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Aerobic Exercise Training Decreases Hepatic Asprosin in Diabetic Rats.

Jeong Rim Ko1, Dae Yun Seo2, Tae Nyun Kim3

  • 1National Research Laboratory for Mitochondrial Signaling, Department of Physiology, BK21 Plus Project Team, College of Medicine, Cardiovascular and Metabolic Disease Center, Inje University, Busan 47392, Korea. kjrsos0217@gmail.com.

Journal of Clinical Medicine
|May 15, 2019
PubMed
Summary
This summary is machine-generated.

Aerobic exercise training reduced asprosin levels in type 1 diabetes mellitus (T1DM) rats. This reduction impacts key signaling pathways, suggesting exercise benefits hepatic glucose metabolism in T1DM.

Keywords:
AMPKPKATGF-βaerobic exerciseasprosinlivertype 1 diabetes

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Area of Science:

  • Endocrinology
  • Metabolic Research
  • Exercise Physiology

Background:

  • Asprosin, a hormone from white adipose tissue, influences hepatic glucose metabolism and is elevated in insulin resistance.
  • The effect of aerobic exercise on asprosin in type 1 diabetes mellitus (T1DM) remains uninvestigated.

Purpose of the Study:

  • To investigate if aerobic exercise training decreases hepatic asprosin levels in streptozotocin (STZ)-induced diabetic rats.
  • To determine if reduced asprosin levels modulate asprosin-dependent downstream signaling pathways.

Main Methods:

  • Male Sprague-Dawley rats were divided into control, STZ-induced diabetes, and STZ with aerobic exercise groups.
  • T1DM was induced using streptozotocin (STZ).
  • The exercise group underwent 8 weeks of treadmill training (60 min/day, 4 days/week).

Main Results:

  • Aerobic exercise training significantly reduced protein levels of asprosin, PKA, and TGF-β in diabetic rats.
  • Exercise training increased the protein levels of AMPK, Akt, PGC-1β, and MnSOD.
  • These changes indicate modulation of hepatic asprosin-dependent pathways.

Conclusions:

  • Aerobic exercise training effectively lowers hepatic asprosin levels in a T1DM rat model.
  • Exercise influences key signaling cascades, including PKA/TGF-β and AMPK pathways, suggesting a mechanism for improved glucose metabolism.