8/8/2019 Postprandial Glucose in Diabetes Time for Action.6

http://slidepdf.com/reader/full/postprandial-glucose-in-diabetes-time-for-action6 1/2

Editorial 

Postprandial Glucose inDiabetes: Time for Action

  Mohsen Eledrisi, MD

The number of patients with type 2 diabetes is increasingat alarming rates in developed and developing countries.1

Many patients with diabetes are not aware of the disease and 

several years often elapse before the diagnosis is made. The

development of type 2 diabetes is characterized by insulin

resistance and a progressive decline in -cell function leading

to reduced insulin secretion. However, metabolic abnormal-

ities start before the development of diabetes mainly in the

form of postprandial hyperglycemia due to loss of first phase

insulin secretion, decreased insulin sensitivity and decreased 

suppression of hepatic glucose production.2,3 Postprandial hy-

 perglycemia is associated with deficiencies in several sub-

stances such as amylin, glucagon-like peptide-1 (GLP-1), and glucose-dependent gastric inhibitory peptide (GIP).4,5 In ad-

dition, it has been shown that there is a gradual loss of post-

 prandial glycemic control that precedes a stepwise deteriora-

tion in fasting glucose levels with worsening diabetes.6

The review by Tibaldi7 on postprandial hyperglycemia in

 patients with type 2 diabetes is important and timely. Epide-

miological data support the role of postprandial hyperglyce-

mia in the development of cardiovascular disease and overall

mortality in patients with impaired glucose tolerance and pa-

tients with diabetes.8–11 However, data on the effect of con-

trolling postprandial hyperglycemia on cardiovascular out-

comes in patients with type 2 diabetes are limited. It is

important to note that the commonly cited large randomized 

clinical trial in this context, the STOP-NIDDM,12 has eval-

uated patients with impaired glucose tolerance—not diabetes.

The other cited study13 was a drug-efficacy and safety trial;

cardiovascular disease was not a primary outcome. The meta-

analysis14 that showed a favorable effect of acarbose on car-

diovascular disease had major issues in its statistical meth-

odology.15 As noted, data on glinides focused on carotid 

intimal media thickness as a surrogate marker; further studies

with attention on clinical outcomes are needed.

So, from the clinical point of view, is it important for the

 physician to monitor postprandial glucose levels? The answer 

should be: Yes. When treating patients with diabetes, clini-

cians strive to achieve near-normal glycemic control to help

reduce the development and progression of long-term com-

  plications. Glycemic targets in patients with diabetes have

traditionally focused on glycated hemoglobin (HbA1c) and 

fasting glucose levels. However, in the last several years, the

role of postprandial hyperglycemia has received attention and 

recent professional guidelines have appreciated this as an

additional target. This target is defined as a 2-hour postmeal

glucose of less than 180 mg/dL as recommended by the Amer-

ican Diabetes Association, while the American Association

of Clinical Endocrinologists and the International Diabetes

Federation recommend a level of less than 140 mg/dL. Post-

 prandial hyperglycemia is observed frequently in patients with

type 1 and type 2 diabetes and can occur even when the

overall metabolic control appears to be reasonable.16,17 The

contribution of postprandial glucose to overall glycemic con-

trol becomes more prominent as HbA1c levels decrease to-

wards the target. Postprandial glucose contributes to overall

hyperglycemia by about 40% when HbA1c levels are more

than 9.3% and by about 70% when levels are 7.3%.18 In

fact, achieving normal fasting glucose levels can still be as-sociated with HbA1c levels that are over the desired target.19

This reinforces the proposition that control of fasting hyper-

glycemia is necessary but usually not adequate for achieving

HbA1c goals, requiring control of postprandial glucose. This

could have significant clinical implications. It is important to

remember that reducing the HbA1c level by only 1% can

decrease the risk of microvascular complications by 25% and 

the risk of any diabetes-related end point by 21%.20

In conclusion, postprandial hyperglycemia has an impor-

tant role in the management of diabetes. Data on the clinical

  benefits of approaches that specifically target postprandial

glucose are needed. Meanwhile, in addition to followingHbA1c and fasting glucose levels, clinicians should consider 

monitoring postprandial glucose levels, particularly in pa-

tients who are getting close to their glycemic targets.

References1. Wild S, Roglic G, Green A, et al. Global prevalence of diabetes esti-

mates for the year 2000 and projections for 2030. Diabetes Care 2004;27:1047–1053.

2. Weyer C, Bogardus C, Mott DM, et al. The natural history of insulin

secretory dysfunction and insulin resistance in the pathogenesis of type

2 diabetes mellitus. J Clin Invest  1999;104:787–794.

3. Pratley RE, Weyer C. The role of impaired early insulin secretion in the

 pathogenesis of type II diabetes mellitus. Diabetologia 2001;44:929– 945.

