Preview

Kuban Scientific Medical Bulletin

Advanced search

Role and significance of asprosin in feeding behaviour and metabolism

https://doi.org/10.25207/1608-6228-2020-27-1-96-104

Abstract

This article presents a review of available information on asprosin — a hormone of white adipose tissue discovered in 2016. The history of its discovery, as well as its action mechanisms and main targets are examined. Changes in the plasma level of asprosin under some pathological conditions are analysed. The importance of studying asprosin is determined by its functions: asprosin regulates physiological processes during fasting and plays an important role in the development of metabolic disorders, such as insulin resistance. There are relatively few studies concerned with asprosin; however, this hormone can already be considered as a diagnostic marker and a potential target in the treatment of certain metabolic disorders, e.g. diabetes mellitus and obesity.

About the Authors

Rustam H. Salimkhanov
Kuban State Medical University
Russian Federation

6th-year Student,

Mitrofana Sedina str., 4, Krasnodar, 350063



Vladislav R. Sharifullin
Kuban State Medical University
Russian Federation

6th-year Student,

Mitrofana Sedina str., 4, Krasnodar, 350063



Yulia R. Kushnareva
Kuban State Medical University
Russian Federation

4th-year Student, General Medicine Department,

Mitrofana Sedina str., 4, Krasnodar, 350063



Azamat Kh. Kade
Kuban State Medical University
Russian Federation

Dr. Sci. (Med.), Prof., Head of the Department of General and Clinical Pathological Physiology,

Mitrofana Sedina str., 4, Krasnodar, 350063



Pavel P. Polyakov
Kuban State Medical University
Russian Federation

Research Assistant, Department of General and Clinical Pathological Physiology,

Mitrofana Sedina str., 4, Krasnodar, 350063



References

1. Zhang Y., Proenca, R., Maffei M., Barone M., Leopold L., Friedman J.M. Positional cloning of the mouse obese gene and its human homologue. Nature. 1994; 372(6505): 425–432. DOI: 10.1038/372425a0.

2. Romere C., Duerrschmid C., Bournat J., Constable P., Jain M., Xia F., Saha P.K., Del Solar M., Zhu B., York B., Sarkar P., Rendon D.A., Gaber M.W., LeMaire S.A., Coselli J.S., Milewicz D.M., Sutton V.R., Butte N.F., Moore D.D., Chopra A.R. Asprosin, a fasting-induced glucogenic protein hormone. Cell. 2016; 165(3): 566– 579. DOI: 10.1016/j.cell.2016.02.063

3. Duerrschmid C., He Y., Wang C., Li C., Bournat J.C., Romere C., Saha P.K., Lee M.E., Phillips K.J., Jain M., Jia P., Zhao Z., Farias M., Wu Q., Milewicz D.M., Sutton V.R., Moore D.D., Butte N.F., Krashes M.J., Xu Y., Chopra A.R. Asprosin is a centrally acting orexigenic hor mone. Nat. Med. 2017; 23(12): 1444– 1453. DOI: 10.1038/nm.4432

4. Paolacci S., Bertola D., Franco J., Mohammed S., Tartaglia M., Wollnik B., Hennekam R. C. WiedemannRautenstrauch syndrome: A phenotype analysis. Am. J. Med. Genet. A. 2017; 173(7): 1763–1772. DOI: 10.1002/ajmg.a.38246

5. Goldblatt J., Hyatt J., Edwards C., Walpole I. Further evidence for a marfanoid syn drome with neonatal progeroid features and severe generalized lipodystrophy due to frameshift mutations near the 3′ end of the FBN1 gene. J. Med. Genet. A. 2011; 155A(4): 717–720. DOI: 10.1002/ajmg.a.33906

6. Graul-Neumann L.M, Kienitz T., Robinson P.N., Baasanjav S., Karow B., Gillessen-Kaesbach G., Fahsold R., Schmidt H., Hoffmann K., Passarge E. Marfan syn drome with neonatal progeroid syndromelike lipodystrophy associated with a novel frameshift mutation at the 3′ terminus of the FBN1-gene. J. Med. Genet. A. 2010; 152A(11): 2749–2755. DOI: 10.1002/ ajmg.a.33690

7. Horn D., Robinson P.N. Progeroid facial features and lipodystrophy associated with a novel splice site mutation in the final intron of the FBN1 gene. J. Med. Genet. A. 2011; 155A(4): 721–724. DOI: 10.1002/ ajmg.a.33905

8. Jacquinet A., Verloes A., Callewaert B., Coremans C., Coucke P., de Paepe A.,Debray F.G. Neonatal progeroid variant of Marfan syndrome with congenital lipodystrophy results from mutations at the 3′ end of FBN1 gene. Eur. J. Med. Genet. 2014; 57(5): 230– 234. DOI: 10.1016/j.ejmg.2014.02.012

9. Takenouchi T., Hida M., Sakamoto Y., Torii C., Kosaki R., Takahashi T., Kosaki K. Severe congenital lipodystrophy and a progeroid appearance: Mutation in the penulti mate exon of FBN1 causing a recognizable phenotype. J. Med. Genet. A. 2013; 161A(12): 3057– 3062. DOI: 10.1002/ajmg.a.36157

10. Passarge E., Robinson P., Graul-Neumann L. Marfanoid-progeroid-lipodystrophy syndrome: a newly recognized fi brillinopathy. Eur. J. Hum. Genet. 2016; 24(9): 1244–1247. DOI: 10.1038/ejhg.2016.6

