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Lada and mody

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Lada and mody

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in this slide i have given a little information about latent autoimmune diabetes in adult and maturity onset diabetes in young

in this slide i have given a little information about latent autoimmune diabetes in adult and maturity onset diabetes in young

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Lada and mody

  1. 1. LADA & MODY Presented By Sriloy Mohanty
  2. 2. LADA- Latent Onset Diabetes In Adult
  3. 3. Introduction  Latent Autoimmune Diabetes in Adults (LADA) is a form of autoimmune (type 1 diabetes) which is diagnosed in individuals who are older than the usual age of onset of type 1 diabetes.  Often, patients with LADA are mistakenly thought to have type 2 diabetes, based on their age at the time of diagnosis.  Progress to insulin requirement within 6 years
  4. 4. Diabetes 1.5
  5. 5. History  1980s  San Raffaele Hospital  Milan (patient)  Stiff Mans Syndrome (SMS)  Type 1 DM  Anti GAD antibodies (Glutamic acid decarboxylase)
  6. 6. GAD  Glutamic acid decarboxylase  Present in cytoplasm of the human beta cells  Catalyses the Conversion of glutamic acid to GABA  GABA is involved in release of insulin from secretory granules
  7. 7.  Adults who should be considered for antibody testing*:  age of onset <50 years  acute symptoms  BMI <25 kg/m2  personal or family history of autoimmune disease  C-Peptide test is positive
  8. 8. Symptoms  Unusual thirst  Frequent urination  Weight loss despite an increase in appetite  Blurred vision  Nausea and vomiting  Extreme weakness and fatigue  Irritability and mood changes  Frequent bladder and skin infections that don't heal easily  High levels of sugar in the blood when tested  High levels of sugar in the urine when tested  Dry, itchy skin  Tingling or loss of feeling in the hands or feet
  9. 9. Diagnosis  C-peptide test (a measure of endogenous insulin)  If positive then….  GAD antibody test  Islet cell antibodies (ICA) are also common  HDL to triglyceride ratio- it exceeds 4 then insulin resistance  If IR then no LADA
  10. 10. Rx for LADA  LADA often does not require insulin at the time of diagnosis and may be managed with diet and exercise  the avoidance of using metformin treatment  May require multiple daily Insulin injections(after 6 months)
  11. 11. Maturity-Onset Diabetes of the Young (MODY) 1975 Definition Type-2 diabetes mellitus in the young plus Autosomal dominant inheritance
  12. 12. Understanding MODY  Mutations in one of the 6 different genes  Onset of diabetes type 2 early in life: childhood, adolescence or young adulthood  Primary defect in insulin secretion, and IR
  13. 13. Maturity Onset diabetes of the young (MODY)  MODY 1 - Mutation in HNF-4-alpha (transcription factor), chromosome 20  MODY 2 - Mutation in glucokinase gene, chromosome 7  MODY 3 - Mutation in HNF-1-alpha (transcription factor), chromosome 12 (most common form)  MODY 4 - Mutation in insulin promoter factor-1 (IPF-1), chromosome 13  MODY 5 - Mutation in HNF-1-beta, chromosome 17  MODY 6 - Mutation in Neurogenic Differentiation Factor-1 (NEUROD1) , chromosome 2
  14. 14. Heterozygous Gene Mutations Identified in MODY Name (Year) Gene Chromosome MODY1 (1991) HNF-4a 20q MODY2 (1993) Glucokinase 7p MODY3 (1996) HNF-1a 12q MODY4 (1997) IPF-1 (PDX-1) 13q MODY5 (1997) HNF-1b 17q MODY6 (1999) Neuro-D1 / BETA-2 2q HNF = Hepatocyte nuclear factor IPF = Insulin promoter factor PDX-1 = Pancreatic duodenal homeobox-1
  15. 15. MODY-Related Proteins Glucokinase  Expressed in b-cells and liver  GSK catalyzes the formation of glucose-6-phosphate from glucose.  Liver – Helps in storage of glucose as glycogen  Mutation causes problem in conversion
  16. 16. Liver-enriched transcription factors HNF-1a, HNF-1b, and HNF-4a  Expressed in liver, pancreatic islets, kidneys and genitalia.  In Beta cells they regulate The expression of the insulin gene Proteins involved in glucose transport and metabolism.  Mutations results in defect of insulin secretion response to glucose, leading to progressive decline in glycemic control.
  17. 17. Transcription factor IPF-1 Rare Expressed in pancreatic islets Central role in development of pancreas. Mediates glucose-induced stimulation of insulin-gene transcription
  18. 18. Transcription factor Neuro-D1 (BETA2) Rare Expressed in pancreatic islets Activates the transcription of the insulin gene Required for normal development of the pancreatic islets
  19. 19. Recognition at young age 1.Mild, asymptomatic increase in blood glucose in a child, adolescent or young adult(<25 years) 2. Prominent family history of diabetes in 2-3 generations 3. Usually not associated with obesity
  20. 20. When to suspect MODY  a “type 1″ diabetes patient who has negative blood testing for autoantibodies.  a “type 1″ diabetes patient who generates a significant amount of insulin for years beyond diagnosis (detectable blood levels of c-peptide, proinsulin, and/ or insulin)  a “type 2″ diabetes patient who is normal weight and shows no signs of insulin resistance.  a diabetes with family history of early onset diabetes for 2-3 generations.  Diabetes paired with pancreatic insufficiency  Individual or family history of diabetes paired with developmental kidney disease or kidney cysts
  21. 21. Rx for MODY Rx depends on the involved gene and other factors  MODY 3 and 1 can be treated initially with sulfonylureas, prompts the body to produce insulin. Usually GCK-MODY requires no treatment at all. Other type of MODY Rx is unclear may require multiple daily Insulin injections.
  22. 22. Thank you…

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