PMID- 32344561
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 2075-1729 (Print)
IS  - 2075-1729 (Electronic)
IS  - 2075-1729 (Linking)
VI  - 10
IP  - 4
DP  - 2020 Apr 24
TI  - Maternal Obesity Modulates Expression of Satb2 in Hypothalamic VMN of Female 
      Offspring.
LID - 10.3390/life10040048 [doi]
LID - 48
AB  - Maternal obesity during pregnancy is associated with a greater risk of poor 
      health outcomes in offspring, including obesity, metabolic disorders, and 
      anxiety, however the incidence of these diseases differs for males and females. 
      Similarly, animal models of maternal obesity have reported sex differences in 
      offspring, for both metabolic outcomes and anxiety-like behaviors. The 
      ventromedial nucleus of the hypothalamus (VMN) is a brain region known to be 
      involved in the regulation of both metabolism and anxiety, and is well documented 
      to be sexually dimorphic. As the VMN is largely composed of glutamatergic 
      neurons, which are important for its functions in modulating metabolism and 
      anxiety, we hypothesized that maternal obesity may alter the number of 
      glutamatergic neurons in the offspring VMN. We used a mouse model of a maternal 
      high-fat diet (mHFD), to examine mRNA expression of the glutamatergic neuronal 
      marker Satb2 in the mediobasal hypothalamus of control and mHFD offspring at 
      GD17.5. We found sex differences in Satb2 expression, with mHFD-induced 
      upregulation of Satb2 mRNA in the mediobasal hypothalamus of female offspring, 
      compared to controls, but not males. Using immunohistochemistry, we found an 
      increase in the number of SATB2-positive cells in female mHFD offspring VMN, 
      compared to controls, which was localized to the rostral region of the nucleus. 
      These data provide evidence that maternal nutrition during gestation alters the 
      developing VMN, possibly increasing its glutamatergic drive of offspring in a 
      sex-specific manner, which may contribute to sexual dimorphism in offspring 
      health outcomes later in life.
FAU - Glendining, Kelly A
AU  - Glendining KA
AD  - Centre for Neuroendocrinology, Department of Anatomy, University of Otago, 
      Dunedin 9054, New Zealand.
FAU - Fisher, Lorryn C
AU  - Fisher LC
AD  - Centre for Neuroendocrinology, Department of Anatomy, University of Otago, 
      Dunedin 9054, New Zealand.
FAU - Jasoni, Christine L
AU  - Jasoni CL
AUID- ORCID: 0000-0002-2945-8301
AD  - Centre for Neuroendocrinology, Department of Anatomy, University of Otago, 
      Dunedin 9054, New Zealand.
LA  - eng
GR  - 14-568/Health Research Council of New Zealand/
PT  - Journal Article
DEP - 20200424
PL  - Switzerland
TA  - Life (Basel)
JT  - Life (Basel, Switzerland)
JID - 101580444
PMC - PMC7235991
OTO - NOTNLM
OT  - developmental programming
OT  - glutamatergic
OT  - maternal nutrition
OT  - neurodevelopment
OT  - ventromedial nucleus of the hypothalamus
COIS- The authors declare no conflict of interest. The funders had no role in the 
      design of the study; in the collection, analyses, or interpretation of data; in 
      the writing of the manuscript, or in the decision to publish the results.
EDAT- 2020/04/30 06:00
MHDA- 2020/04/30 06:01
PMCR- 2020/04/01
CRDT- 2020/04/30 06:00
PHST- 2020/03/11 00:00 [received]
PHST- 2020/04/16 00:00 [revised]
PHST- 2020/04/21 00:00 [accepted]
PHST- 2020/04/30 06:00 [entrez]
PHST- 2020/04/30 06:00 [pubmed]
PHST- 2020/04/30 06:01 [medline]
PHST- 2020/04/01 00:00 [pmc-release]
AID - life10040048 [pii]
AID - life-10-00048 [pii]
AID - 10.3390/life10040048 [doi]
PST - epublish
SO  - Life (Basel). 2020 Apr 24;10(4):48. doi: 10.3390/life10040048.