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.
Highlights
Diabetes mellitus, a global epidemic disease, is the most common metabolic disorder caused by the impairment of insulin secretion and glucose metabolism [1]
Asprosin has been identified as a novel hormone which is cleaved from the C-terminal end of profibrillin, released from white adipose tissue [5]
To determine whether aerobic exercise training influences hepatic asprosin and protein kinase A (PKA) levels, the rats were made to run on a treadmill 60 min/day, 4 days/week, for 8 weeks
Summary
A global epidemic disease, is the most common metabolic disorder caused by the impairment of insulin secretion and glucose metabolism [1]. Type 1 diabetes mellitus (T1DM) is characterized by a deficiency in insulin secretion from β-cells, resulting in hyperglycemia and impaired glucose metabolism [2]. The role of the cAMP/PKA signaling pathway in the liver of streptozotocin (STZ)-induced diabetic models remains unclear. Increased asprosin levels in the liver promote cAMP and PKA signaling pathways, which results in acceleration of glucose release in the circulation. The activation of the cAMP/PKA signaling pathways negatively regulates glucose production through AMP-activated protein kinase (AMPK) inactivation in humans and animals [9,10]. Our previous study has shown that aerobic exercise training activates AMPK by increasing peroxide proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), fibronectin type III domain-containing protein 5 (FNDC5), and uncoupling proteins (UCPs), suggesting that these AMPK signaling pathways improve insulin resistance and glucose intolerance in STZ-induced T1DM rats [12]. The signaling pathway downstream of asprosin in the liver of T1DM rats during aerobic exercise training remains to be elucidated
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