Adiponectin is an adipokine increasing glucose and fatty acid metabolism and improving insulin sensitivity. The aim of this study was to investigate the role of adiponectin in the regulation of adipocyte lipolysis. Human adipocytes isolated from biopsies obtained during surgical operations from 16 non-obese and 17 obese subjects were incubated with 1) human adiponectin (20 μg/ml) or 2) 0.5 mM AICAR - activator of AMPK (adenosine monophosphate activated protein kinase). Following these incubations, isoprenaline was added (10-6 M) to investigate the influence of adiponectin and AICAR on catecholamine-induced lipolysis. Glycerol concentration was measured as lipolysis marker. We observed that adiponectin suppressed spontaneous lipolysis by 21 % and isoprenaline-induced lipolysis by 14 % in non-obese subjects. These effects were not detectable in obese individuals, but statistically significant differences in the effect of adiponectin between ob ese and non-obese were not revealed by two way ANOVA test. The inhibitory effect of AICAR and adiponectin on lipolysis was reversed by Compound C. Our results suggest, that adiponectin in physiological concentrations inhibits spontaneous as well as catecholamine-induced lipolysis. This effect might be lower in obese individuals and this regulation seems to involve AMPK., Z. Wedellová ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Adipose tissue is a hormonally active tissue, producing adipocytokines which may influence activity of other tissues. Adiponectin, abundantly present in the plasma increases insulin sensitivity by stimulating fatty acid oxidation, decreases plasma triglycerides and improves glucose metabolism. Adiponectin levels are inversely related to the degree of adiposity. Anorexia nervosa and type 1 diabetes are associated with increased plasma adiponectin levels and higher insulin sensitivity. Decreased plasma adiponectin levels were reported in insulin-resistant states, such as obesity and type 2 diabetes and in patients with coronary artery disease.Activity of adiponectin is associated with leptin, resistin and with steroid and thyroid hormones, glucocorticoids, NO and others.
Adiponectin suppresses expression of extracellular matrix adhesive proteins in endothelial cells and atherosclerosis potentiating cytokines. Anti-atherogenic and anti-inflammatory properties of adiponectin and the ability to stimulate insulin sensitivity have made adiponectin an important object for physiological and pathophysiological studies with the aim of potential therapeutic applications.
Adiponektin je hormon tukové tkáně, který je přítomen v krvi v poměrně vysokých koncentracích. Působí jako protektivní faktor při iniciaci a progresi aterosklerózy díky svým protizánětlivým a protiaterogenním vlastnostem. Jeho sérové hladiny jsou sníženy u obézních jedinců, pacientů s diabetem 2. typu, u pacientů s onemocněním koronárních arterií atd. Hladina adiponektinu pozitivně koreluje s hladinou HDL cholesterolu, negativně naopak s markery zánětu, inzulinové rezistence, triacylglyceroly a markery metabolismu na triacylglyceroly bohatých lipoproteinových částic, a dalšími adipokiny. Adiponektin působí jako ochranný faktor v rozvoji onemocnění spojených s obezitou. Protizánětlivý efekt může být hlavní složkou jeho kladného působení při potlačování kardiovaskulárních a metabolických onemocnění včetně aterosklerózy a inzulinové rezistence. Navíc se zdá, že vykazuje přímou biologickou aktivitu, a to mj. indukcí klasické cesty aktivace komplementu. Gen pro adiponektin je polymorfní a v jeho blízkosti leží také susceptibilní lokusy pro DM 2. typu a metabolický syndrom. Tato přehledná práce se zabývá adiponektinem a jeho vztahem k ateroskleróze, popisuje některé polymorfi smy na genu pro adiponektin a všímá si jeho protizánětlivého účinku., Adiponectin is an adipose tissue-derived hormone which circulates at relatively high concentrations in blood. Adiponectin has protective actions in the initiation and progression of atherosclerosis through anti-infl ammatory and anti-atherogenic effects. Adiponectin serum levels are decreased in obesity, type 2 diabetes, and patients with coronary artery disease, etc. The level of circulating adiponectin correlates positively with HDL cholesterol, and negatively with infl ammatory markers, markers of insulin resistance, triglyceride-rich lipoprotein particles, and other adipokines. Adiponectin displays protective actions on development of various obesity-linked diseases. The anti-infl ammatory properties may be the major component of its benefi cial effects on cardiovascular and metabolic disorders including atherosclerosis and insulin resistance. In addition, adiponectin displays a direct biological activity through the induction of a classical pathway of complement activation. The polymorphic gene for adiponectin is located in the close proximity of susceptibility loci for type 2 diabetes and metabolic syndrome. This review deals with adiponectin and its relationship to atherosclerosis, describes some adiponectin gene polymorphisms and focuses on its anti-infl ammatory effects., Novotný Dalibor, Vaverková H., Karásek D., Halenka M., and Lit.: 28
