title: Akt activation protects liver cells from apoptosis in rats during acute cold exposure.
abstract: Accidental deaths due to exposure to extremely low natural temperature happen every winter. Exposure to extreme cold causes injury of multiple organs. However, early responses of the bodies to acute extreme cold exposure remain incompletely understood. In this study, we found that hepatic glycogen was rapidly reduced in rats exposed to -15°C, and the key enzymes required for glycogenesis were upregulated in the livers of the cold-exposed rats. In line with the rapid consumption of glycogen, acute cold exposure induced a transient elevation of cellular ATP level, which lasted about one hour. The ATP level went back to basal level after two hours of cold exposure. Four hours of cold exposure resulted in cellular ATP depletion and cell apoptosis. The dynamic change of cellular ATP levels was well associated with Akt activation in cold-exposed liver cells. The activation of Akt was required for cold exposure-induced ATP elevation. Blockade of Akt activation diminished the transient increase of intracellular ATP content and exacerbated cell apoptosis during acute cold exposure. These results suggest that Akt activation plays a pivotal role in maintaining cellular bioenergy balance and promoting liver cell survival during acute cold exposure.
authors.affiliation: Department of Occupational and Environmental Health, Faculty of Military Preventive Medicine, Fourth Military Medical University, 169 Changle West Road, Xi'an, Shaanxi 710032, China.
authors.forename: Jiye
authors.initials: J
authors.lastname: Wang
authors.forename: Yaoming
authors.initials: Y
authors.lastname: Chen
authors.forename: Wenbin
authors.initials: W
authors.lastname: Zhang
authors.forename: Gang
authors.initials: G
authors.lastname: Zheng
authors.forename: Shanshan
authors.initials: S
authors.lastname: Meng
authors.forename: Honglei
authors.initials: H
authors.lastname: Che
authors.forename: Tao
authors.initials: T
authors.lastname: Ke
authors.forename: Jingrun
authors.initials: J
authors.lastname: Yang
authors.forename: Jingyuan
authors.initials: J
authors.lastname: Chen
authors.forename: Wenjing
authors.initials: W
authors.lastname: Luo
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000730:Androstadienes / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D015153:Blotting, Western; D003080:Cold Temperature; D017931:DNA Primers / Q000235:genetics; D004734:Energy Metabolism / Q000502:physiology*; D004789:Enzyme Activation / Q000502:physiology; D006003:Glycogen / Q000378:metabolism; D020287:In Situ Nick-End Labeling; D007274:Injections, Intraperitoneal; D008099:Liver / Q000166:cytology* / Q000378:metabolism*; D008297:Male; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013312:Stress, Physiological / Q000502:physiology*; D000077191:Wortmannin
chemical_list: D000730:Androstadienes; D017931:DNA Primers; D000081082:Phosphoinositide-3 Kinase Inhibitors; D000255:Adenosine Triphosphate; D006003:Glycogen; D051057:Proto-Oncogene Proteins c-akt; D000077191:Wortmannin
keywords: ATP; Akt.; Apoptosis; Cold exposure; Liver; Rat