Diabesity Educational Forum
 Diabesity - 21st century pandemic
Diabesity is now the single greatest
contributor to chronic disease
Obesity will soo...
Aims of this forum
Open forum to discuss management of Diabesity
Forum will be interactive
New studies in this field wi...
Aims of this forum
External speaker
Discussion of case studies
Website to be launched
Expand to regional forum and Nat...
Meeting Three monthly
Clinical leads in Primary care (Two doctors and
two nurses)
Members will be contacted via email
Obesity overview
Incretin based drug
Case studies
Obesity can alter the natural history of T2DM
by virtue of the role of visceral fat with its
Proinflammatory
Prothrombotic...
Incretins
Ramlo-Halsted BA, et al. Prim Care 1999;26:771–789.
Impaired insulin production
& secretion
The underlying defects:
insuli...
Heloderma suspectum
Physiological functions
• Incretins are hormones secreted by
intestinal endocrine cells in response to
nutrient intake
• G...
Incretins were identified when it was observed that orally
ingested glucose provoked a higher insulin response
than compar...
The two primary incretin hormones are GLP-1 and
GIP
• Circulating GIP and GLP-1 levels are regulated by multiple factors2
...
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)
*
* *
** *...
GLP-1 is a more potent insulin secretagogue
than GIP in patients with type 2 diabetes
Mean (SE); N = 18.
Nauck MA, et al. ...
Therapeutic potential
GIP secretion is normal, but its action is
diminished
GLP-1 secretion is diminished, but its actio...
GLP-1 effects in humans
Understanding the natural role of incretins
Adapted from 1
Nauck MA, et al. Diabetologia 1993;36:7...
Change in body weight over time,
Exenatide with metformin
ITT population, N = 336 (Placebo, N = 113; exenatide 5 µg, N = 1...
Change in body weight over time,
Exenatide with sulphonylurea
ITT population, N = 377 (Placebo, N = 123; exenatide 5 µg, N...
Case studies
DR age 48 years
T2DM 14 years
Metformin, Gliclazide, Lantus 56 units
Weight 142Kg BMI 52 Kg/m2
HbA1C 7.6%
Fasting blood glucose 5.6mmol/l
Post prandial 8.8 mmol/l
Recurrent hypoglycaemia at night
Daily supper
Lantus switched to ...
Reduce Lantus
Correct Post prandial Glucose
Stop Supper
Weight loss after 6 months 23KG
HbA1C 6.8%
Lantus reduced to 22uni...
Case Study 2
EB 56 years House wife
Type 1 diabetes sine age 22years
Weight 112Kg BMI 48 Kg/m2
Also is hypertensive and ha...
HbA1C 8.6%
Add Metformin
Weight 106 Kg after three months
Lantus down to 50 units
HbA1C 8.0%
Metformin full dose
After thr...
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
D...
OSA ruled out
? Hypogonad
Testosterone 6.6 nmol/l
Testosterone replacement
After 4 months reduced Lantus to 32 units BD du...
Next Forum
Presentation of GAME and LOOKAHEAD
Case discussion
External Speaker (TBC)
Thank you!
Visit http://www.simplyweight.co.uk for more information
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
Diabesity (Diabetes and Obesity)
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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.

