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The majority of type 2 diabetics are middle-aged and overweight, hence the basic defect is insulin resistance. However there are cases of Maturity Onset Diabetes in the Young (MODY). These are inherited as autosomal dominant conditions and are due to variable defects in beta cells with minimal of insulin resistance and can be divided into:
MODY 1. Caused by mutation of hepatocytes nuclear factor 4 α and accounts for 10% of MODY cases. Treatment is initially with sulfonylurea.
MODY 2. Caused by Glucokinase mutation and account for 32% of MODY cases. It is usually mild and only requires treatment occasionally during pregnancy.
MODY 3. Mutation is at HNF1α and is at chromosome 12. This accounts for 52% of MODY cases. It usually presents in late teens a responds well to sulfonylurea .
MODY 4. Mutation at Pdx 1 Homeobox gene on chromosome 13. Only one family is identified with agenesis of the pancreas.
MODY 5. Mutation at HNF1β(Transcription factor 2) , can be associated with renal cysts ( RCAD Syndrome). This occurs less frequently than the other first three MODY types .
MODY 1. Caused by mutation of hepatocytes nuclear factor 4 α and accounts for 10% of MODY cases. Treatment is initially with sulfonylurea.
MODY 2. Caused by Glucokinase mutation and account for 32% of MODY cases. It is usually mild and only requires treatment occasionally during pregnancy.
MODY 3. Mutation is at HNF1α and is at chromosome 12. This accounts for 52% of MODY cases. It usually presents in late teens a responds well to sulfonylurea .
MODY 4. Mutation at Pdx 1 Homeobox gene on chromosome 13. Only one family is identified with agenesis of the pancreas.
MODY 5. Mutation at HNF1β(Transcription factor 2) , can be associated with renal cysts ( RCAD Syndrome). This occurs less frequently than the other first three MODY types .
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