4. Fineman MS, Koda JE, Shen LZ, et al. The human amylin analog,

  pramlintide, corrects postprandial hyperglucagonemia in patients with

type 1 diabetes. Metabolism 2002;51:636–641.

5. Holst JJ, Gromada J. Role of incretin hormones in the regulation of 

insulin secretion in diabetic and nondiabetic humans. Am J Physiol 

  Endocrinol Metab 2004;287:E199–E206.

6. Monnier L, Colette C, Dunseath GJ, et al. The loss of postprandial

glycemic control precedes stepwise deterioration of fasting with wors-

ening diabetes. Diabetes Care 2007;30:263–269.

7. Tibaldi J. The importance of postprandial glucose levels as a target for 

glycemic control in type 2 diabetes. Southern Med J  2009;102:60–66.

From the Division of Endocrinology and Metabolism, Department of InternalMedicine, National Guard Medical Center, Dammam, Saudi Arabia.

Reprint requests to Mohsen Eledrisi, MD, PO Box 4616, Dammam, SaudiArabia 31412. Email: eledrisim@ngha.med.sa

Accepted August 13, 2008.

Copyright © 2009 by The Southern Medical Association

0038-4348/02000/10200-0010

10 © 2009 Southern Medical Association

8/8/2019 Postprandial Glucose in Diabetes Time for Action.6

http://slidepdf.com/reader/full/postprandial-glucose-in-diabetes-time-for-action6 2/2

8. Cavalot F, Petrelli A, Traversa M, et al. Postprandial blood glucose is a

stronger predictor of cardiovascular events than fasting blood glucose in

type 2 diabetes mellitus, particularly in women: lessons from the San

Luigi Gonzaga Diabetes Study. J Clin Endocrinol Metab 2006;91:813– 

819.

9. Sorkin JD, Muller DC, Fleg JL, et al. The relation of fasting and 2-h

 postchallenge plasma glucose concentrations to mortality: data from the

Baltimore Longitudinal Study of Aging with a critical review of the

literature. Diabetes Care 2005;28:2626–2632.

10. DECODE Study Group, the European Diabetes Epidemiology Group.

Glucose tolerance and cardiovascular mortality: comparison of fasting

and 2-hour diagnostic criteria. Arch Intern Med  2001;161:397– 405.

11. Levitan EB, Song Y, Ford ES, et al. Is nondiabetic hyperglycemia a risk 

factor for cardiovascular disease? A meta-analysis of prospective stud-

ies. Arch Intern Med  2004;164:2147–2155.

12. Chiasson JL, Josse RG, Gomis R, et al; STOP-NIDDM Trial Research

Group. Acarbose treatment and the risk of cardiovascular disease and 

hypertension in patients with impaired glucose tolerance: the STOP-

 NIDDM trial. JAMA 2003;290:486–494.

13. Johnston PS, Lebovitz HE, Coniff RF, et al. Advantages of alpha-glu-

cosidase inhibition as monotherapy in elderly type 2 diabetic patients. J Clin Endocrinol Metab 1998;83:1515–1522.

14. Hanefeld M, Cagatay M, Petrowitsch T, et al. Acarbose reduces the risk 

for myocardial infarction in type 2 diabetic patients: meta-analysis of 

seven long- term studies. Eur Heart J  2004;25:10–16.

15. Van de Laar FA, Lucassen PL. No evidence for a reduction of myocar-

dial infarctions by acarbose. Eur Heart J  2004;25:1179; author reply

1179–1180.

16. Bonora E, Corrao G, Bagnardi V, et al. Prevalence and correlates of 

 post-prandial hyperglycaemia in a large sample of patients with type 2

diabetes mellitus. Diabetologia 2006;49:846–854.

17. Erlinger TP, Brancati FL. Postchallenge hyperglycemia in a national

sample of U.S. adults with type 2 diabetes. Diabetes Care 2001;24:1734–1738.

18. Monnier L, Lapinski H, Colette C. Contributions of fasting and post-

 prandial 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.

19. Woerle HJ, Neumann C, Zschau S, et al. Impact of fasting and post-

 prandial glycemia on overall glycemic control in type 2 diabetes Impor-

tance of postprandial glycemia to achieve target HbA1c levels. Diabetes

 Res Clin Pract  2007;77:280–285.

20. UK Prospective Diabetes Study Group. Intensive blood-glucose control

with sulphonylureas or insulin compared with conventional treatment

and risk of complications in patients with type 2 diabetes (UKPDS 33).

 Lancet  1998;352:837–853.

  Please see “Importance of Postprandial Glucose

 Levels as a Target for Glycemic Control in Type 2

 Diabetes” on page 60 of this issue.

“Music expresses that which cannot be said and onwhich it is impossible to be silent.” 

 —Victor Hugo

Editorial

 Southern Medical Journal • Volume 102, Number 1, January 2009 11