Models of the onset of two phrases of type 2 DM Insulin resistance Insulin resistance NGT IGR(IFG、IGT) DM β cell exhaustion
Models of the onset of two phrases of type 2 DM NGT IGR(IFG、IGT) DM cell exhaustion Insulin resistance Insulin resistance
WHO plasma glucose guidel ine FPG (mmol/L) DM 7.0 IFG 6.1 NGT IGT 7811.1 75gOGTT chPG (mmol/L)
WHO plasma glucose guideline IG T IFG NGT DM 75gOGTT 2hPG (mmol/L) FPG (mmol/L) 7.0 6.1 FPG 7.8 11.1 IGT
Comparison of type 1 and type 2 DM type I DM type2 DM Usual age of onset 30 years Years Mode of onset acute chronic weight norma overweight or obesity or weight loss symptoms polyuria, polydipsia, similar but usually weight loss less severe presentation Acute complications often Chronic complications Large vessel disease less then type 2 DM leading cause of death Renal disease leading cause of death 5%~10% Insulin and c-peptide low or lack peak value delayed, high or deficiency mmune marker usually usuall Therapy insulin dependence oral antidiabetic agents are available
Comparison of type 1 and type 2 DM type1 DM type2 DM Usual age of onset <30 years >40years Mode of onset acute chronic weight normal overweight or obesity or weight loss symptoms polyuria,polydipsia, similar but usually weight loss less severe presentation Acute complications often few Chronic complications Large vessel disease less then type 2 DM leading cause of death Renal disease leading cause of death 5%10% Insulin and c-peptide low or lack peak value delayed ,high or deficiency Immune marker usually + usually - Therapy insulin dependence oral antidiabetic agents are available
Chronic complications Macrovascular disease ● Microangiopathy Diabetic retinopathy Diabetic renal disease Diabetic neuropathy o Diabetic dermatopathy ● Infection
Chronic complications ⚫ Macrovascular disease ⚫ Microangiopathy – Diabetic retinopathy – Diabetic renal disease – Diabetic neuropathy ⚫ Diabetic dermatopathy ⚫ Infection
Mechanism of complications o Activation of polyol (or sorbitol) pathway o Formation of non-enzyme saccharification products Change of hemodynamics ● Activation of pko o Microangiopathy theory
Mechanism of complications ⚫ Activation of polyol （or sorbitol）pathway ⚫ Formation of non-enzyme saccharification products ⚫ Change of hemodynamics ⚫ Activation of PKC ⚫ Microangiopathy theory