Recommended
Recommended
More Related Content
What's hot
What's hot (19)
Similar to Optimising glycaemic control and body weight
Similar to Optimising glycaemic control and body weight (20)
Recently uploaded
Recently uploaded (20)
Optimising glycaemic control and body weight
- 1. Optimising glycaemic control and body weight A Mix50 Insulin Experience Dr C Rajeswaran Consultant Physician Diabetes & Endocrinology Director. simplyweight www.simplyweight.co.uk
- 2. UKPDS: A 1% decrease in HbA1c is associated with a reduction in complications Stratton IM et al. BMJ 2000; 321: 405–412. Microvascular complications e.g. kidney disease and blindness * 37% * p<0.0001 ** p=0.035 1% HbA1c
- 3. UKPDS: A 1% decrease in HbA1c is associated with a reduction in complications Stratton IM et al. BMJ 2000; 321: 405–412. Microvascular complications e.g. kidney disease and blindness * 37% Amputation or fatal peripheral blood vessel disease* 43% * p<0.0001 ** p=0.035 1% HbA1c
- 4. UKPDS: A 1% decrease in HbA1c is associated with a reduction in complications Deaths related to diabetes*21% Stratton IM et al. BMJ 2000; 321: 405–412. Microvascular complications e.g. kidney disease and blindness * 37% Amputation or fatal peripheral blood vessel disease* 43% * p<0.0001 ** p=0.035 1% HbA1c
- 5. UKPDS: A 1% decrease in HbA1c is associated with a reduction in complications Deaths related to diabetes*21% Stratton IM et al. BMJ 2000; 321: 405–412. Microvascular complications e.g. kidney disease and blindness * 37% Amputation or fatal peripheral blood vessel disease* 43% Heart attack*14% * p<0.0001 ** p=0.035 1% HbA1c
- 6. UKPDS: A 1% decrease in HbA1c is associated with a reduction in complications Deaths related to diabetes*21% Stratton IM et al. BMJ 2000; 321: 405–412. Microvascular complications e.g. kidney disease and blindness * 37% Amputation or fatal peripheral blood vessel disease* 43% 12% Stroke** Heart attack*14% * p<0.0001 ** p=0.035 1% HbA1c
- 7. β-cell dysfunction, a core defect in T 2 Diabetes • Genetic and environmental pathophysiology • One of the two core defects in Type 2 diabetes • Impaired ability of β-cells to compensate for insulin resistance • Reduced ability of β-cells to secrete insulin • Therapeutic strategies should address both defects Insulin resistance β-cell dysfunction Type 2 diabetes + = Del Prato S & Marchetti P. Diabetes Technol Ther. 2004; 6:719–731.
- 10. ATP-sensitive K+ channel Insulin Ca2+ -dependent K+ channel Na+ channel Cl- channel UK SmPC Nov 2006’
- 12. Adapted from Riddle et al. Diabetes Care. 1990;13:676-686. Contribution of Postprandial Glucose (PPG) to 24 hour hyperglycaemic profile Mainly target Basal hyperglycaemia: Metformin Secretagogues TZD’s Basal insulin Mainly target Postprandial hyperglycaemia: Repaglinide Nateglinide Acarbose Rapid-acting insulin Glucose(mmol/l) 10.0 5.0 0 0600 1200 Hours 1800 0000 0600 7.5 12.5 2.5 Basal Hyperglycemia Postprandial Hyperglycemia
- 14. As patients get closer to HbA1c target, the need to manage PPG increases Monnier L, et al. Diabetes Care. 2003;26:881-885. 30% 40% 45% 70% 60% 55% >10.2 10.2-9.3 9.2-8.5 8.4-7.3 <7.3 %Contribution toHbA1c HbA1c Range (%) 0 20 40 60 80 100 Fasting Plasma Glucose (FPG) Post Prandial Glucose (PPG)
- 15. 50% 50% As patients get closer to HbA1c target, the need to manage PPG increases Monnier L, et al. Diabetes Care. 2003;26:881-885. 30% 40% 45% 70% 60% 55% >10.2 10.2-9.3 9.2-8.5 8.4-7.3 <7.3 %Contribution toHbA1c HbA1c Range (%) 0 20 40 60 80 100 Fasting Plasma Glucose (FPG) Post Prandial Glucose (PPG)
