PMID- 37288271
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230613
IS  - 2644-2884 (Electronic)
IS  - 2644-2884 (Linking)
VI  - 6
IP  - 2
DP  - 2023
TI  - Placental Fatty Acid Metabolism and Transport in a Rat Model of Gestational 
      Diabetes Mellitus.
PG  - 56-67
LID - 10.26502/fjwhd.2644-288400108 [doi]
AB  - Gestational diabetes mellitus (GDM) is a form of heightened insulin resistance 
      triggered during gestation. This study examines how insulin resistance alters 
      placental long-chain polyunsaturated fatty acid (LCPUFA) transport and metabolism 
      in a rat model of lean GDM. Pregnant Sprague Dawley rats were administered with 
      S961, an insulin receptor antagonist (30 nmol/kg s.c. daily), or vehicle from 
      gestational day (GD) 7 to 20. Daily maternal body weight, food, and water intake 
      were measured. Blood pressure assessment and glucose tolerance test were done on 
      GD20. Fetal plasma and placenta were collected on GD20 and processed for fatty 
      acid measurement using LC-mass spectrometry. The expression of fatty acid 
      metabolism-related genes in the placenta was assessed using RT(2) Profiler PCR 
      arrays. The results were validated by qRT-PCR. Blockade of insulin receptors with 
      S961 in pregnant rats resulted in glucose intolerance with increased fasting 
      glucose and insulin levels. Maternal body weight gain and food and water intake 
      were not affected; however, S961 significantly increased maternal blood pressure 
      and heart rate. The placenta n3 and n6 LCPUFA concentrations were significantly 
      decreased by 8% and 11%, respectively, but their levels in the fetal plasma were 
      increased by 15% and 4%. RT2 profiler arrays revealed that placental expressions 
      of 10 genes related to fatty acid beta-oxidation (Acaa1a, Acadm, Acot2, Acox2, 
      Acsbg1, Acsl4, Acsm5, Cpt1b, Eci2, Ehhadh) and 3 genes related to fatty acid 
      transport pathway (Fabp2, Fabp3, Slc27a3) were significantly upregulated. In 
      summary, lack of insulin action increased the expression of genes related to 
      placental fatty acid beta-oxidation and transport with an increased transfer of 
      LCPUFA to the fetus. The increased lipid levels routed toward the fetus may lead 
      to fat adiposity and later-life metabolic dysfunction.
FAU - Mishra, Jay S
AU  - Mishra JS
AD  - Department of Comparative Biosciences, School of Veterinary Medicine, University 
      of Wisconsin, Madison, Wisconsin, United States of America.
FAU - Kumar, Sathish
AU  - Kumar S
AD  - Department of Comparative Biosciences, School of Veterinary Medicine, University 
      of Wisconsin, Madison, Wisconsin, United States of America.
AD  - Department of Obstetrics and Gynecology, School of Medicine and Public Health, 
      University of Wisconsin, Madison, Wisconsin, United States of America.
AD  - Endocrinology-Reproductive Physiology Program, University of Wisconsin, Madison, 
      Wisconsin, United States of America.
LA  - eng
GR  - R01 ES033345/ES/NIEHS NIH HHS/United States
GR  - R01 HL134779/HL/NHLBI NIH HHS/United States
PT  - Journal Article
DEP - 20230504
PL  - United States
TA  - J Womens Health Dev
JT  - Journal of women's health and development
JID - 101751455
PMC - PMC10246410
MID - NIHMS1899830
OTO - NOTNLM
OT  - Fatty Acid
OT  - Gestational Diabetes
OT  - Insulin Resistance
OT  - Placenta
OT  - Pregnancy
COIS- Conflicts of interest: None
EDAT- 2023/06/08 06:42
MHDA- 2023/06/08 06:43
PMCR- 2023/06/07
CRDT- 2023/06/08 04:32
PHST- 2023/06/08 06:43 [medline]
PHST- 2023/06/08 06:42 [pubmed]
PHST- 2023/06/08 04:32 [entrez]
PHST- 2023/06/07 00:00 [pmc-release]
AID - 10.26502/fjwhd.2644-288400108 [doi]
PST - ppublish
SO  - J Womens Health Dev. 2023;6(2):56-67. doi: 10.26502/fjwhd.2644-288400108. Epub 
      2023 May 4.