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Nutrient signaling pathways are integrated networks of biochemical cascades that allow cells to sense and adapt to changes in the availability of energy and macronutrients like glucose, amino acids, and lipids (Efeyan et al., 2015, Nature). These pathways include key molecular sensors such as the mechanistic target of rapamycin (mTOR), which promotes anabolic processes during nutrient abundance, and AMP-activated protein kinase (AMPK), which triggers catabolic energy-producing processes during scarcity (Saxton & Sabatini, 2017, Cell; Hardie et al., 2012, Nat Rev Mol Cell Biol). Other critical components include sirtuins and the insulin/IGF-1 signaling axis, which coordinate cellular metabolism with systemic energy status (Imai & Guarente, 2014, Trends Cell Biol). Dysregulation of these pathways is a central driver in the development of metabolic syndrome, type 2 diabetes, obesity, and various cancers where nutrient sensing is hijacked to support uncontrolled proliferation (González & Hall, 2017, EMBO Mol Med). Therapeutic strategies often involve small molecules that modulate specific nodes within these pathways, such as metformin for AMPK activation or rapalogs for mTOR inhibition, to restore metabolic balance or suppress tumor growth. However, targeting these fundamental pathways presents challenges due to their ubiquitous role in normal physiology, potentially leading to side effects like immunosuppression or metabolic instability.
Modulation of intracellular metabolic sensors (e.g., AMPK activation, mTOR inhibition) and hormonal receptors (e.g., Insulin receptor) to regulate energy homeostasis and cellular growth.
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