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Diabesity (Diabetes and Obesity)


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Are you Struggling to Control of your Diabetes and Weight?

People who are overweight or obese are more prone to developing Type 2 diabetes. Those who have Type 1 and Type 2 diabetes with weight problems struggle to control their blood sugar levels. Research shows that people with diabetes find it more difficult to lose weight than those without diabetes.

Weight loss significantly improves blood sugar control and also reduces the risk of getting complications from diabetes. However, whilst attempting to lose weight, people with diabetes find it hard to restrict their intake of food since eating less may trigger hypoglycaemia (low blood sugar). All these facts explain the need for specialist input in management of weight in people with diabetes.

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Diabesity (Diabetes and Obesity)

  1. 1. Diabesity Educational Forum
  2. 2.  Diabesity - 21st century pandemic Diabesity is now the single greatest contributor to chronic disease Obesity will soon become the leading cause of death
  3. 3. Aims of this forum Open forum to discuss management of Diabesity Forum will be interactive New studies in this field will be presented Emerging treatments in Diabesity will be discussed
  4. 4. Aims of this forum External speaker Discussion of case studies Website to be launched Expand to regional forum and National
  5. 5. Meeting Three monthly Clinical leads in Primary care (Two doctors and two nurses) Members will be contacted via email
  6. 6. Obesity overview Incretin based drug Case studies
  7. 7. Obesity can alter the natural history of T2DM by virtue of the role of visceral fat with its Proinflammatory Prothrombotic Proinsulin resistant environments.
  8. 8. Incretins
  9. 9. Ramlo-Halsted BA, et al. Prim Care 1999;26:771–789. Impaired insulin production & secretion The underlying defects: insulin resistance and β-cell dysfunction Insulin resistance (IR) - Hyperinsulinaemia - Normal glucose tolerance IR + declining insulin levels + impaired glucose tolerance - Failure of β-cell to adapt to IR Impaired responsiveness to insulin ↑FFA levels Sedentary lifestyle Diet Obesity Type 2 diabetes Glucotoxicity β-cell dysfunction Genetic predispositions
  10. 10. Heloderma suspectum
  11. 11. Physiological functions • Incretins are hormones secreted by intestinal endocrine cells in response to nutrient intake • Glucose-dependent insulin secretion, postprandial glucagon suppression and slowing of gastric emptying
  12. 12. Incretins were identified when it was observed that orally ingested glucose provoked a higher insulin response than comparable glucose administered intravenously This well-described phenomenon is called the ‘incretin effect’ The incretin effect accounts for ~60% of total insulin release following a meal
  13. 13. The two primary incretin hormones are GLP-1 and GIP • Circulating GIP and GLP-1 levels are regulated by multiple factors2 – Low in the basal fasting state, rise rapidly following a meal due to neuronal, neuroendocrine, and direct nutrient stimulation of intestinal cells 1 Wei Y, et al. FEBS Lett 1995;358:219–224; 2 Drucker DJ. Diabetes Care 2003;26:2929–2940. GLP-1 GIP 30 amino acid peptide1 42 amino acid peptide2 Synthesised and released by L cells of ileum and colon2 Synthesised and released from K cells of jejunum and duodenum2 Sites of action1 : Pancreatic β-cells and α-cells GI tract CNS Lungs Heart Sites of action2 : Pancreatic β-cells Adipocytes
  14. 14. The incretin effect is reduced in patients with Type 2 diabetes 0 20 40 60 80 0 30 60 90 120 150 180 Time (min) * * * ** * * 0 20 40 60 80 0 30 60 90 120 150 180 Time (min) Oral Glucose
