RESUMO
Disorders in the kidneys lead to disturbance of homeostasis. As the glomerular filtration rate decreases, the metabolism of numerous biologically active substances, including pituitary hormones, decreases. The article presents an overview of pituitary dysfunction in patients with chronic kidney disease (CKD) and discusses the possible reasons of the pathogenetic mechanisms. Particular focus is being given to the assessment of changes in the concentration of pituitary hormones in patients with end-stage chronic kidney disease (CKD) and discusses the pathogenetic mechanisms of their formation. Particular attention is paid to the assessment of changes in the concentration of pituitary hormones in patients receiving renal replacement therapy (RRT). CKD leads to an increase in the level of prolactin, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Concentrations of growth hormone (GH), isulin-like growth factor-1 (IGF-1), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH) and vasopressin may remain within normal values or increase in this group of patients. RRT does not reduce the levels of prolactin, LH, FSH, while the concentration of growth hormone, IGF-1, TSH tends to normalize. The content of ACTH and vasopressin may remain unchanged or decrease. Kidney transplantation in most cases corrects hormonal disorders. Correction of hormonal changes can improve the clinical outcome and quality of life of patients with end stage CKD.
Assuntos
Hormônio do Crescimento Humano , Falência Renal Crônica , Doenças da Hipófise , Insuficiência Renal Crônica , Humanos , Prolactina/metabolismo , Fator de Crescimento Insulin-Like I , Qualidade de Vida , Hormônios Hipofisários/metabolismo , Hormônio Luteinizante/metabolismo , Hormônio do Crescimento/uso terapêutico , Hormônio Foliculoestimulante/metabolismo , Tireotropina , Hormônio Adrenocorticotrópico , Doenças da Hipófise/tratamento farmacológico , Falência Renal Crônica/terapia , Falência Renal Crônica/tratamento farmacológico , Vasopressinas , Insuficiência Renal Crônica/terapia , Insuficiência Renal Crônica/tratamento farmacológicoRESUMO
Adipose tissue is an endocrine organ which produces a large number of secretory bioactive substances also known as adipocytokines affecting directly insulin resistance (IR), glucose and lipid metabolism, angiogenesis and inflammation. The studies show a close connection between the imbalance of adipocytokines formed as a result of excessive deposit of adipose tissue in the course of the development of type 2 diabetes mellitus and cardiovascular diseases. In the present review, we summarize current data on the effect of the adipocytokines on the liver, skeletal muscles, adipose tissue, endothelial cells and inflammatory processes, as well as attempt to define the term «adipocytokines¼ and classify adipocytokines according to their influence on metabolic processes and pro-inflammatory status. Some of adipocytokines (adiponectin, omentin, leptin, resistin, tumor necrosis factor-α and interleukin-6) are divided into two groups: adipocytokines reducing IR, and adipocytokines increasing IR.
Assuntos
Diabetes Mellitus Tipo 2 , Resistência à Insulina , Adipocinas/metabolismo , Adiponectina , Células Endoteliais/metabolismo , Humanos , Resistência à Insulina/fisiologiaRESUMO
In 2008 the Food and Drug Administration has revised approval process for new antidiabetic agents and introduced a requirement to demonstrate the cardiovascular safety in an international multicenter trial. Currently cardiovascular outcome trials of dipeptidyl peptidase-4 (DPP-4) inhibitors (SAVOR-TIMI53, EXAMINE and TECOS), sodium-glucose cotransporter 2 inhibitors (EMPAREG, CANVAS), glucagon-like peptide-1 receptor agonists (ELIXA, EXSCEL LEADER and SUSTAIN-6), ultralong-acting and insulin (DEVOTE) have been completed. The trials confirmed cardiovascular safety of these glucose-lowering medications, and in addition, EMPA-REG OUTCOME (empagliflozin), CANVAS (canagliflozin) and LEADER (liraglutide) have also demonstrated cardioprotective effect of sodium-glucose cotransporter 2 inhibitors and glucagon-like peptide-1 receptor agonists. These data led to the changes of clinical guidelines for the management of type 2 diabetes.