title: In preeclampsia, maternal third trimester subcutaneous adipocyte lipolysis is more resistant to suppression by insulin than in healthy pregnancy.
abstract: Obesity increases preeclampsia risk, and maternal dyslipidemia may result from exaggerated adipocyte lipolysis. We compared adipocyte function in preeclampsia with healthy pregnancy to establish whether there is increased lipolysis. Subcutaneous and visceral adipose tissue biopsies were collected at caesarean section from healthy (n=31) and preeclampsia (n=13) mothers. Lipolysis in response to isoproterenol (200 nmol/L) and insulin (10 nmol/L) was assessed. In healthy pregnancy, subcutaneous adipocytes had higher diameter than visceral adipocytes (P<0.001). Subcutaneous and visceral adipocyte mean diameter in preeclampsia was similar to that in healthy pregnant controls, but cell distribution was shifted toward smaller cell diameter in preeclampsia. Total lipolysis rates under all conditions were lower in healthy visceral than subcutaneous adipocytes but did not differ after normalization for cell diameter. Visceral adipocyte insulin sensitivity was lower than subcutaneous in healthy pregnancy and inversely correlated with plasma triglyceride (r=-0.50; P=0.004). Visceral adipose tissue had lower ADRB3, LPL, and leptin and higher insulin receptor messenger RNA expression than subcutaneous adipose tissue. There was no difference in subcutaneous adipocyte lipolysis rates between preeclampsia and healthy controls, but subcutaneous adipocytes had lower sensitivity to insulin in preeclampsia, independent of cell diameter (P<0.05). In preeclampsia, visceral adipose tissue had higher LPL messenger RNA expression than subcutaneous. In conclusion, in healthy pregnancy, the larger total mass of subcutaneous adipose tissue may release more fatty acids into the circulation than visceral adipose tissue. Reduced insulin suppression of subcutaneous adipocyte lipolysis may increase the burden of plasma fatty acids that the mother has to process in preeclampsia.
authors.affiliation: Women and Children's Unit, Forth Valley Royal Hospital, Stirling Rd, Larbert FK5 4WR, United Kingdom. shahzya.huda@nhs.net.
authors.forename: Shahzya S
authors.initials: SS
authors.lastname: Huda
authors.forename: Rachel
authors.initials: R
authors.lastname: Forrest
authors.forename: Nicole
authors.initials: N
authors.lastname: Paterson
authors.forename: Fiona
authors.initials: F
authors.lastname: Jordan
authors.forename: Naveed
authors.initials: N
authors.lastname: Sattar
authors.forename: Dilys J
authors.initials: DJ
authors.lastname: Freeman
mesh_terms: D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D000328:Adult; D001706:Biopsy; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007328:Insulin / Q000494:pharmacology*; D007333:Insulin Resistance / Q000502:physiology; D050152:Intra-Abdominal Fat / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007545:Isoproterenol / Q000494:pharmacology; D020738:Leptin / Q000378:metabolism; D008066:Lipolysis / Q000187:drug effects* / Q000502:physiology; D008071:Lipoprotein Lipase / Q000378:metabolism; D011225:Pre-Eclampsia / Q000378:metabolism* / Q000503:physiopathology; D011247:Pregnancy; D011263:Pregnancy Trimester, Third / Q000378:metabolism*; D022702:Receptors, Adrenergic, beta-3 / Q000378:metabolism; D050151:Subcutaneous Fat / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D014280:Triglycerides / Q000097:blood
chemical_list: C568534:ADRB3 protein, human; D007328:Insulin; D020738:Leptin; D022702:Receptors, Adrenergic, beta-3; D014280:Triglycerides; C548261:LPL protein, human; D008071:Lipoprotein Lipase; D007545:Isoproterenol
keywords: adipocytes; lipolysis; preeclampsia; pregnancy