This Slideshow gives you insight to Diabesity

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  • DISCUSSION The development of type 2 diabetes involves defects in multiple organ systems which can be exacerbated by a number of factors, including diet and lifestyle, genetic causes and dysregulation of lipid and carbohydrate metabolism. Initially, insulin resistance is associated with hyperinsulinaemia and normal glucose tolerance. β -cell dysfunction manifests as impaired insulin production and failure to secrete sufficient insulin to compensate for insulin resistance. Eventually, demand for insulin outweighs β -cell capacity, leading to impaired glucose tolerance, escalating hyperglycaemia, and type 2 diabetes. Ramlo-Halsted BA, et al. Prim Care 1999;26:771–789.
  • DISCUSSION GLP-1 and GIP represent the dominant peptides responsible for the ‘incretin effect’. Bioactive forms of both GLP-1 and GIP are short-lived, with active plasma half-lives of ~2–7 minutes. Degradation is by dipeptidyl peptidase IV (DPP-IV). Drucker DJ. Diabetes Care 2003;26:2929–2940.
  • DISCUSSION The β -cell secretory response to glucose ingestion, as measured by increases in plasma insulin, was reduced in patients with type 2 diabetes. Patients with type 2 diabetes exhibited a greater β -cell secretory response than control subjects, as indicated by higher insulin secretion levels, during the 180-minute course of intravenous glucose infusion. BACKGROUND Differences in insulin response to oral and intravenous glucose administration, which are attributed to factors other than glucose itself, describe the incretin effect; the incretin effect appears to be reduced in patients with type 2 diabetes. Measured insulin and C-peptide responses to a 50 g oral glucose load and an isoglycaemic intravenous infusion. Additionally, an attempt was made to correlate incretin effects to GIP responses. Insulin measurements are shown here. Plasma insulin responses were studied for 14 patients with type 2 diabetes in this study and 8 metabolically healthy control subjects. Nauck MA, et al. Diabetologia 1986;29:46–52
  • DISCUSSION In patients with type 2 diabetes, GLP-1, in contrast to GIP, retains much of its insulinotropic activity. Both GIP and GLP-1 augmented insulin secretion in a dose-dependent fashion. With GLP-1 infusion, the maximum insulin effect in patients with type 2 diabetes approached 71% of the maximum insulin effect in subjects without diabetes (no statistical difference). With GIP infusion, the maximum insulin effect in patients with type 2 diabetes was 46% of the maximum insulin effect in subjects without diabetes ( P < 0.05). BACKGROUND The graphs represent immunoreactive insulin plotted against time (minutes) during hyperglycaemic clamp experiments with and without the infusion of synthetic human GIP or GLP-1. The data for the graphs of this slide were derived from a study of the insulinotropic effect of intravenously administered synthetic human GLP-1 and GIP (N = 9 for each patient group). Nauck MA, et al. J Clin Invest 1993;91:301–307
  • DISCUSSION Decreased GLP-1 secretion is found in patients with type 2 diabetes 1 ; however, it’s ability to stimulate glucose-dependent insulin secretion is preserved 1,2 . Another hormone, glucagon, is secreted by the α - cells of the pancreas and is elevated in type 2 diabetes. Glucagon stimulates hepatic glucose release. GLP-1 suppresses glucagon secretion from pancreatic α - cells in a glucose-dependent manner 3 , suppressing hepatic glucose output 4 . Therefore, incretin hormones, specifically GLP-1, have sparked interest in the treatment of type 2 diabetes 5 . 1 Nauck MA, et al. J Clin Invest 1993;91:301–307 2 Nauck M, et al. Diabetologia 1986;29:46–52 3 Nauck MA, et al. Diabetologia 1993;36:741–744 4 Larsson H, et al. Acta Physiol Scand 1997;160:413–422 5 Drucker DJ. Diabetes Care 2003;26:2929–2940 .
  • DISCUSSION This diagram demonstrates the GLP-1 effects in humans and the role these effects play in normal physiology. Upon the ingestion of food, plasma glucose levels increase postprandially. GLP-1 is secreted from intestinal L cells and provides a stimulus to the β -cells to release insulin in a glucose-dependent manner. When plasma glucose levels return to normal, the action of GLP-1 decreases 1 . GLP-1 also suppresses glucagon levels that are inappropriately elevated in patients with type 2 diabetes 1 . Lower glucagon levels leads to decreased hepatic glucose output 2 . In the stomach, GLP-1 slows the rate of gastric emptying, which reduces the rate at which meal-derived glucose appears in the circulation 3 . In the brain, GLP-1 promotes satiety and reduces appetite, which leads to a feeling of fullness and a reduction in food intake 4,5 . All these actions help maintain overall glucose homeostasis. 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.
  • DISCUSSION Progressive, dose-dependent reduction in weight was seen in exenatide-treated patients. At Week 30, weight changes from baseline were -2.8 ± 0.5 kg (10 µg), -1.6 ± 0.4 kg (5 µg) for exenatide treated patients ( P < 0.001 vs placebo 10 μ g and P < 0.001 vs placebo 5 μ g). No special weight loss programmes, exercise programmes, or standardised diets were used in the study. STUDY BACKGROUND A 30-week triple-blind, phase III study; patients with type 2 diabetes randomised to placebo, exenatide 5 or 10 µg BD with metformin, ITT, N = 336.
  • DISCUSSION Reduction in weight was seen in both exenatide arms, but greater weight loss was observed in the exenatide 10 µg BD arm. At Week 30, weight changes from baseline were -1.6 ± 0.3 kg (10 µg), -0.9 ± 0.3 kg (5 µg; not significantly different vs placebo) and -0.6 ± 0.3 kg (placebo). No special weight loss programmes, exercise programmes, or standardised diets were used in the study. STUDY BACKGROUND A 30-week triple-blind, phase III study; patients with type 2 diabetes randomised to placebo or exenatide 5 or 10 µg BD with sulphonylurea, ITT, N = 377.
  • 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 http://www.simplyweight.co.uk for more information

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