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Therapy for Type II Diabetes

Therapy for Type II Diabetes. Non-Insulin Therapy for Hyperglycemia in Type 2 Diabetes, Match Patient Characteristics to Drug Characteristics. -. -. -. Peripheral glucose uptake. 1.Pancreatic insulin Secretion: Incretin, ranolazine. 5. Gut CHO Absorption: Incretin, Pramlintide,

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Therapy for Type II Diabetes

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  1. Therapy for Type II Diabetes

  2. Non-Insulin Therapy for Hyperglycemia in Type 2 Diabetes,Match Patient Characteristics to Drug Characteristics - - - Peripheral glucose uptake 1.Pancreatic insulin Secretion: Incretin, ranolazine 5.Gut CHO Absorption: Incretin, Pramlintide, Glucosidase inh. 7.Brain- TZD,INCRETIN, bromocryptine 2.Pancreatic glucagon Secretion- Incretin 8.Kidney- SGLT2 HYPERGLYCEMIA De 3.Muscle- TZD, Incretin Hepatic glucose production: Metformin, incretin 4.Liver 6.Fat- TZD, metformin

  3. AACE/ACE:Recommendations Based on A1C at Diagnosis/ or When you see in OfficeEMPHASIS on Using Combination Therapy to ADDRESS multiple etiologies of hyperglycemia in Octet Lifestyle Modifications Monotherapy Dual therapy Triple therapy A1C 6.5%-7.5% A1C 7.6%-9.0% A1C >9.0% If under treatment If drug naive Symptoms No symptoms Dual therapy Insulin plus other agent(s)* Insulin plus other agent(s)* Triple therapy Triple therapy Use Sulfonylureas/Glinides LAST, IF AT ALL Therapeutic Choice, based on Safety/ Efficacy, Should Match The Drug Characteristics With Patient Characteristics Rodbard HW, et al. Endocr Pract. 2009;15:540-559.

  4. TZD (Pioglitazone), metformin, bromocriptine QR Combo therapy-in AACE >7.5 PICK RIGHT DRUG FOR RIGHT PT. . Postmeal Glucose Insulin Level • Consider therapyfor prevention (future) • Early treatment,even with IGT • FASTTHERAPEUTICCHANGES • Not 1st,2nd ,3rd line; • not competition betw. • classes; • early combo therapy Incretins* (GLP-1 RA, DPP-4 Inh.) SGLT-2 Inhibitors *with caution re:Immune Sup. Levels Insulin Delay Need for Insulin No need for Early Insulin If need Insulin, Continue Non-Insulin RX (Avoids need for Meal-Time Insulin- Decrease Risk Hypoglycemia 85%- Get Patients off insulin Who had been given early Insulin Nutrition Exercise, NO SMOKING Onset of Diabetes 350 300 250 200 150 100 50 Glucose (mg/dl) Fasting Glucose Insulin-Resistance 250 200 150 100 50 0 Relative -cell Function (%) Insulin Insulin -10 -5 -0 5 10 15 20 25 30 RxPRINCIPLES-Uses Across Continuum of Care ModifiedfromBergenstal RM, International Diabetes Center.

  5. There is No perfect Exogenous Insulin:All result in HyperInsulinemia and Potential Hypoglycemia Hypoglycemia CONCLUSION: DELAY INSULIN THERAPY; AVOID BOLUS RX if possible NORMAL: Insulin into portal system and B-cell= Perfect glucose sensor- Insulin secretion modulator Exogenous Insulin

  6. Concurrent Therapy

  7. Treating the ABCs Reduces Diabetic Complications 1 UKPDS Study Group (UKPDS 33). Lancet. 1998;352:837-853. 2 Hansson L, et al. Lancet. 1998;351:1755-1762. 3 UKPDS Study Group (UKPDS 38). BMJ. 1998;317:703-713. 4 Grover SA, et al. Circulation. 2000;102:722-727. 5 Pyŏrälä K, et al. Diabetes Care. 1997;20:614-620.

  8. Aggressive medical therapy in diabetes-ADD SGLT-2 Inh. Bromocriptine QR Pioglitazone Incretins, Metformin Ranolazine Hyperglycemia/ Insulin resistance Atherosclerosis, CV Outcomes, CV Risk Factors, Mortality ACE inhibitorsARBs β-blockersCCBsDiuretics Hypertension StatinsFibric acid derivatives Colsevalam PCSK-9 Inh Dyslipidemia Platelet activationand aggregation ASAClopidogrelTiclopidine Adapted from Beckman JA et al. JAMA. 2002;287:2570-81.

  9. Summary Treat aggressively-benefit on cost and complications Treat elements of pathophysiology Resistance-glycemia,endothelial dysfunction,lipids,BP,coag. Secretion-first phase,incretin,importance of PPG Multi-hormonal issues Use SIDE-BENEFITS of the various agents Treat to new goals using combinations that make pathophysiologic sense Guidelines should help pick right drug(s) for right patients

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