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Expression of a hypomorphic Pomc allele alters leptin dynamics during late
Authors Yu H, Thompson Z, Kiran S, Jones GL, Mundada L, Rubinstein M, Low MJ
Submitted By Submitted Externally on 3/31/2020
Status Published
Journal The Journal of endocrinology
Year 2020
Date Published 4/1/2020
Volume : Pages 245 : 115 - 127
PubMed Reference 32027603
Abstract Proopiomelanocortin (POMC) neurons in the hypothalamic arcuate nucleus (ARC) are
essential for normal energy homeostasis. Maximal ARC Pomc transcription is
dependent on neuronal Pomc enhancer 1 (nPE1), located 12 kb upstream from the
promoter. Selective deletion of nPE1 in mice decreases ARC Pomc expression by
70%, sufficient to induce mild obesity. Because nPE1 is located exclusively in
the genomes of placental mammals, we questioned whether its hypomorphic mutation
would also alter placental Pomc expression and the metabolic adaptations
associated with pregnancy and lactation. We assessed placental development, pup
growth, circulating leptin and expression of Pomc, Agrp and alternatively
spliced leptin receptor (LepR) isoforms in the ARC and placenta of Pomc?1/?1 and
Pomc+/+ dams. Despite indistinguishable body weights, lean mass, food intake,
placental histology and Pomc expression and overall pregnancy outcomes between
the genotypes, Pomc ?1/?1 females had increased pre-pregnancy fat mass that
paradoxically decreased to control levels by parturition. However, Pomc?1/?1
dams had exaggerated increases in circulating leptin, up to twice of that of the
typically elevated levels in Pomc+/+ mice at the end of pregnancy, despite their
equivalent fat mass. Pomc?1/?1dams also had increased placental expression of
soluble leptin receptor (LepRe), although the protein levels of LEPRE in
circulation were the same as Pomc+/+ controls. Together, these data suggest that
the hypomorphic Pomc?1/?1 allele is responsible for the perinatal super
hyperleptinemia of Pomc?1/?1 dams, possibly due to upregulated leptin secretion
from individual adipocytes.


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