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Human Nutrition and Metabolism

Postprandial Hyperglycemia and Insulin Sensitivity Differ among Lean Young Adults of Different Ethnicities

S. Dickinson^*, S. Colagiuri, E. Faramus, P. Petocz^** and J. C. Brand-Miller

^* Human Nutrition Unit, School of Molecular and Microbial Biosciences, University of Sydney, Sydney, Australia; Department of Endocrinology, Diabetes and Metabolism, Prince of Wales Hospital, Sydney, Australia; and ^** Department of Mathematical Sciences, University of Technology, Sydney, Australia

¹To whom correspondence should be addressed. E-mail: s.dickinson{at}mmb.usyd.edu.au.

	ABSTRACT

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Both postprandial hyperglycemia and insulin resistance (IR) have implications for the development of cardiovascular disease. The present study was designed to examine differences in postprandial glycemia and insulin sensitivity among young adults of different ethnic origins. Lean, healthy subjects (n = 60) from five ethnic groups [20 European Caucasians, 10 Chinese, 10 South East (SE) Asians, 10 Asian Indians and 10 Arabic Caucasians] were matched for age, body mass index, waist circumference, birth weight and current diet. A 75-g white bread carbohydrate challenge was fed to assess postprandial glycemia and insulinemia. Insulin sensitivity was assessed in three groups by the euglycemic-hyperinsulinemic clamp and in all subjects by homeostasis model assessment (HOMA) modeling. Postprandial hyperglycemia (incremental area under the curve) and insulin sensitivity (M-value) both showed a twofold variation among the groups (P < 0.001) and were significantly related to each other (R² = 56%, P < 0.001). Young SE Asians had the highest postprandial glycemia and lowest insulin sensitivity, whereas European and Arabic Caucasian subjects were the most insulin sensitive and carbohydrate tolerant. These findings suggest that IR is evident even in lean, young adults of some ethnic groups and is associated with significant increases in postprandial glycemia and insulinemia in response to a realistic carbohydrate load.

KEY WORDS: • carbohydrate tolerance • insulin resistance • glycemic and insulin responses • postprandial hyperglycemia

	INTRODUCTION

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Recent studies have documented the importance of postprandial hyperglycemia as a risk factor for all-cause and cardiovascular mortality in the normal population. In this context, the blood glucose concentration 2-h after a standard 75-g glucose tolerance test has been used as a measure of postprandial glycemia. In the Hoorn study (1 ), for example, there was a significant association between the 8-y risk of cardiovascular death and 2-h postload glucose in subjects with normal fasting glucose levels, even after adjustment for known risk factors. The DECODE study was a meta-analysis of >20 studies that clearly demonstrated that the increased rates of mortality and morbidity associated with high blood glucose levels were not confined solely to people with diabetes (2 ). Observational studies have documented an independent association between dietary glycemic load (carbohydrate content x glycemic index) and relative risk of coronary infarct (3 ).

High blood glucose concentration appears to be damaging to the endothelium through a variety of mechanisms. In nondiabetic individuals, high glucose levels are associated with increased thickness of the carotid intima media, an established predictor of coronary infarct. High glucose levels interfere with vasodilation by inhibiting nitrous oxide synthase and reducing the production of nitrous oxide (4 ). Excessive postprandial hyperglycemia is also directly "toxic" to the endothelium, increasing protein glycation, generating oxidative stress and causing impaired endothelial function (5 –7 ). Hyperinsulinemia itself, a consequence of hyperglycemia, may also be pathogenic (8 ,9 ). Insulin resistance (IR)² and compensatory hyperinsulinemia are implicated in the development of dyslipidemia (high VLDL cholesterol, high triglycerides and low HDL cholesterol), hypertension, impaired fibrinolysis and other abnormalities that contribute to increased risk of coronary heart disease (10 –12 ).

Insulin resistance may be the underlying cause of impaired glucose tolerance (13 ,14 ). Although the exact mechanisms that cause IR are not fully understood, both environmental and genetic factors are involved. Insulin resistance has been linked with one or more genes (15 ) with varying frequencies among different ethnic groups. Pima Indians and Asian Indians are more insulin resistant than European Caucasians of similar age and body mass index (BMI), as assessed by the euglycemic-hyperinsulinemic clamp (16 ,17 ). In most studies, however, the subjects have been middle-aged and/or overweight, with IR already well developed. Studies in young lean subjects are required to determine whether reduced insulin sensitivity and postprandial hyperglycemia/hyperinsulinemia can be present without overt signs of the metabolic syndrome.

