Torpor is a crucial adaptive strategy employed by mammals to cope with low-temperature environments and/or seasonal food shortages. Investigating the torpor behavior of animals not only helps to elucidate their ecological adaptation mechanisms under conditions of food scarcity and harsh environments but also provides potential scientific insights for exploring organ transplantation, delaying aging, and extending lifespan. In this study, we established a torpor model using C57BL mice subjected to fasting and water deprivation at environmental temperatures of 22℃, 17℃, and 12℃. Through a combination of ultrastructural histology, proteomics, molecular biology, network analysis, and bioinformatics, we systematically analyzed the changes in protein expression and phosphorylation modification regulation in the kidney, liver, heart, and brown adipose tissue (BAT) of torpid mice. Notably, proteins such as phosphoenolpyruvate carboxykinase (PCK), tyrosine aminotransferase (TAT), and microtubule-associated protein 2 (MAP2) play significant roles during the torpor state in mice. These findings lay a crucial foundation for a deeper understanding of the molecular regulatory mechanisms underlying mammalian torpor and their tolerance strategies in adverse environments.