- 16. As patients get closer to HbA1c target, the need to manage PPG increases Monnier L, et al. Diabetes Care. 2003;26:881-885. 30% 40% 45% 50% 70% 60% 55% 50% 70% 30% >10.2 10.2-9.3 9.2-8.5 8.4-7.3 <7.3 %Contribution toHbA1c HbA1c Range (%) 0 20 40 60 80 100 Fasting Plasma Glucose (FPG) Post Prandial Glucose (PPG)
- 17. Insulin and body weight Weight gain appears unavoidable when patients with Type 2 diabetes are commenced on insulin Body weight increases by 2Kg for each percentage point decrease in HbA1C during the first year1 Gain in weight mainly represents an increase in fat mass, which enhances insulin resistance and increases the risk of obesity related complications. Insulin in T2 DM is aimed at inhibition of hepatic glucose output and improvement of peripheral glucose utilisation 1.Makimattila et al Diabetologia 1999;42;406-412
- 18. Insulin and weight • Reduced glyosuria • Anabolic action of insulin • Fluid retention • Hypoglycaemia and increased calorie consumption • Excess insulin administration
- 19. Hyperinsulinaemia should be avoided to prevent weight gain and optimise glycaemic control GAME regimen: insulin aspart and glimepride HbA1c decreasedf rom 9.4 to 7.0 and net change in weight 4-5 Kg less than predicted.
- 20. Mix 50 Advantages The TDS regime uses appropriate dose of prandial insulin (to improve glycaemic control) in conjunction with a reduction in the total daily dose of insulin( facilitating weight loss) while maintaining adequate basal insulin therapy (given TDS) over a 24 hour period Absorption is better when the dose is split and prevents stacking Simple dosage regime and single delivery device
- 21. Mix 50 Once a day With biggest meal along with Metformin Substituting Mix30 with Mix 50 reduced HbA1C by 0.49%, whereas patients on Mix 30 had a mean Hba1c increase of 0.33%.1 An alternate regime for initiation of insulin with lesser hypoglycaemic episodes 1.Hui et al Comparitive analysis of twice daly insulin regimes during the month of Ramadan in patients with Type 2 diabetes Diabetic Medicine,24(suppl 1), 79-199
- 22. Titration Total insulin dose - 10% 3 = Dose of Mix 50
- 23. Mix 50 case studies NJ Asian 54 years with T2DM
- 24. Summary • As patients Get Closer to HbA1c target (≤8.0%) post prandial glucose becomes the most significant contributing factor • Whilst trying to optimise glycaemic control, increase in body weight should be avoided . • Mix 50 is a credible option in a select group of patients both as once a day and TDS regime
- 25. Thank you! Visit http://www.simplyweight.co.uk for more information
Editor's Notes
- Reducing HbA 1c is a key to addressing other potential complications. CORE SLIDE Observational data based on the UKPDS has demonstrated the association of good blood glucose control with a reduced burden of microvascular and macrovascular complications. 1 Link to next slide: How are we doing currently? Reference Stratton IM et al . BMJ 2000; 321 : 405–412.
- Reducing HbA 1c is a key to addressing other potential complications. CORE SLIDE Observational data based on the UKPDS has demonstrated the association of good blood glucose control with a reduced burden of microvascular and macrovascular complications. 1 Link to next slide: How are we doing currently? Reference Stratton IM et al . BMJ 2000; 321 : 405–412.
- Reducing HbA 1c is a key to addressing other potential complications. CORE SLIDE Observational data based on the UKPDS has demonstrated the association of good blood glucose control with a reduced burden of microvascular and macrovascular complications. 1 Link to next slide: How are we doing currently? Reference Stratton IM et al . BMJ 2000; 321 : 405–412.
