Diabetes mellitus zvyšuje riziko vzniku srdečního selhání nezávisle na ischemické chorobě srdeční a hypertenzi a může způsobovat syndrom označovaný jako diabetická kardiomyopatie. Diabetická kardiomyopatie je definována jako dysfunkce srdečních komor u diabetiků, která vzniká nezávisle na známých příčinách, jako jsou koronární ateroskleróza, chlopenní vady nebo hypertenze. Projevuje se systolickou a/nebo diastolickou dysfunkcí. Klíčová slova: srdeční selhání – diabetická kardiomyopatie – dysfunkce srdečních komor, Diabetes mellitus increases the risk of heart failure independent of coronary heart disease and hypertension and may cause diabetic cardiomyopathy. Diabetic cardiomyopathy has been defined as ventricular dysfunction that occurs in diabetic patients independent of recognised causes (coronary heart disease, valve defects, hypertension). Left ventricular dysfunction is manifested by systolic and/or diastolic dysfunction. Keywords: heart failure – diabetic cardiomyopathy – left ventricular dysfunction, and Kubíčková M., Šmahelová A.
Inzulinový růstový faktor typu 1 (IGF-1) a inzulin mají kromě specifických účinků týkajících se metabolizmu glukózy také účinek mitogenní, který se prostřednictvím receptorů pro IGF1 (IGF1-R) a pro inzulin (IR), přítomných velmi často na nádorových buňkách, realizuje i v podobě potenciace nádorového růstu. Úzká vazba mezi kancerogenezí a metabolizmem glukózy vede potom k ovlivňování obou těchto procesů léky používanými v léčbě jedné z diagnóz. Pochopení molekulárních mechanizmů zprostředkovaných oběma receptory umožňuje klinikům předvídat nežádoucí účinky léčby i kontrolu onkologické bezpečnosti terapie diabetu., In addition to having specific effects in terms of glucose metabolism, the insulin-like growth factor type 1 (IGF-1) and insulin also possess a mitogenic effect that, by means of IGF1 receptors (IGF1-R) and insulin receptors (IR) often present on tumour cells, may be exerted by potentiation of tumour growth. The close link between carcinogenesis and glucose metabolism then results in interference of both these processes by drugs used to treat either condition. An understanding of the molecular mechanisms mediated by both receptors allows the clinician to predict adverse effects of treatment as well as to control the oncological safety of diabetes treatment., Petra Tesařová, and Lit.: 22
The article shows pediatric diabetes as a truly heterogenous condition. Diabetes in children is most often caused by islet cell autoimmunty that leads to absolute lack of insulin; we discuss the recent advances in research of its etiology. A considerable proportion (estimates range from 1 to 3 %) of diabetic chldren suffer from so called MODY diabetes, a monogenic autosomal dominant condition that is cause by a secretory defect in the beta cell. Revealing the mutation causing MODY may enable more effective diabetes therapy.
Diabetic macular edema (DME) is a major factor contributing to visual disabilities in diabetic patients, and the number of patients is increasing. Animal models play a key role in the development of novel therapies. In this study, pathophysiological analyses of ocular lesions in Spontaneously Diabetic Torii (SDT) fatty rats were performed. First, vascular endothelial growth factor (VEGF) concentrations in vitreous humor, retinal vascular permeability and retinal thickness were measured in SDT fatty rats (Experiment 1). Furthermore, the pharmacological effects of two anti-diabetic drugs, phlorizin and pioglitazone, on retinal lesions were evaluated (Experiment 2). As results, the SDT fatty rats exhibited VEGF increase in vitreous humor at 8 and 16 weeks of age, and both retinal vascular hyperpermeability and retinal thickening at 16 weeks of age. In particular, the layers between the retinal internal limiting membrane and the outer nuclear layer were thickened. Phlorizin treatment from 4 to 16 weeks of age improved hyperglycemia and normalized retinal thickness; however, the effect of pioglitazone on retinal thickness was not strong despite the normalization of hyperglycemia. These data demonstrate that the male SDT fatty rat is a useful model for developing new therapeutic approaches in DME., Y. Motohashi, Y. Kemmochi, T. Maekawa, H. Tadaki, T. Sasase, Y. Tanaka, A. Kakehashi, T. Yamada, T. Ohta., and Obsahuje bibliografii