TABLE 1.

Molecular pathway deletion or inhibition in the neuronal subgroups and the outcomes.

Neuronal target	Deletion or inhibition of neuronal molecular pathways	Species	Outcome	References
AgRP	AMPK	Mice AMPKα2KO	Eutrophic phenotype, light level of glucose intolerance	(55)
	mTOR	Mice lacking Rictor in AgRP	mTORC2 did not change energy homeostasis	(53)
	Autophagic pathway	Atg7F/F-AgRP-Cre mice	Better food intake control and eutrophic phenotype	(61)
POMC	AMPK	Mice AMPK α2KO	Hyperphagia, obesity, hyperglycemia	(55)
	mTOR	Mice lacking Rictor in POMC and C57BL/6JPOMC-rptor-KO	Rictor/mTORC2: decreased energy expenditure and induced obese phenotype, did not induce leptin resistance mTORC1: limited ROS capacity to inhibit food intake	(53, 75)
	Autophagic pathway	Atg7F/F-POMC-Cre mice	Limited lipolysis capacity and obese phenotype	(60)
NPY/AgRP and POMC simultaneously	AMPK	In vitro and in vivo (male C57BL/6)	Dysregulation of autophagic pathway and reduction in body weight	(59)
	mTOR	Mice lacking Rictor in all neurons	Increased adiposity, glucose intolerance, leptin resistance	(53)
	Autophagic pathway	Mediobasal hypothalamus Atg7 KD mice	Hyperphagia, reduced energy expenditure, and hypothalamic inflammation	(77)

AMP-dependent protein kinase (AMPK), Rapamycin target protein (mTOR), Reactive oxygen species (ROS).