Glucoreceptors located in the brain mediate NPY release induced by hypoglycemia in normal men

• Published in: Regulatory peptides Vol. 172; no. 1-3; pp. 41 - 43
• Main Authors: Coiro, Vittorio, Volpi, Riccardo, Cataldo, Simona, Magotti, Maria Grazia, Giumelli, Claudio, Russo, Francesca, Stella, Adriano, Chiodera, Paolo
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier B.V 10.12.2011; Elsevier
• Subjects: Adult; Biological and medical sciences; Blood-Brain Barrier - drug effects; Blood-Brain Barrier - metabolism; Blood–brain-barrier; Brain - drug effects; Brain - metabolism; Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges; Fructose; Fructose - pharmacology; Fundamental and applied biological sciences. Psychology; Glucose; Glucose - pharmacology; Humans; Hypoglycemia; Hypoglycemia - chemically induced; Hypoglycemia - physiopathology; Insulin - pharmacology; Male; Neuropeptide Y - blood; NPY; Receptors, Cell Surface; Vertebrates: endocrinology; Vertebrates: nervous system and sense organs; Glucose; Hypoglycemia; Blood–brain-barrier; NPY; Fructose; Human; Neuropeptide Y; Peptide hormone; Central nervous system; Metabolic diseases; Blood brain barrier; Encephalon; Blood-brain-barrier; Release
• ISSN: 0167-0115; 1873-1686
• DOI: 10.1016/j.regpep.2011.08.005

The NPY secretory pattern after an insulin tolerance test (ITT) (0.15IU/kg body weight) was evaluated in 8 normal men. They were infused with normal saline (control test), glucose or fructose. Insulin-induced hypoglycemia produced a significant increment in serum NPY in the control test. The infusion of fructose was unable to change the NPY secretory pattern during insulin-induced hypoglycemia. In contrast, the NPY increase during ITT was completely abolished when the concomitant infusion of glucose prevented insulin-induced hypoglycemia. These results exclude a direct role of hyperinsulinemia in the mechanism underlying the stimulation of NPY secretion during ITT. Furthermore, since glucose but not fructose crosses the blood–brain-barrier (BBB), the NPY increase during ITT appears to be generated by low glucose concentrations at the level of glucosensitive areas located inside the brain. ► Plasma neuropeptide Y (NPY) levels rose in response to insulin induced hypoglycemia. ► Glucose, but not fructose infusion abolished NPY rise during insulin tolerance test. ► Hypoglycemia, but not hyperinsulinemia induced the plasma NPY response. ► Neuroglucopenia stimulated NPY inside the brain at sites not reached by fructose.