  15. 15. GLP-1 is a more potent insulin secretagogue than GIP in patients with type 2 diabetes Mean (SE); N = 18. Nauck MA, et al. J Clin Invest 1993;91:301–307. Low-dose GIP or GLP-1 (7–36 amide) High-dose GIP or GLP-1 (7–36 amide) GLP-1 (7–36 amide) GIP Hyperglycaemic clamp Insulin(pmol/L) 0 30 60 90 120 150 180 210 0 250 500 750 1000 1250 1500 1750 2000 Time (min) 0 30 60 90 120 150 180 210 0 250 500 750 1000 1250 1500 1750 2000 Time (min) Patients with type 2 diabetesNormal subjects
  16. 16. Therapeutic potential GIP secretion is normal, but its action is diminished GLP-1 secretion is diminished, but its action is preserved Glucagon, secreted from pancreatic α-cells, is also elevated in type 2 diabetes GLP-1 suppresses glucagon secretion from pancreatic α-cells in a glucose-dependent manner, suppressing hepatic glucose outputt
  17. 17. GLP-1 effects in humans Understanding the natural role of incretins Adapted from 1 Nauck MA, et al. Diabetologia 1993;36:741–744; 2 Larsson H, et al. Acta Physiol Scand 1997;160:413–422; 3 Nauck MA, et al. Diabetologia 1996;39:1546–1553; 4 Flint A, et al. J Clin Invest 1998;101:515–520; 5 Zander et al. Lancet 2002;359:824–830. GLP-1 secreted upon the ingestion of food 1.β-cell: enhances glucose-dependent insulin secretion in the pancreas1 3.Liver: reduces hepatic glucose output2 2.α-cell: suppresses postprandial glucagon secretion1 4.Stomach: slows the rate of gastric emptying3 5.Brain: promotes satiety and reduces appetite4,5
  18. 18. Change in body weight over time, Exenatide with metformin ITT population, N = 336 (Placebo, N = 113; exenatide 5 µg, N = 110; exenatide 10 µg, N = 113) *P ≤ 0.05 ** P ≤ 0.001 compared to placebo DeFronzo RA, et al. Diabetes Care 2005;28:1092–1100. * ** * -0.3 ± 0.3 kg -2.8 ± 0.5 kg -1.6 ± 0.4 kg Time (weeks) 5 10 15 20 25 300 -4 -3 -2 -1 0 1 ** ** ** ** * Mean(±SE)changeinbody weightfrombaseline(kg) Placebo BD Exenatide 5 µg BD Exenatide 10 µg BD
  19. 19. Change in body weight over time, Exenatide with sulphonylurea ITT population, N = 377 (Placebo, N = 123; exenatide 5 µg, N = 125; exenatide 10 µg, N = 129); *P ≤ 0.05 vs placebo Buse J, et al. Diabetes Care 2004;27:2628–2635. -0.6 kg -0.9 kg -1.6 kg Mean(±SE)changeinbody weightfrombaseline(kg) Time (weeks) 0 10 20 30 -2.00 -1.50 -1.00 -0.50 0 * -1.75 -1.25 -0.75 -0.25 5 15 25 Placebo BD Exenatide 5 µg BD Exenatide 10 µg BD
  20. 20. Case studies
  21. 21. DR age 48 years T2DM 14 years Metformin, Gliclazide, Lantus 56 units Weight 142Kg BMI 52 Kg/m2 HbA1C 7.6%
  22. 22. Fasting blood glucose 5.6mmol/l Post prandial 8.8 mmol/l Recurrent hypoglycaemia at night Daily supper Lantus switched to morning Solution??
  23. 23. Reduce Lantus Correct Post prandial Glucose Stop Supper Weight loss after 6 months 23KG HbA1C 6.8% Lantus reduced to 22units
  24. 24. Case Study 2 EB 56 years House wife Type 1 diabetes sine age 22years Weight 112Kg BMI 48 Kg/m2 Also is hypertensive and has angina On Lantus 66 units Novarapid 12 units TDS
  25. 25. HbA1C 8.6% Add Metformin Weight 106 Kg after three months Lantus down to 50 units HbA1C 8.0% Metformin full dose After three months Orlistat added with guidance Lantus 36 units HbA1C 7.4% Weight 98 Kg
  26. 26. MA 62 years T2DM 8 years Weight 102 Kg BMI 56 Kg/m2 HbA1C 10.3 % On Metformin, Lantus 64 units BD Increasingly tired And Day time sleepiness
  27. 27. OSA ruled out ? Hypogonad Testosterone 6.6 nmol/l Testosterone replacement After 4 months reduced Lantus to 32 units BD due to hypoglycaemia Weight 90KG HbA1C 8.1% No day time sleepiness !!!!!!!
  28. 28. Next Forum Presentation of GAME and LOOKAHEAD Case discussion External Speaker (TBC)
  29. 29. Thank you! Visit for more information