ABSTRACT
Gitelman syndrome is a rare hereditary nephropathy, which causes chronic metabolic alkalosis with low potassium and magnesium levels. There is no known coherence between Gitelman syndrome and Type-1 diabetes but patients with both diseases that develop diabetic ketoacidosis might present with normal acid status and receive incorrect treatment. In our case report the patient was known with both diseases and quickly diagnosed and treated but the condition is rare and previously only described in two other case reports.
ABSTRACT
Studies on isolated pancreatic islets suggest that neuromedin U (NMU), a brain and gastrointestinal peptide, acts as a decretin hormone, inhibiting glucose-stimulated insulin secretion. We investigated whether this effect could be reproduced in vivo and in isolated perfused rat pancreas. Unlike the incretin hormone, glucagon-like peptide 1 (GLP-1), intravenous NMU administration had no effects on blood glucose and plasma insulin and glucagon in vivo. Moreover, NMU neither changed insulin, glucagon, or somatostatin secretion from isolated perfused rat pancreas, nor affected GLP-1-stimulated insulin and somatostatin secretion. For NMU to act as a decretin hormone, its secretion should increase following glucose ingestion; however, glucose did not affect NMU secretion from isolated perfused rat small intestine, which contained extractable NMU. Furthermore, the two NMU receptors were not detected in endocrine rat or human pancreas. We conclude that NMU does not act as a decretin hormone in rats.
