Abstract
The main danger of cold stress to animals in cold regions is systemic metabolic changes and protein synthesis inhibition. Cold-induced RNA-binding protein is a cold shock protein that is rapidly up-regulated under cold stimulation in contrast to the inhibition of most proteins and participates in multiple cellular physiological activities by regulating targets. Therefore, this study was carried out to investigate the possible mechanism of CIRP-mediated glucose metabolism regulation and survival promotion in skeletal muscle after acute cold exposure. Skeletal muscle and serum from mice were obtained after 0, 2, 4 and 8 h of acute hypothermia exposure. Subsequently, the changes of CIRP, metabolism and apoptosis were examined. Acute cold exposure increased energy consumption, enhanced glycolysis, increased apoptosis, and up-regulated CIRP and phosphorylation of AKT. In addition, CIRP overexpression in C2C12 mouse myoblasts at each time point under 37°C and 32°C mild hypothermia increased AKT phosphorylation, enhanced glucose metabolism, and reduced apoptosis. CIRP knockdown by siRNA interference significantly reduced the AKT phosphorylation of C2C12 cells. Wortmannin inhibited the AKT phosphorylation of skeletal muscle after acute cold exposure, thereby inhibiting glucose metabolism and aggravating apoptosis. Taken together, acute cold exposure up-regulates CIRP in mouse skeletal muscle, which regulates glucose metabolism and maintains energy balance in skeletal muscle cells through the AKT signaling pathway, thus slowing down the apoptosis of skeletal muscle cells.
Highlights
A low-temperature environment is a common and unavoidable stressor for humans and livestock in cold regions
We examined the AKT/ GSK3β/GS pathway, as the above results indicated that skeletal muscle demonstrates an increased need for skeletal muscle glycogen synthesis during acute cold exposure
We found that the phosphorylation of PFKFB2 at Ser483 was enhanced after acute cold exposure, which indicated that the glycolytic activity in skeletal muscle of mice was enhanced after acute cold exposure
Summary
A low-temperature environment is a common and unavoidable stressor for humans and livestock in cold regions. Such environments affect neuroendocrine, immune, reproductive, and cardiovascular systems, and cause oxidative stress and apoptosis (Solianik et al, 2014; Cong et al, 2018; Lian et al, 2018). Acute cold exposure cause metabolic disorders, such as increased systemic energy expenditure and increased energy utilization in peripheral tissues (Hao et al, 2015; Yao et al, 2018). Skeletal muscle plays an essential role in the thermogenic metabolic induced by cold. Cytoprotection of CIRP Under Cold Stress exposure due to its ability to produce shivering and non-shivering thermogenesis (Haman, 2006; Brychta and Chen, 2017). Glucose conversion is mostly mediated by skeletal muscle metabolic activation during cold exposure (Blondin et al, 2015), and the maintenance of glucose under cold exposure is of great significance for animal survival (Shibata et al, 1989; Labbé et al, 2015)
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