Asprosin, a C-Terminal Cleavage Product of Fibrillin 1 Encoded by the FBN1 Gene, in Health and Disease


OVALI M. A., Bozgeyik I.

MOLECULAR SYNDROMOLOGY, cilt.13, sa.3, ss.175-183, 2022 (SCI-Expanded) identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 13 Sayı: 3
  • Basım Tarihi: 2022
  • Doi Numarası: 10.1159/000520333
  • Dergi Adı: MOLECULAR SYNDROMOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, EMBASE
  • Sayfa Sayıları: ss.175-183
  • Anahtar Kelimeler: Asprosin, FBN1, Marfan syndrome, Neonatal progeroid syndrome, Fibrillin 1, MARFAN-SYNDROME, CONGENITAL LIPODYSTROPHY, 3' END, MUTATIONS, FEATURES
  • Çanakkale Onsekiz Mart Üniversitesi Adresli: Evet

Özet

Background: Asprosin is a novel fasting-induced, glucogenic, and orexigenic protein hormone that is discovered with the help of genetic studies in patients with neonatal progeroid syndrome. Asprosin is encoded by the penultimate 2 exons (65 and 66) of the fibrillin 1 (FBN1) gene. Profibrillin 1 is the unprocessed protein product of FBN1 and undergoes a proteolytic cleavage by furin enzyme to produce mature fibrillin 1 and asprosin. The main organ responsible for the asprosin production seems to be white adipose tissue. Summary: Asprosin promotes hepatic glucose release in the liver and appetite stimulation in the hypothalamus through activation of the cAMP signaling circuitry through interacting with its G protein-coupled receptor, called OR4M1. Increasing mass of evidence suggests that asprosin is involved in the development and progression of various clinical conditions including diabetes, obesity, cardiomyopathy, cancer, and polycystic ovarian syndrome. It regulates various cellular and physiological processes such as appetite stimulation, glucose release, insulin secretion, apoptotic cell death, and inflammatory response. In this review, we discuss the current literature on asprosin and try to shed light on the yet undiscovered functions of asprosin. Key Message: Asprosin is a key regulatory factor for preserving the homeostasis of energy metabolism.