Table 2.
Maternal Diabetes
|
Maternal BMI*
|
|||||
---|---|---|---|---|---|---|
β | (95% CI) | P | β | (95% CI) | P | |
Separate exposure models† | ||||||
Insulin resistance/sensitivity | ||||||
HOMA2-IR‡ | 1.18 | (1.05, 1.33) | 0.01 | 1.11 | (1.07, 1.15) | <0.001 |
Matsuda‡ | 0.81 | (0.70, 0.95) | 0.01 | 0.90 | (0.85, 0.95) | <0.001 |
β-cell function | ||||||
HOMA2-β‡ | 1.09 | (1.003, 1.18) | 0.04 | 1.06 | (1.03, 1.09) | <0.001 |
Early insulin response (pmol/mmol) | 38.6 | (−193.1, 270.2) | 0.74 | 9.9 | (−67.1, 86.9) | 0.80 |
Oral disposition index (mM−1) | −0.22 | (−2.22, 1.77) | 0.83 | −0.30 | (−0.96, 0.37) | 0.38 |
Combined exposure model§ | ||||||
Insulin resistance/sensitivity | ||||||
HOMA2-IR‡ | 1.13 | (1.01, 1.27) | 0.04 | 1.10 | (1.06, 1.14) | <0.001 |
Matsuda‡ | 0.84 | (0.72, 0.98) | 0.03 | 0.90 | (0.86, 0.95) | <0.001 |
β-cell function | ||||||
HOMA2-β‡ | 1.06 | (0.98, 1.15) | 0.17 | 1.06 | (1.03, 1.09) | <0.001 |
Early insulin response (pmol/mmol) | 35.4 | (−198.6, 269.3) | 0.77 | 8.4 | (−69.3, 86.2) | 0.83 |
Oral disposition index (mM−1) | −0.11 | (−2.13, 1.90) | 0.91 | −0.29 | (−0.96, 0.38) | 0.39 |
Combined exposure model adjusted for offspring BMI§ | ||||||
Insulin resistance/sensitivity | ||||||
HOMA2-IR‡ | 1.12 | (1.01, 1.24) | 0.03 | 1.00 | (0.97, 1.04) | 0.95 |
Matsuda‡ | 0.83 | (0.72, 0.95) | 0.01 | 0.99 | (0.94, 1.04) | 0.77 |
β-cell function | ||||||
HOMA2-β‡ | 1.06 | (0.98, 1.14) | 0.14 | 1.00 | (0.98, 1.03) | 0.90 |
Early insulin response (pmol/mmol) | 43.8 | (−189.1, 276.6) | 0.71 | −29.1 | (−114.8, 56.7) | 0.51 |
Oral disposition index (mM−1) | −0.11 | (−2.12, 1.91) | 0.92 | −0.32 | (−1.06, 0.42) | 0.40 |
HOMA2-IR, updated homeostatic model of insulin resistance; HOMA2-β, updated homeostatic model of β-cell function.
Results for HOMA2-IR and HOMA2-β include repeated measurements collected on the same individuals at visit 1 and visit 2. Results for Matsuda, early insulin response, and oral disposition index include measurements collected at visit 2 only.
Per 5 kg/m2 increase in maternal pregnancy BMI.
Models constructed separately for maternal diabetes and obesity. Models are adjusted for offspring sex, race/ethnicity, age, Tanner stage, and for HOMA2-IR and HOMA2-β only, age by Tanner interaction.
Data were natural log-transformed for analysis; interpret β as percentage change in outcome with status change in maternal diabetes exposure and 5-kg/m2 increase in maternal pregnancy BMI.
Single model constructed with both maternal diabetes and obesity as predictors. Model is also adjusted for offspring sex, race/ethnicity, age, Tanner stage, age by Tanner interaction.