Hypocretin/orexin modulates body weight and the metabolism of glucose and insulin

Ernest Adeghate, Mohamed Lotfy, Crystal D'Souza, Saleh Meqbel Alseiari, Abdulla Ali Alsaadi, Saif Abdo Qahtan

Research output: Contribution to journalReview articlepeer-review

13 Citations (Scopus)


The hypocretin/orexin (Hcrt/orexin) unit affects the functions of the nervous, cardiovascular, gastrointestinal, and reproductive systems. Hcrt/orexin ligands and receptors have been localized to different parts of the central and peripheral nervous systems, cerebrospinal fluid and blood, exocrine (pancreas, salivary, lacrimal) as well as endocrine (pancreatic islets, pituitary, adrenal) glands. Several factors including stress, glucagon-like peptide-1 agonists, glutamate, nicotine, glucose, and hypoglycaemia stimulate the expression of Hcrt/orexin system, but it is inhibited by ageing, bone morphogenetic protein, hypoxia/hypercapnia, melanocortin receptor accessory protein 2, and glucagon. Literature reports show that Hcrt/orexin can significantly increase insulin secretion from normal and diabetic rat pancreata. Hcrt/orexin decreases blood glucose concentration and reduces insulin resistance partly via increased tissue expression of glucose transporter type 4. It reduces obesity by increasing browning of fat cells and energy expenditure. Taken together, Hcrt/orexin modulates obesity and the metabolism of glucose and insulin. The Hcrt/orexin system may thus be a target in the development of new therapies for the treatment of diabetes mellitus.

Original languageEnglish
Article numbere3229
JournalDiabetes/Metabolism Research and Reviews
Issue number3
Publication statusPublished - Mar 1 2020


  • diabetes mellitus
  • glucose
  • hypocretin/orexin
  • insulin
  • obesity

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


Dive into the research topics of 'Hypocretin/orexin modulates body weight and the metabolism of glucose and insulin'. Together they form a unique fingerprint.

Cite this