Table 1. Diabetes: Fetal origins of adult diseasea
| Maternal | Fetal | Adult | Offspring |
|---|---|---|---|
| a Fetal exposure to nutritional disturbances affects pancreatic development and influences the insulin response in adulthood that becomes manifest as diabetes. Furthermore, these offspring have an increased rate of gestational diabetes, which in turn increases the risk for future development of type 2 diabetes in their offspring. In this manner, obesity may play a role in escalating the incidence of obesity and its associated diseases, including renal disease. | |||
| Mild hyperglycemia | Asymmetric macrosomia, ↑ insulin, ↑ IGF-1 | Type 2 diabetes, normal pancreatic mass | ↑ Risk for type 2 diabetes |
| Gestational diabetes | Islet hypertrophy and hyperplasia | Impaired glucose tolerance, impaired insulin secretion, ↑ risk for breast cancer | |
| Severe hyperglycemia | Asymmetric microsomia, ↓ insulin, ↓ IGF-1 | Type 2 diabetes, ↑ pancreatic mass | ↑ Risk for type 2 diabetes |
| Poorly controlled diabetes | ↓ Insulin receptors, degranulation of β cells | Insulin resistance, ↑ insulin, cardiovascular disease and renal disease | |
| Protein restriction | Reduced nephron number, ↓ insulin, ↓ pancreatic mass, ↓ β cells | Type 2 diabetes, women are insulin resistant, hypertension | ↑ Risk for type 2 diabetes |
| Intrauterine growth retardation | |||