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Lipid stress inhibits endocytosis of melanocortin-4 receptor from modified clathrin-enriched sites and impairs receptor desensitization.
Cooney, Kimberly A; Molden, Brent M; Kowalczyk, Nicholas S; Russell, Susan; Baldini, Giulia.
Afiliación
  • Cooney KA; From the Department of Biochemistry and Molecular Biology University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205-7199.
  • Molden BM; From the Department of Biochemistry and Molecular Biology University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205-7199.
  • Kowalczyk NS; From the Department of Biochemistry and Molecular Biology University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205-7199.
  • Russell S; From the Department of Biochemistry and Molecular Biology University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205-7199.
  • Baldini G; From the Department of Biochemistry and Molecular Biology University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205-7199 gbaldini@uams.edu.
J Biol Chem ; 292(43): 17731-17745, 2017 10 27.
Article en En | MEDLINE | ID: mdl-28878020
Melanocortin-4 receptor (MC4R) is a G-protein-coupled receptor expressed in the brain's hypothalamus where it regulates energy homeostasis. MC4R agonists function to lower food intake and weight. In this respect, although obesity promotes hyperlipidemia and hypothalamic injury, MC4R agonists are nevertheless more effective to reduce food intake within hours of administration in overweight, rather than lean, mice. MC4R undergoes constitutive internalization and recycling to the plasma membrane with agonist binding inducing receptor retention along the intracellular route and, under prolonged exposure, desensitization. Here, we found that, in neuronal cells, lipid stress by exposure to elevated palmitate leaves unchanged the rate by which MC4R and transferrin receptor are constitutively excluded from the cell surface. However, lipid stress disrupted later steps of MC4R and transferrin receptor internalization to endosomes as well as traffic of agonist-occupied MC4R to lysosomes and MC4R desensitization. In the lipid-stressed cells, MC4R and clathrin were redistributed to the plasma membrane where they colocalized to sites that appeared by super-resolution microscopy to be modified and to have higher clathrin content than those of cells not exposed to elevated palmitate. The data suggest that lipid stress disrupts steps of endocytosis following MC4R localization to clathrin-coated sites and exclusion of the receptor from the extracellular medium. We conclude that increased effectiveness of MC4R agonists in obesity may be an unexpected outcome of neuronal injury with disrupted clathrin-dependent endocytosis and impaired receptor desensitization.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Membrana Celular / Clatrina / Receptor de Melanocortina Tipo 4 / Endocitosis / Hiperlipidemias / Obesidad Límite: Animals Idioma: En Revista: J Biol Chem Año: 2017 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Membrana Celular / Clatrina / Receptor de Melanocortina Tipo 4 / Endocitosis / Hiperlipidemias / Obesidad Límite: Animals Idioma: En Revista: J Biol Chem Año: 2017 Tipo del documento: Article Pais de publicación: Estados Unidos