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Published on: May 14, 2018
Aged PROP1 deficient dwarf mice maintain ACTH production
Igor O Nasonkin1, Robert D Ward, David L Bavers
1Department of Human Genetics, University of Michigan, Ann Arbor, Michigan, United States of America.
Plos One
|December 7, 2011
Summary
Prophetin (PROP1) mutations cause multiple pituitary hormone deficiencies in humans. Mouse models show elevated pituitary-adrenal axis hormones, unlike human patients with progressive hormone loss.
Area of Science:
- Endocrinology
- Genetics
- Developmental Biology
Background:
- PROP1 mutations lead to multiple pituitary hormone deficiencies (MPHD) in humans, affecting growth and other anterior pituitary hormones.
- The Prop1 mouse models (Prop1(-/-) and Prop1(df/df)) exhibit congenital deficiencies in growth hormone (GH), prolactin, and thyroid-stimulating hormone.
- Corticotroph and pituitary adrenal axis function in Prop1 mouse models remain incompletely understood.
Purpose of the Study:
- To investigate the pituitary-adrenal axis function in Prop1-deficient mice.
- To characterize the phenotype associated with PROP1 mutations in the C57BL6 mouse background.
Main Methods:
- Phenotypic analysis of Prop1(-/-) mice on a C57BL6 background.
- Measurement of circulating adrenocorticotropic hormone (ACTH) and corticosterone levels.
- Assessment of pituitary-adrenal axis response to restraint stress.
Main Results:
- Prop1(-/-) mice on C57BL6 background exhibit a wasting phenotype and premature death, associated with severe hypoglycemia.
- Elevated circulating ACTH and corticosterone levels were observed in juvenile and aged Prop1 mutants.
- Prop1-deficient mice maintained the ability to elevate ACTH and corticosterone in response to stress.
Conclusions:
- The Prop1 mouse model displays distinct pituitary-adrenal axis characteristics compared to human PROP1 mutation patients.
- Hypoglycemia in Prop1-deficient mice likely contributes to elevated corticosterone levels.
- The C57BL6 background exacerbates the phenotype, leading to a wasting syndrome in Prop1 mutants.
