Background Low birth weight is associated with an increased risk of developing type-2 diabetes in later life. The fathers of low birth weight offspring are themselves more likely to have type-2 diabetes in later life. As part of a larger study to determine whether offspring with fetal growth restriction (FGR) inherit insulin resistance (IR) from their fathers, we designed a case-control study to compare IR and endothelial function in men who father FGR offspring (cases) with men who father normal birth weight offspring (controls).
Methods We recruited 30 fathers of ongoing FGR pregnancies, defined as fetal growth <10th customised centile and confirmed post-natally. We excluded pregnancies with chromosomal or structural abnormalities or maternal diseases. Fathers of normal grown offspring, 10th to 95th centile, were controls (n=50). In all fathers, we measured IR (HOMA index, from fasting serum glucose and insulin levels), endothelial function by flow-mediated dilatation (FMD), weight, waist-circumference and blood pressure.
Results Fathers of FGR pregnancies had greater IR, (p=0.0015), impaired FMD (p=0.029), higher systolic (p=0.007) and diastolic (p=0.0001) blood pressures, greater waist circumferences (p<0.0042) and weight (p=0.058) than fathers of normal weight offspring.
Conclusions Fathers of FGR pregnancies have a metabolic and vascular phenotype that predisposes to type 2 diabetes and cardiovascular disease at the time of an affected pregnancy. We are investigating whether this observation can be explained by altered insulin control genes inherited by the growth-restricted fetus from the father.
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