Deletion of codons 88-92 of the melanocortin-4 receptor gene: a novel deleterious mutation in an obese female

J Clin Endocrinol Metab. 2003 Dec;88(12):5841-5. doi: 10.1210/jc.2003-030903.

Abstract

Genetic and pharmacological studies have shown that the melanocortin-4 receptor (MC4R) is an important regulator of food intake and energy homeostasis. Consistent with these studies, several mutations of the MC4R gene have been identified as being associated with early-onset severe obesity. We report here the first in-frame deletion mutation of the MC4R gene (delta88-92) in an obese female patient with onset of obesity at less than 5 yr of age. Functional analysis revealed that the mutant receptor is expressed well on the cell surface but completely devoid of ligand binding and cAMP generation in response to agonist stimulation. We conclude that this novel mutation is the cause of obesity of this patient.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adolescent
  • Adult
  • Amino Acid Sequence / genetics
  • Base Sequence / genetics
  • Binding, Competitive
  • Cell Line
  • Codon / genetics*
  • Cyclic AMP / biosynthesis
  • Female
  • Gene Deletion*
  • Humans
  • Ligands
  • Male
  • Middle Aged
  • Mutation
  • Obesity / genetics*
  • Receptor, Melanocortin, Type 4 / agonists
  • Receptor, Melanocortin, Type 4 / genetics*
  • Receptor, Melanocortin, Type 4 / metabolism

Substances

  • Codon
  • Ligands
  • Receptor, Melanocortin, Type 4
  • Cyclic AMP