Endocrine Abstracts

Fibro-adipogenic progenitors (FAPs), a muscle-resident stem cell population, have recently emerged as important actors of muscle regeneration by interacting with myogenic progenitors (MPs) to promote the formation of new muscle fibers. However, in pathological condition, as muscle dystrophies, this coordinated response is lost and then an accumulation of FAPs is observed. In particular, in a mouse model of Duchenne muscle dystrophy (mdx), the accumulation of a specific subpopu...

Dysregulation of types 2 and 3 deiodinases (D2 and D3) alters the metabolism of thyroid hormones in the patients with nonthyroidal illness syndrome (NTIS). Previous studies have demonstrated that deiodinase expression varies in the muscle in different disease models. Nevertheless, the location of D2 and D3 and the effect of oxidative stress on reticulum endoplasmic (ER) and mitochondrial function are not described in human muscle with different types of acute disease and NTIS....

Diabetes mellitus is one of the greatest health crises of our time. In response to diabetic stress, pancreatic beta-cells undergo a set of profound phenotypical alterations, including dedifferentiation, polyploidisation and hypertrophy, and apoptosis. Although we know that thyroid hormone (TH) signalling controls these phenomena in response to various injuries, little is known about its role in the pathobiology of diabetic pancreas. The aim of this study was to investigate the...

Purpose: Treatment with tyrosine kinase inhibitors (TKI) has been associated with alterations in circulating thyroid hormone levels, possibly related to perturbations in peripheral thyroid hormone metabolism. In this study, we evaluated the effect of the multi-kinase inhibitor vandetanib on the expression of the three deiodinase selenoenzymes.Materials and Methods: Cell models that endogenously express either D1 (HepG2 and HEK-293), D2 (HeLa and KMH-2) o...

Objectives: Acute liver failure (ALF) is a rare but life-threatening condition with severe liver dysfunction. In ALF liver regeneration capacity is exceeded due to loss of hepatocyte function. A well-known trigger of ALF is paracetamol (acetaminophen, APAP) intoxication. Unfortunately, based on the poor prognosis and rapidly increasing mortality rate liver transplantation offers the so far only effective therapeutic strategy. Even if the underlying mechanisms of ALF are not ye...