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Objective By stimulating intermittent cold exposure to mice for a long term, to investigate the effect of cold exposure on amelioration of glucose homeostasis and prevention of glucose homeostasis disorder induced by high-fat diet (HFD), and analyze the regulative effect of adipose tissue in the process. Methods A total of 24 male C57 BL/6J male mice (8 weeks old) were equally divided into 4 groups, that is, control group (normal diet+room temperature), cold exposure group (normal diet+4 ℃, 2 h/d), HFD group (HFD feeding+room temperature), and HFD and cold exposure group. Intraperitoneal glucose tolerance test (IPGTT) and insulin tolerance test (IPITT) were carried out in 1, 8, 16 and 22 weeks after intervention. In 22 weeks after intervention, scapular brown adipose tissue (BAT) and inguinal white adipose tissue (WATi) were collected for transcriptome profiling analysis. Results When having no effect on the bodyweight, intermittent cold exposure for 22 weeks significantly reduced the weight of WATi (0.221±0.016 vs 0.338±0.024 g, P < 0.05), but increased the weight of BAT (0.095±0.005 vs 0.079±0.003 g, P < 0.05) when compared with the control group, and elevated glucose tolerance by 25.9% (P < 0.01) and enhanced insulin sensitivity by 50.4% (P < 0.01). The amelioration of glucose homeostasis was positively correlated with the length of cold exposure. However, in the mice with HFD feeding, the cold exposure inhibited the increase of bodyweight (43.3±1.8 vs 32.9±0.7 g, P < 0.01) and WATi (1.186±0.215 vs 0.434±0.059 g, P < 0.05), and improved insufficient glucose tolerance by 25.5% (P < 0.01) and insulin resistance by 33.9% (P < 0.01) when compared to the mice of HFD and cold exposure group. Transcriptome profiling analysis showed that long-term intermittent cold exposure obviously activated the glycolysis in the brown fat and white fat tissues, and the PI3K-Akt and insulin signaling pathways (P < 0.01), but HFD reversed the activation of glycolysis-related pathways in white fat tissues. Conclusion Long-term intermittent cold exposure may promote glucose homeostasis and prevent glucose homeostasis disorder induced by HFD via activating glycolysis, PI3K-Akt and insulin signaling pathways in adipose tissue.

PTEN-induced putative kinase 1 (PINK1), a Parkinson's disease (PD)-related protein, has two isoforms, the mitochondria-localized full-length isoform PINK1FL and the cytoplasm-localized short isoform PINK1-cyto. Studies have suggested that PINK1FL can selectively accumulate at the surface of damaged mitochondria and cooperate with another Parkinson's Disease-related protein PARKIN to trigger the degradation of MIRO1, a mitochondria trafficking regulator. The functions of PINK1-cyto are, however, not yet clear. To investigate the functions of PINK1-cyto, we expressed different proteins in cultured HEK293 cells by transfecting it with different plasmids, and detected the protein levels by Western blot after expressing for 24 h. We found that in cultured HEK293 cells, PINK1-cyto could also cooperate with PARKIN degrade MIRO1 in the presence of CK23, and the regulatory subunit of Casein Kinase II. Interestingly, this function of CK2P was not dependent on CK2alpha, the catalytic subunit of Casein Kinase II. We also found that CK2P could promote the direct interaction between PINK1-cyto and MIRO1 by immunocoprecipitation analysis. This result suggested that in addition to CK2alpha, CK2beta could also form a kinase complex.