Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2019 May 12;8(5):666.
doi: 10.3390/jcm8050666.

Aerobic Exercise Training Decreases Hepatic Asprosin in Diabetic Rats

Affiliations

Aerobic Exercise Training Decreases Hepatic Asprosin in Diabetic Rats

Jeong Rim Ko et al. J Clin Med. .

Abstract

Asprosin, a novel hormone released from white adipose tissue, regulates hepatic glucose metabolism and is pathologically elevated in the presence of insulin resistance. It is unknown whether aerobic exercise training affects asprosin levels in type 1 diabetes mellitus (T1DM). The aim of this study was to determine whether (1) aerobic exercise training could decrease asprosin levels in the liver of streptozotocin (STZ)-induced diabetic rats and (2) the reduction in asprosin levels could induce asprosin-dependent downstream pathways. Five-week-old male Sprague-Dawley rats were randomly divided into control, STZ-induced diabetes (STZ), and STZ with aerobic exercise training groups (n = 6/group). T1DM was induced by a single dose of STZ (65 mg/kg intraperitoneally (i.p.)). The exercise group was made to run on a treadmill for 60 min at a speed of 20 m/min, 4 days per week for 8 weeks. Aerobic exercise training reduced the protein levels of asprosin, PKA, and TGF-β but increased those of AMPK, Akt, PGC-1β, and MnSOD. These results suggest that aerobic exercise training affects hepatic asprosin-dependent PKA/TGF-β and AMPK downstream pathways in T1DM.

Keywords: AMPK; PKA; TGF-β; aerobic exercise; asprosin; liver; type 1 diabetes.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic diagram of the experimental timeline. CON: control, STZ: streptozotocin, EXE, exercise.
Figure 2
Figure 2
Aerobic exercise training decreased asprosin and PKA levels, but increased AMPK and Akt levels in the liver of type 1 diabetic rats. (A) Representative western blot, (B) Western blot analysis of liver asprosin levels in type 1 diabetic rats, (C) Western blot analysis of PKA levels in type 1 diabetic rats, (D) Western blot analysis of CRBN levels in type 1 diabetic rats, (E) Western blot analysis of AMPK levels in type 1 diabetic rats, (F) Western blot analysis of Akt levels in type 1 diabetic rats. Results are expressed as the mean ± standard error (SE); * p < 0.5, ** p < 0.05, and *** p < 0.001; NS, not significant.
Figure 3
Figure 3
Aerobic exercise training increased PGC-1β levels in the liver of type 1 diabetic rats. (A) Representative western blot. (B) Western blot analysis of liver GLUT-4 levels in type 1 diabetic rats, (C) Western blot analysis of liver PGC-1α levels in type 1 diabetic rats (D) Western blot analysis of liver PGC-1β levels in type 1 diabetic rats (E) Western blot analysis of liver FNDC5 levels in type 1 diabetic rats, (F) Western blot analysis of liver UCP3 levels in type 1 diabetic rats. Results are expressed the mean ± SE. * p < 0.5; NS, not significant.
Figure 4
Figure 4
Aerobic exercise increased MnSOD levels and decreased TGF-β levels in the liver of type 1 diabetic rats. (A) Representative western blot. (B) Western blot analysis of liver MnSOD, (C) Western blot analysis of liver CuZnSOD, (D) Western blot analysis of liver p-38MAPK, (E) Western blot analysis of liver TGF-β. Results are expressed as the mean ± SE. * p < 0.5; NS, not significant.
Figure 5
Figure 5
Schematic diagram of the possible mechanisms activated by asprosin in the liver of type 1 diabetic rat following aerobic exercise training.

References

    1. Debnam E.S., Smith M.W., Sharp P.A., Srai S.K., Turvey A., Keable S.J. The effects of streptozotocin diabetes on sodium-glucose transporter (SGLT1) expression and function in rat jejunal and ileal villus-attached enterocytes. Pflugers Arch. 1995;430:151–159. doi: 10.1007/BF00374645. - DOI - PubMed
    1. Daneman D. Type 1 diabetes. Lancet. 2006;367:847–858. doi: 10.1016/S0140-6736(06)68341-4. - DOI - PubMed
    1. Gerich J.E. Role of the kidney in normal glucose homeostasis and in the hyperglycaemia of diabetes mellitus: Therapeutic implications. Diabet. Med. 2010;27:136–142. - PMC - PubMed
    1. Dey A., Chandrasekaran K. Hyperglycemia induced changes in liver: In vivo and in vitro studies. Curr. Diabetes Rev. 2009;5:67–78. doi: 10.2174/157339909788166864. - DOI - PubMed
    1. Romere C., Duerrschmid C., Bournat J., Constable P., Jain M., Xia F., Saha P.K., Del Solar M., Zhu B., York B., et al. Asprosin, a fasting-induced glucogenic protein hormone. Cell. 2016;165:566–579. doi: 10.1016/j.cell.2016.02.063. - DOI - PMC - PubMed

LinkOut - more resources