The aim of the present study was to examine differences in postprandial glycemia and insulinemia after a white bread meal and their relation to insulin sensitivity and IR among young adults of different ethnic origins. Insulin sensitivity was assessed by the euglycemic-hyperinsulinemic clamp in three ethnic groups and by homeostasis model assessment (HOMA) modeling in all five.

	SUBJECTS AND METHODS

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Subjects.

Volunteers (n = 60) from five different ethnic groups were recruited from the student population at the University of Sydney. They included 20 European Caucasian, 10 Chinese, 10 South East (SE) Asian (2 Thai, 8 Vietnamese), 10 Indian and 10 Arabic Caucasian subjects who satisfied the following selection criteria: 18–35 y of age, moderate physical activity, BMI between 18 and 25 kg/m², waist-to-hip ratio (WHR) < 0.9 in men and < 0.8 in women, birth weight > 2.75 kg, and no medication that could interfere with glucose tolerance.

All but eight of the subjects were Australian-born (one subject was born in Canada and 7 in Hong Kong). Birth weights were reported by the subject’s mother, but seven birth weights (4 European Caucasian and 3 Chinese subjects) were not available. The study was approved by the Ethical Review Committee of the University of Sydney and the Eastern Sydney Area Health Service. All subjects gave written, informed consent.

Carbohydrate tolerance test.

Subjects from all five ethnic groups consumed a 170-g portion of regular white bread (Sunblest, Tip Top Bakeries, Chatswood, NSW, Australia) providing 75 g of available carbohydrate as calculated using the manufacturer’s data. Two capillary blood samples were taken from fasting subjects by finger-prick (-5 and 0 min), and the meal was consumed within 12 min. Water was consumed so that the total meal volume equaled 600 mL. Further capillary blood samples were taken at 15-min intervals during h 1 and at 30 min during h 2. Samples (700 µL) were collected into heparinized Eppendorf tubes, immediately centrifuged at 6000 x g for 1 min and the plasma drawn off and stored at -20°C before being assayed for glucose and insulin.

Euglycemic-hyperinsulinemic clamp.

Whole-body insulin sensitivity was assessed using the euglycemic-hyperinsulinemic clamp technique in three ethnic groups. Fifteen subjects from the European Caucasian group (6 men, 9 women), nine subjects from the Chinese group (3 men, 6 women) and seven subjects from the SE Asian group (3 men, 4 women) participated. The remaining subjects from those ethnic groups either declined participation (n = 8) or could not be cannulated (n = 1). Subjects fasted for 10 h before testing. Two intravenous cannulae were inserted into the arms of each subject. One cannula was kept patent with a slow saline infusion and was used for periodic blood sampling. Glucose (250 g/L dextrose solution) and unmodified human insulin (Actrapid, Novo Nordisk, Copenhagen, Denmark) were infused simultaneously through the other cannula. Using the methods outlined by Pacini and Bergman (18 ), the clamp was controlled using the PACBERG computer software program. After the collection of three basal blood glucose samples from fasting subjects (-30, -15 and 0 min), insulin was infused at 40 mU/(m² · min) according to the subject’s body surface area. Plasma insulin concentrations were increased to the steady state (500 pmol/L) by an Imed 800 pump (Milton Trading Estate, Abingdon, UK). To clamp the fasting blood glucose concentration throughout the test, the dextrose infusion rate was adjusted every 5 min using an AVI 470 infusion pump (3M, St. Paul, MN) based on blood glucose concentration readings. The infusion of glucose and insulin was continued for 2 h. The amount of glucose required to maintain euglycemia (in mmol/min) during the steady state in the last 30 min of the clamp was calculated. Dividing the mean value of glucose infusion in mmol/min by the subject’s surface area in m² gave a measure of the individual’s insulin sensitivity (M-value). Additional blood samples (2 mL) were collected before the test at -30, -15 and 0 min to assess fasting insulin concentrations. Samples were also taken at 10-min intervals during the steady-state period of the clamp to calculate the final insulin concentration.

Biochemistry.

