Abstract
ObjectiveTo profile the differential gene expression of the KEGG Adipocytokine Signaling pathway in omental compared to subcutaneous tissue in normal pregnancy.Study DesignSubjects included 14 nonobese, normal glucose tolerant, healthy pregnant women. Matched omental and subcutaneous tissue were obtained at elective cesarean delivery. Gene expression was evaluated using microarray and validated by RT-PCR. Differential gene expression was defined as ≥1.5 fold increase at p < 0.05.ResultsSix genes were significantly downregulated with two upregulated genes in omental tissue. Downregulation of Adiponectin and Insulin Receptor substrate, key genes mediating insulin sensitivity, were observed with borderline upregulation of GLUT-1. There were downregulations of CD36 and acyl-CoA Synthetase Long-chain Family Member 1which are genes involved in fatty acid uptake and activation. There was a novel expression of Carnitine palmitoyltransferase 1C.ConclusionDifferential gene expression of Adipocytokine Signaling Pathway in omental relative to subcutaneous adipose tissue in normal pregnancy suggests a pattern of insulin resistance, hyperlipidemia, and inflammation.
Highlights
Pregnancy is associated with changes in the regulation of glucose metabolism and the development of insulin resistance during the second and third trimesters [1] of all pregnancies.there is no consensus regarding the precise pathophysiology of insulin resistance, which is perceived as causative of gestational diabetes mellitus
It has been suggested that the observed increase in body fat mass from the 1st trimester throughout pregnancy may be causally associated with decrease in insulin sensitivity [2]
Martin et al have noted a significant association between visceral adipose tissue-depth above upper quartile value on ultrasound with positive glucose challenge test in later pregnancy, with no such associations seen for subcutaneous adipose tissue [5]
Summary
Pregnancy is associated with changes in the regulation of glucose metabolism and the development of insulin resistance during the second and third trimesters [1] of all pregnancies. There is no consensus regarding the precise pathophysiology of insulin resistance, which is perceived as causative of gestational diabetes mellitus. It has been suggested that the observed increase in body fat mass from the 1st trimester throughout pregnancy may be causally associated with decrease in insulin sensitivity [2]. Intra-abdominal (omental or visceral) adipose has been implicated as a major factor in pathophysiology of insulin resistance [3]. It has been observed that visceral fat accumulation increases during pregnancy [4]. Martin et al have noted a significant association between visceral adipose tissue-depth above upper quartile value on ultrasound with positive glucose challenge test in later pregnancy, with no such associations seen for subcutaneous adipose tissue [5]
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