Obezita je v kombinaci s dalšími složkami syndromu inzulinové rezistence výrazným rizikovým faktorem aterosklerózy a jejich komplikací. Přesné mechanizmy propojení uvedených onemocnění jsou dosud objasněny pouze zčásti. Jedním z možných pojítek je porucha endokrinní funkce tukové tkáně, která při obezitě produkuje zvýšené množství prozánětlivých a proaterogenních hormonů a cytokinů a méně faktorů protektivních. Prakticky jediným z hormonů tukové tkáně s prokázaným protizánětlivým a antiaterosklerotickým účinkem je hormon adiponektin. Tento hormon je produkován převážně adipocyty a jeho hladiny jsou sníženy právě u pacientů s obezitou, inzulinovou rezistencí a aterosklerózou. Cílem tohoto článku je shrnout současné experimentální a klinické poznatky o vztahu adiponektinu k ateroskleróze a diskutovat možné využití tohoto hormonu v predikci aterosklerózy a případné perspektivy jeho využití v prevenci a léčbě tohoto onemocnění., Denisa Haluzíková, T. Roubíček, Martin Haluzík, and Lit. 39
High -energy intake which exceeds energy expenditure leads to the accumulation of triglycerides in adipose tissue, predominantly in large -size adipocytes. This metabolic shift, which drives the liver to produce atherogenic dyslipidemia, is well documented. In addition, an increasing amount of monocytes/macrophages, predominantly the proinflammatory M1- type, cumulates in ectopic adipose tissue. The mechanism of this process, the turnover of macrophages in adipose tissue and their direct atherogenic effects all remain to be analyzed., R. Poledne, I. Králová Lesná, S. Čejková., and Obsahuje bibliografii
Excessive LDL cholesterol concentration together with subclinical inflammation, in which macrophages play a central role, are linked pathologies. The process starts with the accumulation of macrophages in white adipose tissue and the switch of their polarization toward a pro-inflammatory phenotype. The proportion of pro-inflammatory macrophages in adipose tissue is related to the main risk predictors of cardiovascular disease. The cholesterol content of phospholipids of cell membranes seems to possess a crucial role in the regulation of membrane signal transduction and macrophage polarization. Also, different fatty acids of membrane phospholipids influence phenotypes of adipose tissue macrophages with saturated fatty acids stimulating pro-inflammatory whereas ω3 fatty acids antiinflammatory changes. The inflammatory status of white adipose tissue, therefore, reflects not only adipose tissue volume but also adipose tissue macrophages feature. The beneficial dietary change leading to an atherogenic lipoprotein decrease may therefore synergically reduce adipose tissue driven inflammation.
For a given bi-continuous semigroup $(T(t))_{t\geq 0}$ on a Banach space $X$ we define its adjoint on an appropriate closed subspace $X^\circ $ of the norm dual $X'$. Under some abstract conditions this adjoint semigroup is again bi-continuous with respect to the weak topology $\sigma (X^\circ ,X)$. We give the following application: For $\Omega $ a Polish space we consider operator semigroups on the space ${\rm C_b}(\Omega )$ of bounded, continuous functions (endowed with the compact-open topology) and on the space ${\rm M}(\Omega )$ of bounded Baire measures (endowed with the weak$^*$-topology). We show that bi-continuous semigroups on ${\rm M}(\Omega )$ are precisely those that are adjoints of bi-continuous semigroups on ${\rm C_b}(\Omega )$. We also prove that the class of bi-continuous semigroups on ${\rm C_b}(\Omega )$ with respect to the compact-open topology coincides with the class of equicontinuous semigroups with respect to the strict topology. In general, if $\Omega $ is not a Polish space this is not the case.
Using the concept of the $ {\mathrm H}_1$-integral, we consider a similarly defined Stieltjes integral. We prove a Riemann-Lebesgue type theorem for this integral and give examples of adjoint classes of functions.