Plasma collected from the 75-g carbohydrate challenge was assayed for glucose on a Cobas Fara single unit centrifugal analyzer (Roche Diagnosta, Basel, Switzerland) using the hexokinase glucose-6-phosphate dehydrogenase enzymatic method. The intra-assay CV was 0.5% and the interassay CV was 1.1% for the glucose assays. Blood samples collected during the euglycemic clamp were assayed for glucose at 5-min intervals using a HemoCue B-glucose analyzer (HemoCue, Ångelholm, Sweden). The intra-assay CV for glucose was 3.5% at 4.5 mmol/L. The interassay CV was 2.5% at 5.5 mmol/L.

Plasma insulin collected during the carbohydrate tolerance test was assayed using the Coat-a-Count Insulin kit protocol (Diagnostic Products, Los Angeles, CA). The mean intra-assay CV for the insulin assay was 3.0% and the mean interassay CV was 3.5%. Plasma collected during the clamp was assayed for insulin by the Department of Endocrinology at Royal Prince of Wales Hospital using the Beckman Access Ultrasensitive Insulin method (Beckman Instruments, Fullerton, CA). The mean interassay CV for the insulin assay was 4.0% and the mean intra-assay CV was 2.6%.

Diet and anthropometry.

Subjects were asked to record all food and beverages consumed for three consecutive days (included one weekend day). Mean daily macronutrient intake, total energy intake and the percentage of energy intake from fat, carbohydrate and protein were calculated using the Foodworks computer program (Version 2.0, Xyris Software, Highgate Hill, Queensland, Australia). Five of the 60 subjects (3 European Caucasians and 2 Chinese) did not complete a 3-d food record. All anthropometric measurements were performed in duplicate by one operator. Waist circumference was measured as the minimum measurement between the xiphoid process and the umbilicus; hip circumference was measured as the most protruding points of the greater trochanters. BMI (kg/m²) and WHR were calculated.

Data and statistical analysis.

The incremental areas under the curve (iAUC) for glucose and insulin were calculated for the carbohydrate tolerance test with the fasting level as baseline. A power analysis based on previous findings showed that 10 subjects in each group gave a power of at least 80% (ß = 0.80) to detect a difference in glucose AUC of 100 U ( = 0.05). The HOMA model was used to assess IR using the formula: fasting insulin (pmol/L) x fasting glucose (mmol/L)/22.5 (19 ). Because the ratio of men to women in each group varied, all comparisons were adjusted for sex differences. Correlation analyses were conducted using a general linear model (one-way ANOVA for group differences with various variables as covariates, e.g., BMI, WHR). Post-hoc comparisons among groups were made using Dunnett’s adjustment to the significance level for multiple comparisons. Regression analyses were carried out to model the M-value in terms of other variables, with a stepwise analysis used to identify potentially useful predictors. All analyses were performed with the Minitab statistical package, version 13.32 (Minitab, State College, PA)

	RESULTS

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Subject characteristics.

After adjustment for sex differences, the five ethnic groups were comparable in age, BMI, waist circumference and birth weight (Table 1 ). European Caucasian subjects were not significantly different from any other group. The Arabic group had the highest WHR, which was higher than that of the Chinese group (0.82 vs 0.75, respectively, P = 0.04, adjusted for sex differences). There were no differences in nutrient intakes (Table 2 ). Total fat and saturated fat consumption tended to be higher in the Arabic group compared with others (P = 0.07 for total fat and 0.06 for saturated fat). All subjects with complete dietary records consumed at least 200 g carbohydrate/d.

On the morning of the carbohydrate tolerance test, fasting glucose concentrations did not differ among the groups but fasting insulin was higher in the SE Asian and Indian groups than in the others (P < 0.001, Table 3 ). Postprandial metabolic responses to the bread meal (75 g carbohydrate) varied markedly among the groups (Fig. 1 , Table 3 ). SE Asian and Chinese subjects showed significantly greater glycemia, with the incremental AUC 100 and 50% higher, respectively, than the European Caucasians (P < 0.001). Plasma glucose concentrations at 120 min were also elevated in the SE Asian subjects; 4 of the 10 subjects had concentrations > 7.8 mmol/L (the cut-off level considered indicative of impaired glucose tolerance during a 75-g glucose tolerance test). Postprandial insulin responses also varied among the ethnic groups (P < 0.001). Compared with European Caucasians, the incremental insulin AUC was 2.7 times higher in the Indian group, 2.4 times higher in the SE Asian group, 90% higher in the Chinese group and 25% higher in the Arabic group (Table 3) .

