Postprandial Glucose Levels May be High Despite Normal HbA1c Levels
February 28, 2002 4 minutes read
Postprandial Glucose Levels May be High Despite Normal HbA1c Levels
Abstract & Commentary
Synopsis: Postmeal glucose levels may be seriously elevated despite a normal fasting plasma glucose and HbA1c levels of less than 7%.
Source: Bonora E, et al. Diabetes Care. 2001;24:2023-2029.
The objective of this study was to evaluate the relationship between the plasma glucose excursions with meals, the relations between levels at different times of the day, and these findings with their relationship to the level of the HbA1c in noninsulin-treated type 2 diabetics.
The UK Prospective Diabetes study made their therapeutic decisions based on the fasting glucose levels possibly assuming that good control in the fasting state would be associated with good control throughout the day. Bonora and colleagues wanted to know how frequently diabetic patients experience broad glucose excursions with meals. How much does fasting plasma glucose influence subsequent glucose levels during the day? How strongly are plasma glucose levels during the day interrelated? And, finally, is the HbA1c influenced more strongly by the fasting or nonfasting glucose?
They assessed 3 groups of patients: 1) outpatients at their clinic (n = 371; 1 daily plasma glucose profile, which consisted of fasting plasma glucose and HbA1c, plasma glucose levels 2 hours post breakfast and lunch, and a before dinner plasma glucose); 2) patients at home (n = 30; 5 daily glucose profiles, as in the first group on nonconsecutive days over 1 month); as well as 3) inpatients (n = 455; profiles of plasma glucose on the day of admission) were examined. Subjects had plasma/blood glucose assessment before and 2-3 hours after breakfast, lunch, and dinner. HbA1c was measured in all the patients.
After meals many subjects had glucose levels > 160 mg/dL and/or glucose excursions > 40 mg /dL. This was also found when HbA1c was satisfactory (< 7%). The coefficients of simple correlation among plasma/blood glucose at different times of the day ranged from 0.52-0.88. Correlations between HbA1c and plasma/blood glucose at different times of the day ranged from 0.44-0.67. Multiple regression analysis showed that premeal, but not postmeal, plasma/blood glucose levels were independent predictors of HbA1c.
These results suggest that: 1) the majority of non-insulin-treated type 2 diabetic patients have exaggerated plasma/blood glucose excursions with meals, and many of them have higher than recommended glucose concentration 2 hours after the meals; 2) plasma/blood glucose levels throughout the day are not as strongly interrelated as one might believe; and 3) HbA1c is more related to preprandial than postprandial plasma/blood glucose levels. These findings have potential implications for treatment and monitoring of metabolic control in type 2 diabetes.
Comment by Ralph R. Hall, MD, FACP
The UKPDS, which did not evaluate postprandial glucose levels, did not find a reduction in cardiovascular disease in patients with a reduction in fasting plasma glucose or reduced HbA1c. However, Bonora and Muggeo, 2 of the authors of the study, have also recently reviewed the growing number of studies that indicate that the plasma postmeal glucose (PMG) and post glucose load (PGL) blood glucose levels are more important indicators of cardiovascular risk than fasting blood glucose levels.1 Therefore, the results of this current study are important.
Bonora et al and others note that the cost of caring for patients with type 2 diabetes is much greater for the treatment of the chronic complications (nephropathy, neuropathy, and retinopathy and cardiovascular disease) than for the pharmacologic control of blood glucose.2 In light of this information, it behooves us to better monitor and control PMG levels if it can be accomplished without a significant loss of "quality of life." There are both dietary and pharmacologic means of improving PMG levels. Obviously, short-acting and oral insulin can be used for this purpose, however, the continuing weight gain may be a problem. Polyunsaturated fatty acids in the diet can improve PMG levels if maintained at levels of 8-10% of the body’s energy requirements.3 However, dietary treatment alone is not as effective as pharmacologic treatment.
The PMG is primarily influenced by hepatic glucose production associated with insulin resistance. The thiazolidinediones increase insulin sensitivity, which results in a decreased hepatic glucose production and an increase in glucose disposal. This dramatically improves post meal plasma/blood glucose levels. In addition, they improve the dyslipidemia associated with type 2 diabetes.4,5 They may constitute the best method of improving the total glucose profile of these patients. They were not used for treatment in the study of Bonora et al.
The alpha-glucosidase inhibitors lower postprandial glucose by interfering with intestinal absorption. They have to be given more frequently than the thiazolidinediones but are effective agents for treating postprandial glucose elevations.
One has to remember, however, that there are still no studies that have demonstrated, with certainty, that lowering the postprandial blood glucose will decrease the incidence of cardiovascular disease. In the Shichiri and colleagues study of nonobese type 2 diabetics, which attempted to have normal fasting blood glucose levels and 2-hour postprandial glucose below 180 mg/dL, did not reduce the incidence of cardiovascular disease but did dramatically lower the incidence of microvascular disease.6
Another interesting way to lower weight, fasting, postprandial glucose levels, and lipids is by using the antiobesity drug sibutramine that induces satiety and thermogenesis. To date, this interesting agent has significantly decreased weight and improved metabolic parameters in type 2 diabetic patients.7
We do have the tools to control both the fasting and postprandial plasma/blood glucose levels and the current evidence favors our attempting to do so!
Dr. Hall, Emeritus Professor of Medicine, University of Missouri-Kansas City School of Medicine, is Associate Editor of Internal Medicine Alert.
References
1. Bonora E, Muggeo M. Diabetologia. 2001;44:2107-2114.
2. Diabetes Care. 1998;21:296-309.
3. Krauss RM, et al. Circulation. 2000;102:2284-2299.
4. Gomez-Perez FJ, et al. Metabolism. 2002;51:44-51.
5. Miyazaki Y, et al. Diabetologia. 2001;44:2210-2219.
6. Shichiri M. Diabetes Care. 2000;23(Suppl 2):B21-B29.
7. Gokcel A, et al. Diabetes Care. 2001;24:1957-1960.
You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content