The article discusses the mechanisms and pathways involved in nutrient sensing, which are crucial for maintaining cellular and organismal homeostasis. Nutrient sensing involves detecting intracellular and extracellular levels of sugars, amino acids, and lipids, and integrating these signals at the organismal level through hormonal responses. During periods of food abundance, nutrient sensing pathways promote anabolism and storage, while scarcity triggers homeostatic mechanisms such as autophagy. Nutrient sensing pathways are often deregulated in human metabolic diseases. The article covers lipid sensing, including the detection of fatty acids by G-protein coupled receptors (GPR40 and GPR120) and the role of the FAT/CD36 receptor in intestinal lipid uptake. Cholesterol sensing is discussed, focusing on the SCAP/SREBP pathway and the HMG-CoA reductase regulatory loop. For amino acid sensing, the article highlights the role of GCN2 in detecting uncharged tRNAs and inhibiting translation initiation, and the activation of mTORC1 by amino acids, particularly leucine. The involvement of taste receptors in sensing extracellular amino acids and glucose is also explored. Finally, the article discusses autophagy as a mechanism for accessing internal nutrient stores during nutrient scarcity, emphasizing the role of AMPK and mTORC1 in regulating autophagy initiation and termination. The importance of autophagy in various physiological processes and its disruption in diseases such as diabetes and neurodegeneration is highlighted.The article discusses the mechanisms and pathways involved in nutrient sensing, which are crucial for maintaining cellular and organismal homeostasis. Nutrient sensing involves detecting intracellular and extracellular levels of sugars, amino acids, and lipids, and integrating these signals at the organismal level through hormonal responses. During periods of food abundance, nutrient sensing pathways promote anabolism and storage, while scarcity triggers homeostatic mechanisms such as autophagy. Nutrient sensing pathways are often deregulated in human metabolic diseases. The article covers lipid sensing, including the detection of fatty acids by G-protein coupled receptors (GPR40 and GPR120) and the role of the FAT/CD36 receptor in intestinal lipid uptake. Cholesterol sensing is discussed, focusing on the SCAP/SREBP pathway and the HMG-CoA reductase regulatory loop. For amino acid sensing, the article highlights the role of GCN2 in detecting uncharged tRNAs and inhibiting translation initiation, and the activation of mTORC1 by amino acids, particularly leucine. The involvement of taste receptors in sensing extracellular amino acids and glucose is also explored. Finally, the article discusses autophagy as a mechanism for accessing internal nutrient stores during nutrient scarcity, emphasizing the role of AMPK and mTORC1 in regulating autophagy initiation and termination. The importance of autophagy in various physiological processes and its disruption in diseases such as diabetes and neurodegeneration is highlighted.