Nutrient excess

Nutrient excess, often termed overnutrition or metabolic overload, is a physiological and pathological state characterized by a chronic surplus of energy intake relative to energy expenditure. This condition leads to the sustained over-activation of nutrient-sensing pathways, most notably the mechanistic target of rapamycin complex 1 (mTORC1), and the concomitant suppression of energy-sensing catabolic pathways, such as those governed by AMP-activated protein kinase (AMPK) [1, 2]. At the cellular level, persistent nutrient excess causes mitochondrial dysfunction, endoplasmic reticulum stress, and the accumulation of toxic lipid intermediates like diacylglycerols and ceramides, which collectively impair insulin signaling [1, 3, 7]. Clinically, it serves as the fundamental driver of the global metabolic disease epidemic, encompassing obesity, type 2 diabetes mellitus, and non-alcoholic fatty liver disease (NAFLD) [10]. While 'nutrient excess' is not a single molecular target, therapeutic interventions for its associated diseases typically involve pharmacological agents that mimic a low-energy state, modulate nutrient-sensing nodes, or enhance insulin sensitivity [5, 7, 8].

Other names

OvernutritionMetabolic overloadNutrient surplusExcess caloric intakeHyperalimentation

Activation of catabolic regulators (e.g., AMPK activation) or inhibition of anabolic drivers (e.g., mTORC1 inhibition) to mitigate the systemic effects of chronic over-nutrition.