Adiponektin je důležitý biomarker metabolického syndromu, který byl v nedávné době identifikován také v mateřském mléce člověka. V naší práci prokazujeme přítomnost adiponektinového receptoru typu 1 (adipoR1) imunoperoxidázovou metodou ve 21 bioptických vzorcích – duodenum (n = 6), terminální ileum (n = 7) a kolon (n = 8) od 14 jedinců (6 žen a 8 mužů ve věku 9 měsíců – 47 let). Ve všech vzorcích jsme prokázali přítomnost adipoR1. Pozitivita byla pozorována v enterocytech, kolonocytech i v lymfocytech submukózy a v hladké svalovině střevní stěny. Předpokládáme, že adiponektin může ovlivňovat intestinální fyziologické děje prostřednictvím adiponektinového receptoru typu 1.

Adiponectin is an important biomarker of metabolic syndrome that was recently identified in human breast milk. We demonstrate the presence of type-1 adiponectin receptor (adipoR1) by immunoperoxidase method in 21 bioptic specimens – duodenum (n = 6), terminal ileum (n = 7) and colon (n = 8) from 14 human subjects (6 females and 8 males aged 9 months-47 years). In all the samples, adipoR1 was detected. The positivity was observed in enterocytes and colonocytes as well as in lymphocytes in the submucosa and in the smooth muscle of the intestinal wall. Thus, adiponectin may influence intestinal physiology through its type-1 receptor.

• Klíčová slova
• nutriční programování,
• MeSH
• adiponektin analýza   MeSH
• dítě MeSH
• dospělí MeSH
• financování organizované MeSH
• imunoenzymatické techniky metody   MeSH
• kohortové studie MeSH
• kojenec MeSH
• lidé středního věku MeSH
• lidé MeSH
• mateřské mléko chemie   MeSH
• mladiství MeSH
• předškolní dítě MeSH
• receptory adiponektinu analýza   MeSH
• střevní sliznice cytologie   metabolismus   MeSH
• Check Tag
• dítě MeSH
• dospělí MeSH
• kojenec MeSH
• lidé středního věku MeSH
• lidé MeSH
• mladiství MeSH
• předškolní dítě MeSH

OBJECTIVE: The number of patients with end-stage renal disease (ESRD) is rising and these patients are at higher risk of cardiovascular disease. We studied the role of hormonal production of adipose tissue in the development of chronic inflammation in patients with ESRD before kidney transplantation. METHODS: Fifteen women with ESRD and 17 healthy women (control) underwent single blood drawing and visceral and subcutaneous adipose tissue sampling during surgery (kidney transplantation in the ESRD group or cholecystectomy in the control group). Serum concentrations of C-reactive protein, interleukin-6, tumor necrosis factor-alpha, leptin, adiponectin, resistin, monocyte chemoattractant protein-1 were measured. Messenger RNA expression of the same hormones, adiponectin receptors 1 and 2 and immunocompetent cell marker CD68 in subcutaneous and visceral samples were measured using real-time polymerase chain reaction. Adipose tissue was examined immunohistochemically for CD68-positive cells. RESULTS: Serum concentrations of C-reactive protein, adiponectin, resistin, interleukin-6, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 were significantly higher in the ESRD versus control group. Subcutaneous and visceral mRNA expressions of tumor necrosis factor-alpha and CD68 were significantly increased in the ESRD versus control group. Adiponectin receptor-1 and monocyte chemoattractant protein-1 mRNA expressions were significantly higher in visceral but not in subcutaneous adipose tissue of the ESRD group. Messenger RNA expressions of resistin, leptin, adiponectin, interleukin-6, and adiponectin receptor-2 in both fat depots did not significantly differ between groups. Increased infiltration of subcutaneous and visceral adipose tissue with CD68-positive immunocompetent cells was found in the ESRD group by histologic examination. CONCLUSION: Subcutaneous and visceral adipose tissues in ESRD express higher amounts of proinflammatory cytokines and may play a role in the development of systemic inflammation.

