Diabetic embryopathy refers to congenital maldevelopments that are linked to maternal diabetes. Prenatal exposure to hyperglycemia can result in spontaneous abortions, perinatal mortality, and malformations. Type 1 and Type 2 diabetic pregnancies both increase the risk of diabetes induced teratogenicity. The rate of congenital malformations is similar in Type 1 and 2 mothers because of increased adiposity and the age of women with type 2 diabetes. Genetic predisposition and different environmental factors both play a significant role in the development of diabetic embryopathy. Metabolic dysfunction in pregnant mothers also increases the risk of fetal malformations. Risk factors
Women with pregestational diabetes are at the highest risk for fetal malformations. The risk of congenital malformations in pregestational type 1 diabetes is directly correlated with glucose and glycohemoglobin levels in the blood. It is also inversely related to the gestational age at first exposure. The comorbidities associated with pregestational type 2 diabetes include advanced maternal age, lipid preroxidation and obesity. Overweight women (BMI ≥ 25) who develop gestational diabetes have an intermediate risk for malformations. Pregnant women who have gestational diabetes but dont have prediabetic markers experience perinatal outcomes that are similar to women without diabetes. Gestational consequences
Malformations
Type 1 diabetes in pregnant women can result in malformations that affect the musculoskeletal , urogenital, and central nervous systems. Most of these malformations occur within the first 4 weeks of gestation. Caudal dysgenesis is one of the most strongly associated diseases to diabetes. This malformation has the highest risk for diabetic embryopathy.
History
Congenital Generalized Lipodystrophy, also known as Berardinelli–Seip lipodystrophy was first described in 1954 by Berardinelli and later by Seip in 1959. The gene for type 1 CGL was identified as AGPAT2 at chromosome 9q34, and later the gene for type 2 CGL was identified as BSCL2 at chromosome 11q13. More recently, type 3 CGL was identified as a separate type of CGL, which was identified as a mutation in the CAV1 gene. Then, a separate type 4 CGL was identified as a mutation in the PTRF gene. See also
Lipodystrophy
Familial partial lipodystrophy
List of cutaneous conditions
Skin lesion
Seipin

References
Further reading
GeneReviews/NCBI/NIH/UW entry on Berardinelli-Seip Congenital Lipodystrophy


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