Detailed metabolic studies were carried out to compare major regulatory steps in @entity413 metabolism in vivo between 25 normal pregnant Latino @entity1 without and 150 pregnant Latino @entity1 with @entity6 ( @entity6 ). The two groups were frequency-matched for age, BMI, and gestational age at testing in the third trimester. After an overnight fast, @entity1 with @entity6 had higher fasting plasma @entity413 (P = 0.0001) and immunoreactive @entity2690 (P = 0.0003) concentrations and higher @entity413 production rates (P = 0.01) but lower @entity413 clearance rates (P = 0.001) compared with normal pregnant @entity1 . During @entity3190 (approximately 600 pmol/l) and euglycemia (approximately 4.9 mmol/l), @entity1 with @entity6 had lower @entity413 clearance rates (P = 0.0001) but higher @entity413 production rates (P = 0.0001) and plasma free @entity844 ( @entity6334 ) concentrations (P = 0.0002) than the normal @entity1 . These intergroup differences persisted when a subgroup of 116 @entity1 with @entity6 who were not diabetic < or = 6 months after pregnancy were used in the analysis. When all subjects were considered, there was a very close correlation between @entity413 production rates and plasma @entity6334 concentrations throughout the @entity413 clamps in control (r = 0.996) and @entity6 (r = 0.995) groups. Slopes and intercepts of the relationships were nearly identical, suggesting that blunted suppression of @entity6334 concentrations contributed to blunted suppression of @entity413 production in the @entity6 group. In addition to these defects in @entity2690 action, @entity1 with @entity6 had a 67% impairment of @entity9451 for @entity2690 resistance compared with normal pregnant @entity1 . These results demonstrate that @entity1 with @entity6 have @entity156 in @entity2690 action together with @entity73 for @entity2690 resistance. Our findings suggest that defects in the regulation of @entity413 clearance, @entity413 production, and plasma @entity6334 concentrations, together with defects in pancreatic beta-cell function, precede the development of @entity164 2 @entity6 in these high-risk @entity1 .

Multiple metabolic defects during late pregnancy in @entity1 at high risk for @entity164 2 XXXX .

@entity1 :: ('9606', 'Species') :: ['women'] @entity844 :: ('CHEBI:35366', 'Chemical') :: ['fatty acid'] @entity6 :: ('MESH:D003920', 'Disease') :: ['gestational diabetes mellitus', 'diabetes', 'GDM'] @entity73 :: ('MESH:D003072', 'Disease') :: ['impaired compensation'] @entity2690 :: ('3630', 'Gene') :: ['insulin'] @entity9451 :: ('MESH:D010195', 'Disease') :: ['pancreatic beta-cell compensation'] @entity156 :: ('MESH:D000015', 'Disease') :: ['multiple defects'] @entity6334 :: ('CHEBI:42638', 'Chemical') :: ['FFA'] @entity3190 :: ('MESH:D006946', 'Disease') :: ['steady-state hyperinsulinemia'] @entity164 :: ('MESH:D017827', 'Disease') :: ['type'] @entity413 :: ('MESH:D005947', 'Chemical') :: ['glucose']
@entity6 :: (MESH:D003920,Disease) :: ['diabetes']
