aim of this article is to review the current state of knowledge about fatty acid binding protein-4 and its relationship to above mentioned diseases including perspectives of modulation of FABP-4 levels in the prevention and treatment of type 2 diabetes mellitus.

• Klíčová slova
• protein vázající mastné kyseliny, hormony tukové tkáně,
• MeSH
• diabetes mellitus MeSH
• inzulinová rezistence genetika   MeSH
• komplikace diabetu genetika   metabolismus   MeSH
• lidé MeSH
• modely u zvířat MeSH
• myši MeSH
• obezita genetika   metabolismus   MeSH
• proteiny vázající mastné kyseliny genetika   metabolismus   MeSH
• tuková tkáň chemie   metabolismus   MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• Publikační typ
• klinické zkoušky kontrolované MeSH

• MeSH
• adiponektin metabolismus   sekrece   terapeutické užití   MeSH
• diferenciální diagnóza MeSH
• hodnocení rizik MeSH
• inzulinová rezistence fyziologie   MeSH
• leptin metabolismus   sekrece   terapeutické užití   MeSH
• lidé MeSH
• metabolický syndrom etiologie   komplikace   metabolismus   MeSH
• morbidita MeSH
• mortalita MeSH
• nemoci endokrinního systému klasifikace   komplikace   MeSH
• nikotinamidfosforibosyltransferasa metabolismus   MeSH
• obezita etiologie   komplikace   MeSH
• prevalence MeSH
• proteiny vázající mastné kyseliny metabolismus   MeSH
• renin-angiotensin systém MeSH
• resistin metabolismus   sekrece   MeSH
• rizikové faktory MeSH
• tuková tkáň metabolismus   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• novinové články MeSH

The paucity of early, predictive, noninvasive biomarkers has impaired our ability to institute potentially effective therapies for acute kidney injury and chronic kidney disease in a timely manner. RECENT FINDINGS: Promising novel biomarkers for acute kidney injury include a plasma panel (neutrophil gelatinase-associated lipocalin and cystatin C) and a urine panel (neutrophil gelatinase-associated lipocalin, interleukin-18, and kidney injury molecule-1). For chronic kidney disease, these include a similar plasma panel and a urine panel (neutrophil gelatinase-associated lipocalin, asymetric dimethylarginine, and liver-type fatty acid-binding protein). The biomarker panels will probably be useful for assessing the duration and severity of kidney disease, and for predicting progression and adverse clinical outcomes. It is also likely that the biomarker panels will help to distinguish between the various etiologies of acute kidney injury or chronic kidney disease. SUMMARY: The tools of functional genomics and proteomics have provided us with promising novel biomarkers for acute kidney injury and chronic kidney disease. It will be important in future studies to validate the sensitivity and specificity of these biomarker panels in clinical samples from large cohorts and in multiple clinical situations. Such studies will be facilitated by the availability of commercial tools for reproducible measurement of these panels.

• MeSH
• akutní poškození ledvin diagnóza   metabolismus   MeSH
• arginin analogy a deriváty   metabolismus   MeSH
• biologické markery krev   metabolismus   MeSH
• chronická renální insuficience diagnóza   metabolismus   MeSH
• cystatiny metabolismus   MeSH
• interleukin-18 metabolismus   MeSH
• lidé MeSH
• lipokaliny metabolismus   MeSH
• membránové glykoproteiny metabolismus   MeSH
• prediktivní hodnota testů MeSH
• prognóza MeSH
• proteiny akutní fáze metabolismus   MeSH
• proteiny vázající mastné kyseliny metabolismus   MeSH
• protoonkogenní proteiny metabolismus   MeSH
• reprodukovatelnost výsledků MeSH
• stupeň závažnosti nemoci MeSH
• virové receptory metabolismus   MeSH
• Check Tag
• lidé MeSH