• MeSH
• adiponektin genetika   metabolismus   MeSH
• antigeny diferenciační myelomonocytární metabolismus   MeSH
• C-reaktivní protein metabolismus   MeSH
• CD antigeny metabolismus   MeSH
• chemokin CCL2 genetika   metabolismus   MeSH
• chronické selhání ledvin metabolismus   MeSH
• cytokiny metabolismus   MeSH
• interleukin-6 genetika   metabolismus   MeSH
• lidé středního věku MeSH
• lidé MeSH
• mediátory zánětu metabolismus   MeSH
• messenger RNA biosyntéza   MeSH
• nitrobřišní tuk metabolismus   MeSH
• podkožní tuk metabolismus   MeSH
• receptory adiponektinu biosyntéza   genetika   MeSH
• resistin genetika   metabolismus   MeSH
• TNF-alfa krev   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• práce podpořená grantem MeSH

We studied the effect of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activation on serum concentrations and tissue expression of resistin, adiponectin, and adiponectin receptor-1 and -2 (AdipoR1 and AdipoR2) mRNA in normal mice and mice with insulin resistance induced by lipogenic, simple-carbohydrate diet (LD). Sixteen weeks of LD feeding induced obesity with liver steatosis and increased insulin levels but did not significantly affect circulating adiponectin or resistin. Treatment with PPAR-alpha agonist fenofibrate decreased body weight and fat pad weight and ameliorated liver steatosis in LD-fed mice with concomitant reduction in blood glucose, free fatty acid, triglyceride, serum insulin levels, and homeostasis model assessment index values. Euglycemic-hyperinsulinemic clamp demonstrated the development of whole-body and liver insulin resistance in LD-fed mice, which were both normalized by fenofibrate. Fenofibrate treatment markedly increased circulating resistin levels on both diets and adiponectin levels in chow-fed mice only. Fat adiponectin mRNA expression was not affected by fenofibrate treatment. Resistin mRNA expression increased in subcutaneous but not gonadal fat after fenofibrate treatment. In addition to fat, a significant amount of adiponectin mRNA was also expressed in the muscle. This expression markedly increased after fenofibrate treatment in chow- but not in LD-fed mice. Adipose tissue expression of AdipoR1 mRNA was significantly reduced in LD-fed mice and increased after fenofibrate treatment. In conclusion, PPAR-alpha activation ameliorated the development of insulin resistance in LD-fed mice despite a major increase in serum resistin levels. This effect could be partially explained by increased AdipoR1 expression in adipose tissue after fenofibrate treatment.

• MeSH
• adiponektin genetika   krev   MeSH
• dieta MeSH
• dietní sacharidy aplikace a dávkování   MeSH
• exprese genu účinky léků   MeSH
• fenofibrát aplikace a dávkování   MeSH
• financování organizované MeSH
• glykemický clamp MeSH
• hmotnostní úbytek účinky léků   MeSH
• inzulin farmakologie   krev   MeSH
• inzulinová rezistence MeSH
• játra chemie   účinky léků   MeSH
• kosterní svaly chemie   MeSH
• krevní glukóza analýza   MeSH
• kyseliny mastné neesterifikované analýza   MeSH
• lipidy biosyntéza   MeSH
• messenger RNA analýza   MeSH
• myši inbrední C57BL MeSH
• myši MeSH
• obezita etiologie   krev   patofyziologie   MeSH
• PPAR alfa agonisté   fyziologie   MeSH
• receptory adiponektinu MeSH
• receptory buněčného povrchu genetika   MeSH
• resistin genetika   krev   MeSH
• triglyceridy krev   MeSH
• tuková tkáň chemie   patologie   MeSH
• velikost orgánu účinky léků   MeSH
• ztučnělá játra etiologie   farmakoterapie   krev   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH