Enterohepatic circulation of triiodothyronine

The major factor regulating thyroid function is thyroid stimulating hormone (TSH), a glycoprotein released by the thyrotropic cells of the pituitary gland. Determinants of the TSH secretion rate are inhibition by thyroxine (T 4), 3, 3', 5-triiodothyronine (T3), dopamine, glucocorticoids and somatostatin, and stimulation by TSH-releasing hormone (TRH), (nor)adrenaline and perhaps neurotensin [156]. In the control of thyroid hormone bioavailability, an important role is also played by iodothyronine transport into cells, enzymatic deiodination and conjugation. Several groups have studied the enterohepatic metabolic pathways of iodothyronines. It has been generally accepted that these pathways have no more than a passive function in the elimination of the hormone. However, if enterohepatic circulation (EHC) of iodothyronines occurs, the intestinal tract may constitute an important pool of exchangeable hormone. Until recently, only few and inconclusive data existed concerning this EHC. In our studies we have attempted to document the possible existence of an EHC of thyroid hormone and the role it may play in regulating overall hormone metabolism and excretion in the rat. Especially, we wanted to assess the importance of the intestinal microflora for this process. We have studied the biliary clearance of T3 and its conjugates, the hydrolysis of iodothyronine conjugates by intestinal bacteria and intestinal contents, and the metabolism of T3 and its conjugates in conventional (CV) and intestine-decontaminated (ID) rats. It is the purpose of this thesis to discuss the role of the EHC of iodothyronines in thyroid hormone metabolism, with special emphasis on the results of my own studies of this subject, described in detail in the appendix papers

Van Docter Bernardo naar Endocriene Weesaandoeningen

Rede, uitgesproken ter gelegenheid van het aanvaarden van het ambt van bijzonder hoogleraar met als leeropdracht Endocriene oncologie aan het Erasmus MC, faculteit van de Erasmus Universiteit Rotterdam op 24 november 201

One hundred years after the discovery of insulin and glucagon:the history of tumors and hyperplasias that hypersecrete these hormones

One century ago, in 1922, Frederick G Banting, Charles H Best, James B Collip and John J R Macleod first published their experiments resulting in the isolation of a hypoglycemic factor, named insulin, from a solution extract from a dog’s pancreas. One year later, in 1923, a hyperglycemic factor named glucagon was isolated by Charles P Kimball and John R Murlin. In the following years, it could be demonstrated that pancreatic islet alpha- and beta-cell neoplasms and hyperplasias could inappropriately secrete excessive amounts of these two hormones. This review is a sequel to the discovery of insulin and glucagon and introduces the history of this fascinating group of neuroendocrine neoplasms and hyperplasias of the pancreas.</p

Clémentine Delait (1865–1934), the most famous bearded lady on the continent in the 20th century

Clémentine Delait Clattaux (1865–1934), the Bearded Woman from Thaon-les-Vosges, France, did not suffer from her extreme hirsutism, but used it to her advantage. Her beard started to grow when she turned 18 and at the age of 25 she decided to stop shaving her beard and let it grow. She had regular menstrual cycles between ages 12 and 35. She was diagnosed with signs and symptoms of hyperandrogenism like hirsutism, impressive strength and muscularity and a deep voice, but also with morbid obesity. She never gave birth to a child. At the age of 39, she was officially allowed by the French Government to wear man’s clothes. She suffered from rheumatism and died because of a stroke. The most probable cause of her hirsutism was polycystic ovary syndrome. Alternatively, an incomplete block in the adrenal steroid synthesis, like nonclassical 21-hydroxylase deficiency can be considered

The Evolution of Neuroendocrine Tumor Treatment Reflected by ENETS Guidelines

In 2016, the third version of guidelines for the diagnosis and treatment of neuroendocrine tumors (NETs) has been published by the European Neuroendocrine Tumor Society (ENETS). These guidelines reflect the progress in treatment of NETs, and by comparing the newest guidelines with the first guidelines of 2001, this progress can be clearly recognized. Diagnostic accuracy has been increased by the introduction of PET-CT with Ga-labelled somatostatin analogs, and multiple new treatments and treatment schedules have been developed, like peptide receptor radiotherapy with radiolabeled somatostatin analogs, or targeted therapies. Evidence and indications for these therapi

Medical treatment of neuroendocrine neoplasms

Medical therapy of clinically nonfunctioning (nonsecreting) low grade (grade 1–2) neuroendocrine neoplasms consists of first-line first generation somatostatin analogs and second-line or third-line peptide receptor radiotherapy with radiolabeled beta-emitting somatostatin analogs, Everolimus, Sunitinib, and interferon-α. Second-generation somatostatin analogs like Pasireotide have no proven superiority over first-generation somatostatin analogs. Chemotherapy is usually reserved as second-line therapy in pancreatic neuroendocrine neoplasms and neuroendocrine carcinomas.</p