This Slideshow gives you insight on the Mix50 insulin
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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.
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
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
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.
