饥饿
蛋白质水解
脂解
酮体
自噬
骨骼肌
生物化学
脂肪生成
生物
饥饿反应
分解代谢
内分泌学
蛋白质分解代谢
内科学
化学
脂肪组织
新陈代谢
酶
氨基酸
细胞凋亡
医学
作者
Patrick F. Finn,J. Fred Dice
出处
期刊:Nutrition
[Elsevier]
日期:2006-07-01
卷期号:22 (7-8): 830-844
被引量:281
标识
DOI:10.1016/j.nut.2006.04.008
摘要
Mammals survive starvation by activating proteolysis and lipolysis in many different tissues. These responses are triggered, at least in part, by changing hormonal and neural statuses during starvation. Pathways of proteolysis that are activated during starvation are surprisingly diverse, depending on tissue type and duration of starvation. The ubiquitin-proteasome system is primarily responsible for increased skeletal muscle protein breakdown during starvation. However, in most other tissues, lysosomal pathways of proteolysis are stimulated during fasting. Short-term starvation activates macroautophagy, whereas long-term starvation activates chaperone-mediated autophagy. Lipolysis also increases in response to starvation, and the breakdown of triacylglycerols provides free fatty acids to be used as an energy source by skeletal muscle and other tissues. In addition, glycerol released from triacylglycerols can be converted to glucose by hepatic gluconeogenesis. During long-term starvation, oxidation of free fatty acids by the liver leads to the production of ketone bodies that can be used for energy by skeletal muscle and brain. Tissues that cannot use ketone bodies for energy respond to these small molecules by activating chaperone-mediated autophagy. This is one form of interaction between proteolytic and lipolytic responses to starvation.
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