11. Lönnqvist D., Reinhardt L., Sakai L., Peltonen L. Evidence for furin-type activity-mediated C-terminal processing of profibrillin-1 and interference in the processing by certain mutations. Hum. Mol. Genet. 1998; 7(13): 2039–2044. DOI: 10.1093/hmg/7.13.2039

12. Milewicz D.M., Grossfield J., Cao S.N., Kielty C., Covitz W., Jewett W. A mutation in FBN1 disrupts profibrillin processing and results in isolated skeletal features of the Marfan syndrome. J. Clin. Invest. 1995; 95(5): 2373–2378. DOI: 13.1172/JCI117930

13. Li E., Shan H., Chen L., Long A., Zhang Y., Liu Y., Jia L., Wei F., Han J., Li T., Liu X., Deng Y., Wang Y. OLFR734 Mediates Glucose Metabolism as a Receptor of Asprosin. Cell Metabolism. 2019; 30(2): 319–328. DOI: 10.1016/j.cmet.2019.05.022

14. Aponte Y., Atasoy D., Sternson S.M. AgRP neurons are sufficient to orches trate feeding behavior rapidly and without training. Nat. Neurosci. 2011; 14(3): 351– 355. DOI: 10.1038/nn.2739

15. Krashes M.J., Koda S., Ye C, Rogan S.C., Adams A.C., Cusher D.S., Maratos-Flier E., Roth B.L., Lowell B.B. Rapid, reversible activation of AgRP neurons drives feed ing behavior in mice. J. Clin. Invest. 2011. 121(4): 1424–1428. DOI: 10.1172/JCI46229

16. Luquet S., Perez F.A., Hnasko T.S., Palmiter, R.D. NPY/AgRP neurons are essen tial for feeding in adult mice but can be ablated in neonates. Science. 2005; 310(5748): 683–685. DOI: 10.1126/science.1115524

17. Atasoy D., Betley J.N., Su H.H., Sternson S.M. Deconstruction of a neural circuit for hunger. Nature. 2012; 488(7410): 172–177. DOI: 10.1038/nature11270

18. Tong Q., Ye C.P., Jones J.E., Elmquist J.K., Lowell B.B. Synaptic release of GABA by AgRP neurons is required for normal regulation of energy balance. Nat. Neuro sci. 2008; 11(9): 998–1000. DOI: 10.1038/nn.2167

19. Denis R.G., Joly-Amado A., Webber E., Langlet F., Schaeffer M., Padilla S.L., Cansell C., Dehouck B., Castel J., Delbès A.S., Martinez S., Lacombe A., Rouch C., Kassis N., Fehrentz J.A., Martinez J., Verdié P., Hnasko T.S., Palmiter R.D., Krashes M.J., Güler A.D., Magnan C., Luquet S. Palatability can drive feeding independent of AgRP neurons. Cell Metabolism. 2015; 22(4): 646–657. DOI: 10.1016/j. cmet.2015.07.011

20. Garfield A.S., Li C., Madara J.C., Shah B.P., Webber E., Steger J.S., Campbell J.N., Gavrilova O., Lee C.E., Olson D.P., Elmquist J.K., Tannous B.A., Krashes M.J., Lowell B.B. A neural basis for melanocortin-4 receptor-regulated appetite. Nat. Neurosci. 2015; 18(6): 863–871. DOI: 10.1038/nn.4011

21. Zhang X., Jiang H., Ma X., Wu H. J. Increased serum level and impaired re sponse to glucose fluctuation of asprosin is associated with type 2 diabetes mellitus. J. Diabetes Investig. 2019; 16. DOI: 10.1111/jdi.13148

22. Wang Y., Qu H., Xiong X., Qiu Y., Liao Y., Chen Y., Zheng Y., Zheng H. Plasma asprosin concentrations are increased in individuals with glucose dysregulation and corre lated with insulin resistance and first phase insulin secretion. Mediators Inflamm. 2018; 2018: 9471583. DOI: 10.1155/2018/9471583

23. Alan M., Gurlek B., Yilmaz A., Aksit M., Aslanipour B., Gulhan İ., Mehmet C., Taner C. E. Asprosin: a novel peptide hormone related to insulin resistance in women with polycystic ovary syndrome. Gynecol. Endocrinol. 2018; 35(3): 220–223. DOI: 10.1080/09513590.2018.1512967

24. Kocaman N., Artaş G. Can novel adipokines, asprosin and meteorin-like, be biomarkers for malignant mesothelioma? Biotech. Histochem. 2019; 1: 1–5. DOI: 10.1080/10520295.2019.1656344

25. Zhang Z., Tan Y., Zhu L., Zhang B., Feng P., Gao E., Xu C., Wang X., Yi W., Sun Y. Asprosin improves the survival of mesenchymal stromal cells in myocardial infarction by inhibiting apoptosis via the activated ERK1/2-SOD2 pathway. Life Sci. 2019; 231: 116554. DOI: 10.1016/j.lfs.2019.116554


Review

For citations:


Salimkhanov R.H., Sharifullin V.R., Kushnareva Yu.R., Kade A.Kh., Polyakov P.P. Role and significance of asprosin in feeding behaviour and metabolism. Kuban Scientific Medical Bulletin. 2020;27(1):96-104. (In Russ.) https://doi.org/10.25207/1608-6228-2020-27-1-96-104

Views: 1142


Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.


ISSN 1608-6228 (Print)
ISSN 2541-9544 (Online)