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Loss of PI3K p110α in the Adipose Tissue Results in Infertility and Delayed Puberty Onset in Male Mice.

Abstract Deletion of PI3K catalytic subunit p110α in adipose tissue (aP2-Cre/p110α(flx/flx), α-/- hereafter) results in increased adiposity, glucose intolerance, and liver steatosis. Because this endocrine organ releases hormones like leptin, which are important in reproductive physiology, we investigated the reproductive phenotype of α-/- males. Compared to controls, α-/- males displayed delayed onset of puberty accompanied by a reduction in plasma LH levels and testicular weight. At postnatal day 30, α-/- mice exhibited normal body weight but elevated fasted plasma leptin levels. Testicular leptin gene expression was increased, whereas expression of the cholesterol transporter StAR and of P450 cholesterol side chain cleavage enzyme was decreased. Adult α-/- males were infertile and exhibited hyperandrogenemia with normal basal LH, FSH, and estradiol levels. However, neither sperm counts nor sperm motility was different between genotypes. The mRNA levels of leptin and of 17-beta-dehydrogenase 3, and enzyme important for testosterone production, were significantly higher in the testis of adult α-/- males. The mRNA levels of ERα, an important regulator of intratesticular steroidogenesis, were lower in the testis of adult and peripubertal α-/- males. We propose that chronic hyperleptinemia contributes to the negative impact that disrupting PI3K signaling in adipocytes has on puberty onset, steroidogenesis, and fertility in males.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title biomed research international
Publication Year Start




PMID- 28357399
OWN - NLM
STAT- MEDLINE
DA  - 20170330
DCOM- 20170418
LR  - 20170418
IS  - 2314-6141 (Electronic)
VI  - 2017
DP  - 2017
TI  - Loss of PI3K p110alpha in the Adipose Tissue Results in Infertility and Delayed
      Puberty Onset in Male Mice.
PG  - 3756089
LID - 10.1155/2017/3756089 [doi]
AB  - Deletion of PI3K catalytic subunit p110alpha in adipose tissue
      (aP2-Cre/p110alphaflx/flx, alpha-/- hereafter) results in increased adiposity,
      glucose intolerance, and liver steatosis. Because this endocrine organ releases
      hormones like leptin, which are important in reproductive physiology, we
      investigated the reproductive phenotype of alpha-/- males. Compared to controls, 
      alpha-/- males displayed delayed onset of puberty accompanied by a reduction in
      plasma LH levels and testicular weight. At postnatal day 30, alpha-/- mice
      exhibited normal body weight but elevated fasted plasma leptin levels. Testicular
      leptin gene expression was increased, whereas expression of the cholesterol
      transporter StAR and of P450 cholesterol side chain cleavage enzyme was
      decreased. Adult alpha-/- males were infertile and exhibited hyperandrogenemia
      with normal basal LH, FSH, and estradiol levels. However, neither sperm counts
      nor sperm motility was different between genotypes. The mRNA levels of leptin and
      of 17-beta-dehydrogenase 3, and enzyme important for testosterone production,
      were significantly higher in the testis of adult alpha-/- males. The mRNA levels 
      of ERalpha, an important regulator of intratesticular steroidogenesis, were lower
      in the testis of adult and peripubertal alpha-/- males. We propose that chronic
      hyperleptinemia contributes to the negative impact that disrupting PI3K signaling
      in adipocytes has on puberty onset, steroidogenesis, and fertility in males.
FAU - Nelson, Victoria L Boughton
AU  - Nelson VL
AD  - Department of Physiology and Biophysics, Stony Brook University Medical Center,
      Stony Brook, NY, USA.
FAU - Negron, Ariel L
AU  - Negron AL
AD  - Department of Physiology and Biophysics, Stony Brook University Medical Center,
      Stony Brook, NY, USA; Graduate Program in Neuroscience, State University of New
      York at Stony Brook, Stony Brook, NY, USA.
FAU - Reid, Inefta
AU  - Reid I
AD  - Department of Physiology and Biophysics, Stony Brook University Medical Center,
      Stony Brook, NY, USA.
FAU - Thomas, Justin A
AU  - Thomas JA
AD  - Department of Physiology and Biophysics, Stony Brook University Medical Center,
      Stony Brook, NY, USA.
FAU - Yang, Leon
AU  - Yang L
AD  - Department of Physiology and Biophysics, Stony Brook University Medical Center,
      Stony Brook, NY, USA.
FAU - Lin, Richard Z
AU  - Lin RZ
AD  - Department of Physiology and Biophysics, Stony Brook University Medical Center,
      Stony Brook, NY, USA; Department of Veterans Affairs Medical Center, Northport,
      NY, USA.
FAU - Acosta-Martinez, Maricedes
AU  - Acosta-Martinez M
AUID- ORCID: 0000-0003-0841-4032
AD  - Department of Physiology and Biophysics, Stony Brook University Medical Center,
      Stony Brook, NY, USA.
LA  - eng
PT  - Journal Article
DEP - 20170305
PL  - United States
TA  - Biomed Res Int
JT  - BioMed research international
JID - 101600173
RN  - 0 (Leptin)
RN  - 3XMK78S47O (Testosterone)
RN  - 9002-67-9 (Luteinizing Hormone)
RN  - 9002-68-0 (Follicle Stimulating Hormone)
RN  - EC 1.1.- (17-Hydroxysteroid Dehydrogenases)
RN  - EC 1.1.1.239 (3-alpha-(17-beta)-hydroxysteroid dehydrogenase (NAD(+)))
RN  - EC 2.7.1.137 (1-phosphatidylinositol 3-kinase p110 subunit, mouse)
RN  - EC 2.7.1.137 (Class I Phosphatidylinositol 3-Kinases)
SB  - IM
MH  - 17-Hydroxysteroid Dehydrogenases/biosynthesis/blood
MH  - Adipose Tissue/*metabolism/pathology
MH  - Animals
MH  - Class I Phosphatidylinositol 3-Kinases/biosynthesis/*genetics
MH  - Follicle Stimulating Hormone/blood
MH  - Gene Expression Regulation
MH  - Genotype
MH  - Humans
MH  - Infertility, Male/blood/*genetics/pathology
MH  - Leptin/blood/genetics
MH  - Luteinizing Hormone/blood
MH  - Male
MH  - Mice
MH  - Mice, Transgenic
MH  - Puberty, Delayed/blood/*genetics/pathology
MH  - Sperm Count
MH  - Sperm Motility/genetics
MH  - Testosterone/biosynthesis
PMC - PMC5357525
COI - There are no competing interests to disclose.
EDAT- 2017/03/31 06:00
MHDA- 2017/04/19 06:00
CRDT- 2017/03/31 06:00
PHST- 2016/10/11 [received]
PHST- 2017/01/05 [revised]
PHST- 2017/01/22 [accepted]
AID - 10.1155/2017/3756089 [doi]
PST - ppublish
SO  - Biomed Res Int. 2017;2017:3756089. doi: 10.1155/2017/3756089. Epub 2017 Mar 5.

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