ABSTRACT
Since macrosomic infants of diabetic mothers tend to remain obese throughout their
lives, and obesity and heredity are factors predisposing to Type II diabetes, it can
be hypothesized that infants who are going to develop diabetes later in life are more
likely to be macrosomic at birth than those who are not going to develop diabetes
as adults. This hypothesis was tested, using the c57/KsJdb+/+m mouse animal model
of gestational diabetes. This animal is frankly diabetic in the homozygous diabetic
form. In the heterozygous form, it develops gestational diabetes, and in the homozygous
normal form, it is normal. The pups of heterozygous males and females that were bred
were weighed, classified by sex, and identified. At 4 weeks of age, the genetic makeup
of the pups was determined. From 37 litters, 140 pups were born and raised to weaning
age. Multiple regression analysis of the data revealed that the homozygous diabetic
pups weighed most at birth; the heterozygous gestationally diabetic pups weighed less,
and the homozygous normal pups weighed the least. All comparisons of these groups
were statistically significant. Sex and interlitter variation also were found to be
significant factors determining birthweight. Controlling for sex and interlitter variation
did not change the significance of the effect of the genetic tendency for diabetes
on birthweight. This study indicates that in Type II diabetes, neonatal macrosomia
in part may be determined by the genetic or congenital susceptibilty to develop diabetes
in the future.