- Reducing HbA 1c is a key to addressing other potential complications. CORE SLIDE Observational data based on the UKPDS has demonstrated the association of good blood glucose control with a reduced burden of microvascular and macrovascular complications. 1 Link to next slide: How are we doing currently? Reference Stratton IM et al . BMJ 2000; 321 : 405–412.
- Reducing HbA 1c is a key to addressing other potential complications. CORE SLIDE Observational data based on the UKPDS has demonstrated the association of good blood glucose control with a reduced burden of microvascular and macrovascular complications. 1 Link to next slide: How are we doing currently? Reference Stratton IM et al . BMJ 2000; 321 : 405–412.
- Beta cell dysfunction remains a core defect in the pathophysiology of Type 2 diabetes alongside insulin resistance. Therapeutic strategies should therefore address both the reduced ability of -cells to secrete insulin as well as improving insulin resistance.
- Repaglinide stimulates insulin secretion from beta-cells only when glucose is also present. This is in contrast with sulphonylureas, which induce insulin secretion even in the absence of glucose. In patients with Type 2 diabetes, stimulation of insulin secretion in the absence of glucose may increase the risk of hypoglycaemia. Repaglinide is the first prandial glucose regulator and has the properties which define the class. Both repaglinide and sulphonylureas act to stimulate insulin secretion by closing ATP-sensitive potassium ion channels in the beta-cell membrane. However, studies have shown that the PGRs and SUs have different patterns of binding to sites on the cell membrane with repaglinide acting on a distinct site for its primary activity being different to that of SUs, and also having different effects on beta-cell activity: Unlike SU’s; Repaglinide does not inhibit the biosynthesis of insulin or other proteins Repaglinide does not directly promote exocytosis of insulin Repaglinide does not stimulate insulin secretion in the absence of glucose Repaglinide is effective in metabolically stressed cells Repaglinide has a fast onset and offset of action, minimising beta-cell stimulation The mechanism of action of repaglinide (and PGRs) is therefore fundamentally different from that of the sulphonylureas.
- In order to achieve overall glycemic control, it is important to target both FPG (basal) and PPG (peaks). A combination of metformin and a postprandial regulator or acarbose therefore present a logical combination strategy. Pharmacological agents that target PPG more specifically are highlighted in blue. Graph adapted from Riddle MC. Evening insulin strategy. Diabetes Care . 1990;13:676-686
- As Patients Get Closer to HbA1C Goal, the Need to Successfully Manage PPG Significantly Increases Postprandial glycemic excursions become more predominant in patients with good control of fasting plasma glucose. Therefore, treatment should focus on both FPG and PPG excursions in order to reach and maintain HbA1C targets. Adapted from Monnier L, Lapinski H, Collette C. Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycemia of Type 2 diabetic patients: variations with increasing levels of HBA(1c). Diabetes Care . 2003;26:881-885.
- As Patients Get Closer to HbA1C Goal, the Need to Successfully Manage PPG Significantly Increases Postprandial glycemic excursions become more predominant in patients with good control of fasting plasma glucose. Therefore, treatment should focus on both FPG and PPG excursions in order to reach and maintain HbA1C targets. Adapted from Monnier L, Lapinski H, Collette C. Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycemia of Type 2 diabetic patients: variations with increasing levels of HBA(1c). Diabetes Care . 2003;26:881-885.
- As Patients Get Closer to HbA1C Goal, the Need to Successfully Manage PPG Significantly Increases Postprandial glycemic excursions become more predominant in patients with good control of fasting plasma glucose. Therefore, treatment should focus on both FPG and PPG excursions in order to reach and maintain HbA1C targets. Adapted from Monnier L, Lapinski H, Collette C. Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycemia of Type 2 diabetic patients: variations with increasing levels of HBA(1c). Diabetes Care . 2003;26:881-885.