Endoplasmic reticulum stress is increased in adipose tissue of XXXX with gestational diabetes.

@entity1 @entity1477 @entity6 @entity28 @entity1356 @entity310 @entity5594 @entity2348 @entity1192 @entity23656 @entity5593
@entity28 and @entity6 ( @entity6 ) are two increasingly common and important obstetric complications that are associated with severe long-term health risks to mothers and babies. @entity1356 , which is increased in @entity28 and @entity6 pregnancies, plays an important role in the pathophysiology of these two pregnancy complications. In non-pregnant tissues, endoplasmic (ER) stress is increased in @entity6 and can induce @entity1356 via inflammasome activation. The aim of this study was to determine whether ER stress is increased in omental adipose tissue of @entity1 with @entity6 , and if ER stress can also upregulate inflammasome-dependent secretion of @entity1356 . ER stress markers @entity5593 , @entity1477 and @entity5594 s were significantly increased in adipose tissue of @entity28 compared to lean pregnant @entity1 . ER stress was also increased in adipose tissue of @entity1 with @entity6 compared to BMI-matched normal glucose tolerant (NGT) @entity1 . Thapsigargin, an ER stress activator, induced upregulated secretion of mature @entity1192 and @entity1356 in @entity1 omental adipose tissue explants primed with @entity2348 , the viral dsRNA analogue poly(I:C) or the pro-inflammatory cytokine @entity310 . Inhibition of capase-1 with Ac-YVAD-CHO resulted in decreased @entity1192 and @entity1356 secretion, whereas inhibition of @entity23656 with carbenoxolone suppressed @entity1356 secretion only. Treatment with anti- @entity6 drugs metformin and glibenclamide also reduced @entity1192 and @entity1356 secretion in infection and cytokine-primed adipose tissue. In conclusion, this study has demonstrated ER stress to activate the inflammasome in pregnant adipose tissue. Therefore, increased ER stress may contribute towards the pathophysiology of @entity28 in pregnancy and @entity6 .
