Body Mass Index Differences in Pseudohypoparathyroidism Type 1aVersusPseudopseudohypoparathyroidism May Implicate Paternal Imprinting of Gαs in the Development of Human Obesity | Zendy

Dominique Long | Zendy; Sarah McGuire | Zendy; Michael A. Levine | Zendy; Lee S. Weinstein | Zendy; Emily L. GermainLee | Zendy

Open Access

Body Mass Index Differences in Pseudohypoparathyroidism Type 1aVersusPseudopseudohypoparathyroidism May Implicate Paternal Imprinting of Gαs in the Development of Human Obesity

Author(s) -

Dominique Long,

Sarah McGuire,

Michael A. Levine,

Lee S. Weinstein,

Emily L. GermainLee

Publication year - 2006

Publication title -

the journal of clinical endocrinology and metabolism

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.206

H-Index - 353

eISSN - 1945-7197

pISSN - 0021-972X

DOI - 10.1210/jc.2006-1497

Subject(s) - imprinting (psychology) , pseudohypoparathyroidism , body mass index , obesity , endocrinology , medicine , genomic imprinting , biology , physiology , genetics , gene , parathyroid hormone , calcium , gene expression , dna methylation

Obesity is a prominent feature of Albright hereditary osteodystrophy (AHO), a disorder caused by heterozygous GNAS mutations that disrupt the stimulatory G protein alpha-subunit Galpha(s). Because Galpha(s) is paternally imprinted in certain hormone target tissues, maternal inheritance of AHO leads to multihormone resistance [pseudohypoparathyroidism type 1a (PHP1a)], whereas paternal inheritance leads to AHO alone [pseudopseudohypoparathyroidism (pseudoPHP)]. Classically, the obesity in AHO is described as occurring similarly in both conditions.

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