@article {69782,
	title = {Melanocortin 3 receptor regulates hepatic autophagy and systemic adiposity.},
	journal = {Nat Commun},
	volume = {16},
	year = {2025},
	month = {2025 Feb 16},
	pages = {1690},
	abstract = {<p>Systemic lipid homeostasis requires hepatic autophagy, a major cellular program for intracellular fat recycling. Here, we find melanocortin 3 receptor (MC3R) regulates hepatic autophagy in addition to its previously established CNS role in systemic energy partitioning and puberty. Mice with Mc3r deficiency develop obesity with hepatic triglyceride accumulation and disrupted hepatocellular autophagosome turnover. Mice with partially inactive human MC3R due to obesogenic variants demonstrate similar hepatic autophagic dysfunction. In vitro and in vivo activation of hepatic MC3R upregulates autophagy through LC3II activation, TFEB cytoplasmic-to-nuclear translocation, and subsequent downstream gene activation. MC3R-deficient hepatocytes had blunted autophagosome-lysosome docking and lipid droplet clearance. Finally, the liver-specific rescue of Mc3r was sufficient to restore hepatocellular autophagy, improve hepatocyte mitochondrial function and systemic energy expenditures, reduce adipose tissue lipid accumulation, and partially restore body weight in both male and female mice. We thus report a role for MC3R in regulating hepatic autophagy and systemic adiposity.</p>
},
	keywords = {Adiposity, Animals, Autophagosomes, Autophagy, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Female, Hepatocytes, Humans, Lipid Metabolism, Liver, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Microtubule-Associated Proteins, Obesity, Receptor, Melanocortin, Type 3, Triglycerides},
	issn = {2041-1723},
	doi = {10.1038/s41467-025-56936-1},
	author = {Patel, Tushar P and Jun, Joo Yun and Seo, Arnold Y and Levi, Noah J and Elizondo, Diana M and Chen, Jocelyn and Wong, Adrian M and Tugarinov, Nicol and Altman, Elizabeth K and Gehle, Daniel B and Jung, Sun Min and Patel, Pooja and Ericson, Mark and Haskell-Luevano, Carrie and Demby, Tamar C and Cougnoux, Antony and Wolska, Anna and Yanovski, Jack A}
}
@article {65695,
	title = {Metabolic rate through the life-course: From the organism to the organelle.},
	journal = {Experimental Gerontology},
	volume = {140},
	year = {2020},
	month = {2020 Aug 13},
	pages = {111059},
	issn = {1873-6815},
	doi = {10.1016/j.exger.2020.111059},
	author = {Seo, Arnold Y and Speakman, John R and Selman, Colin}
}
@article {49527,
	title = {MYC induces a hybrid energetics program early in cell reprogramming.},
	journal = {Stem Cell Reports},
	volume = {11},
	year = {2018},
	month = {2018 Dec 11},
	pages = {1479-92},
	abstract = {<p>Cell reprogramming is thought to be associated with a full metabolic switch from an oxidative- to a glycolytic-based metabolism. However, neither the dynamics nor the factors controlling this metabolic switch are fully understood. By using cellular, biochemical, protein array, metabolomic, and respirometry analyses, we found that c-MYC establishes a robust bivalent energetics program early in cell reprogramming. Cells prone to undergo reprogramming exhibit high mitochondrial membrane potential and display a hybrid metabolism. We conclude that MYC proteins orchestrate a rewiring of somatic cell metabolism early in cell reprogramming, whereby somatic cells acquire the phenotypic plasticity necessary for their transition to pluripotency in response to either intrinsic or external cues.</p>
},
	issn = {2213-6711},
	doi = {10.1016/j.stemcr.2018.10.018},
	author = {Prieto, Javier and Seo, Arnold Y and Le{\'o}n, Marian and Santacatterina, Fulvio and Torresano, Laura and Palomino-Sch{\"a}tzlein, Martina and Gim{\'e}nez, Karen and Vallet-S{\'a}nchez, Azahara and Ponsoda, Xavier and Pineda-Lucena, Antonio and Cuezva, Jos{\'e} M and Lippincott-Schwartz, Jennifer and Torres, Josema}
}
