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AMP-activated protein kinase (AMPK) is a key enzyme in the regulation of cellular energy homeostasis. Recent studies demonstrated that AMPK also plays an important role in the modulation of inflammation, an energy-intensive molecular response. The commonly used AMPK activators include 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) and A-769662. In addition, the biological activities of metformin and adiponectin are closely related to activation of AMPK. Numerous studies have shown that these AMPK activators play an effectively protective role in animal models of acute lung injury, asthma, colitis, hepatitis, atherosclerosis and other inflammatory diseases. Therefore, AMPK activators may have promising potential for the prevention and treatment of inflammation related diseases.

Hypoxic exposure activates hypoxia inducible factors (HIFs) to up-regulate the expression of its target genes. These genes encode glucose metabolism related proteins, such as glucose transporters (GLUTs) and glycolysis related enzymes, including lactate dehydrogenase A (LDHA) and aldolase A (ALDA). Therefore, HIFs participate in oxygenolysis of glucose and play an important role in mediating hypoxia response and weight loss. Exercise training influences fatty acid metabolism, insulin sensitivity and body energy balance through activating peroxisome proliferator-activated receptors (PPARs), which plays an active role in losing weight. In addition, hypoxic exposure or exercise training can activate energy sensor 5'-AMP activated protein kinase (AMPK) in cells and promote oxidation of glucose and fatty acid and weight loss. It has been shown that hypoxic training exerts a better effects on controlling weight, compared with either hypoxic exposure or exercise training alone. This paper reviewed synergistic interactions among HIFs, PPARs and AMPK under hypoxic training and proposed possible mechanisms of hypoxic training-induced weight loss via AMPK-HIFs axis or AMPK-PPARs axis, thus providing theoretical guidance for application of hypoxic training in weight control.

Objective: To observe the effect of high-mobility group box 1 (HMGB1) on autophagy and chemotherapy resistance in human leukemiacell line (K562) cells, and to explore the underlying mechanisms.
 Methods: The K562 cells were cultured in vitro and divided into 6 groups: a chemotherapeutic group, a chemotherapeutic control group, a HMGB1 preconditioning group, a HMGB1 preconditioning control group, a HMGB1 siRNA group and a siRNA control group. The chemotherapeutic group was further divided into a vincristine (VCR) group, an etoposide (VP-16) group, a cytosine arabinoside (Ara-C) group, a adriamycin (ADM) group and a arsenic trioxide (As2O3) group. The cell activity was evaluated by cell counting kit-8. The protein levels of HMGB1, microtubule-associate protein1light chain3 (LC3), AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (m-TOR) were determined by Western blotting. The level of serum HMGB1 was evaluated by enzyme-linked immunosorbent assay (ELISA). The autophagy was examined by monodansylcadaverine staining and observed under transmission electron microscopy.
 Results: Compared with the control group, the cell activity was significantly decreased and the level of serum HMGB1 was significantly increased in the chemotherapeutic (VCR, VP-16, Ara-C, ADM and As2O3) groups (all P<0.05). Compared with the control group, the cell activity and the level of serum HMGB1 were significantly increased in the HMGB1 preconditioning group (both P<0.05). Compared with the siRNA control group, the cell activity and the level of serum HMGB1 were significantly decreased in the HMGB1 siRNA group (both P<0.05). Compared with the control group, the expression of LC3-II and the formation of autophagic bodies were increased in the HMGB1 preconditioning group (both P<0.05), the p-AMPK expression was increased and p-mTOR expression was decreased (both P<0.05).
 Conclusion: HMGB1 can increase the autophagy and promote chemotherapy resistance through the pathway of AMPK/m-TOR in K562 cells.

The AMP-activated protein kinase (AMPK) widely exists in skeletal muscle, liver, pancreas, adipose tissue and central nervous system. As a "cellular energy regulator", activation of AMPK can improve insulin resistance in various mechanisms. To overall understand the importance of AMPK in exercise, the article summarized the research progress on AMPK exercise activation in skeletal muscle, liver and adipose tissue as well as exercise improving cardiovascular insulin resistance by AMPK, and looked forward to the study future of AMPK exercise activation.