Endocrine Abstracts

IntroductionIn the background of persistent hyperinsulinemic hypoglycemia the insulinomas of the pancreatic beta cells may be present, but in some rare cases we fail to identify a well-defined lesion and the insulin hypersecretion is caused by nesidioblastosis, a diffuse proliferation of the pancreatic islet cells. However, the localization of the lesion is necessary for proper treatment, in certain cases finding the insulinoma is difficult and can only ...

Background: Hypothyroidism due to autoimmune thyroiditis leads to atherogenic lipid profile and metabolic changes. The formation of advanced glycation end products (AGEs) increases with hyperglycemia, hyperlipidemia and oxidative stress. Degradation of AGEs after AGEs-receptor 1-mediated intracellular uptake and renal clearance of soluble AGEs generated by certain cells like macrophages play a crucial role in the decrement of circulating AGEs level. Chemerin is an adipokine pr...

Background: Fibroblast growth factor 21 (FGF21) is a hormonal regulator of lipid and glucose metabolism exerting protection against atherosclerosis by multiple actions on the blood vessels, liver, and adipose tissues. Enhanced FGF21 production in diabetes and obesity reduces the level of LDL-C and triglycerides by suppression of hepatic SREBP-2. Hypothyroidism has also been shown to have unfavorable effects on atherogenesis and dyslipidemia. To date, the association of lipid p...

Background: Advanced glycation end products (AGEs) are heterogenous group of irreversible chemical moieties originated from non-enzymatic glycation and oxidation of proteins, nucleic acids, and lipids. The engagement of AGEs with their chief cellular receptor (RAGE) activates signaling pathways contributing to the progression of chronic diseases like autoimmune thyroiditis, type 2 diabetes mellitus and its complications. Soluble RAGE (sRAGE) prevents AGE-RAGE interaction in a ...