Abstract
OBJECTIVE: To determine relationships between measurements of total body, visceral, and ectopic (liver, skeletal muscle) fat with insulin sensitivity in pregnancy. RESEARCH DESIGN AND METHODS: Pregnant women of varying prepregnancy weights were prospectively studied in early (n = 59) and late (n = 47) gestation. At each visit, participants underwent body composition measurements including fat mass (FM), fat-free mass (FFM), abdominal subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT), ectopic lipid amounts in liver (intrahepatic lipid [IHL]) and calf skeletal muscle (intramyocellular lipid [IMCL] and extramyocellular lipid), and hyperinsulinemia-euglycemic clamp to determine insulin sensitivity (rate of glucose disposal [Rd]), endogenous glucose production (EGP), hepatic insulin sensitivity index (HISI), and free fatty acid (FFA) levels. RESULTS: In early pregnancy, Rd ([mg/kg FFM/min]/µIU/mL) inversely correlated (P values <0.05) with BMI, FM, SAT, VAT, IHL, IMCL, and FFA. HISI inversely correlated (P values <0.05) with BMI, FM, SAT, VAT, IMCL, and FFA, but not with IHL. In late pregnancy, however, neither EGP ([mg/kg FFM/min]/µIU/mL) nor Rd correlated with regional or ectopic fat measures, but HISI remained inversely correlated with BMI, FM, SAT, VAT, and IMCL. Early-pregnancy IHL levels did not predict late-pregnancy insulin sensitivity. Pregnant women with prepregnancy obesity were more insulin resistant but gained less gestational weight, VAT, and SAT, and experienced less decline in insulin sensitivity, than normal prepregnancy weight women. CONCLUSIONS: Insulin resistance in early pregnancy is strongly associated with total, regional, and ectopic adiposity. However, in late pregnancy, factors other than regional and ectopic adiposity predominately influence insulin sensitivity. Prepregnancy weight categories proportionately alter gestational weight gain, adiposity distribution, and glucometabolic responses.