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Nutritional status refers to the physiological condition of an individual resulting from the balance between nutrient intake and the body's requirements, as well as the ability to digest, absorb, and utilize those nutrients [10, 12]. It is not a single molecular entity or receptor but a systemic clinical state monitored and regulated by an intricate network of nutrient sensors [1, 5]. Key molecular players that detect and respond to nutritional status include the mechanistic target of rapamycin (mTOR), which senses amino acids and energy, and AMP-activated protein kinase (AMPK), which serves as a cellular energy gauge [1, 5, 6]. Additionally, G protein-coupled receptors (GPCRs) on the cell surface act as sensors for macronutrients such as free fatty acids and sugars to coordinate metabolic responses [2]. Dysregulation of nutritional status or its sensing pathways is central to the development of metabolic diseases like obesity and Type 2 diabetes, as well as conditions like cancer cachexia and sarcopenia [4, 8, 9]. Therapeutic interventions targeting these states often involve modulating the underlying sensors, such as using rapamycin to inhibit mTOR or metformin to activate AMPK [5, 6].
Modulation of nutrient-sensing signaling pathways (e.g., mTOR, AMPK) and metabolic homeostasis
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