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While GHSR1a constitutive activity is required for amplification of MC3R signaling, it has minimal effect on GHSR1a-MC3R dimer internalization, as treatment with the GHSR1a inverse agonist SP-analog only results in a small, nonsignificant reduction in internalization (Schellekens et al., 2013)

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Many years ago, it was postulated that a retention of phosphate in the extracellular space due to the decrease in glomerular filtration rate and the accompanying reduction in plasma ionized calcium concentration was the primary event in the pathogenesis of secondary hyperparathyroidism