View larger version (26K): [in this window] [in a new window]   FIGURE 1 Postprandial glucose and insulin responses to a 75-g carbohydrate portion of white bread in Caucasian vs. South East (SE) Asian(panel A), Chinese (panel B), Indian (panel C) and Arabic (panel D) subjects. Values are means ± SEM. The following AUC differed from those of Caucasians: (A) SE Asian, glucose AUC, P < 0.001, insulin AUC, P < 0.01; (B) Chinese, glucose AUC, P < 0.05; (C) Indian, insulin AUC, P < 0.001.

Fasting glucose and insulin concentrations did not differ among the three groups tested on the morning of the euglycemic-hyperinsulinemic clamp. The M-value of the European Caucasian group was 100% higher than the that of the SE Asian group and 40% higher than the Chinese group (P < 0.001, Table 4 , Fig. 2 ). The degree of IR was also predicted by HOMA modeling (HOMA-IR) using the fasting glucose and insulin concentrations recorded on the day of the bread test (Fig. 2 , Table 3 ). Insulin sensitivity differed among the groups (P = 0.001). The European Caucasians were the most insulin sensitive (HOMA-IR = 13.1 ± 0.8 mmol/L · pmol/L) and the SE Asians were the least (HOMA-IR = 21.1 ± 2.1 mmol/L · pmol/L).

View larger version (40K): [in this window] [in a new window]   FIGURE 2 Insulin sensitivity determined by the euglycemic-hyperinsulinemic clamp (M-value) in (A) Caucasian vs. Chinese and SE Asian subjects. Values are means ± SEM. The following differed from Caucasians: SE Asian, P < 0.01; Indian, P < 0.01: Chinese, P < 0.05; South East (SE) Asian, P < 0.001. (B) The homeostasis model assessment (HOMA) in SE Asian, Indian, Arabic, Chinese and Caucasian subjects.

Regression analysis indicated that the M-value could be predicted from the postprandial glucose AUC and HOMA-IR (R² = 56%, P < 0.001) but not by other variables. Postmeal 2-h glucose and glucose AUC were predicted by ethnic group (P < 0.001), and marginally by BMI (P = 0.06) but not by WHR (adjusted for sex differences). In contrast, fasting glucose was predicted by WHR (P < 0.01). Fasting insulin, 2-h insulin and insulin AUC were predicted by ethnic group and BMI (P < 0.01).

	DISCUSSION

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
The novel finding in the present study is that lean, young adults of Thai, Vietnamese (i.e., SE Asian) and Chinese origin displayed marked postprandial hyperglycemia and hyperinsulinemia compared with matched Caucasian subjects. This corresponded to reduced insulin sensitivity as determined by the euglycemic-hyperinsulinemic clamp and HOMA modeling, although the level of insulin sensitivity was still within the normal range for healthy individuals. The differences among ethnic groups were evident despite similarities in age (mean 20–22 y), BMI (20–23 kg/m²), waist circumference (72–82 cm), birth weight (3.2–3.5 kg) and diet. The findings suggest that reduced insulin sensitivity and impaired carbohydrate tolerance might precede the development of other features of the metabolic syndrome. Chronic postprandial hyperglycemia and/or hyperinsulinemia may therefore be the only phenotypic evidence of reduced insulin sensitivity for many years. Abnormalities in fat deposition and blood lipids characteristic of the IR syndrome may develop as a consequence of postprandial hyperglycemia or hyperinsulinemia. Excessive glycemia and/or insulin demand on a chronic basis may eventually affect insulin secretory capacity and precipitate type 2 diabetes.

Obesity, particularly visceral adiposity, is associated with IR and often assumed to be causative. According to the "lipid supply" hypothesis, higher concentrations of fatty acids resulting from higher fat intake or higher visceral or intramuscular fat, inhibit carbohydrate oxidation and thereby produce IR (20 ). In the present study, however, the Arabic Caucasian subjects had the highest measure of abdominal fat (as judged by WHR) but were among the most insulin sensitive. Furthermore, the Arabic Caucasian group reported the greatest fat intake (36% of energy vs. only 28% in the European Caucasian group), but the two groups were indistinguishable on the basis of HOMA-IR or postprandial responses to the bread meal. Hence differences in "lipid supply" do not account for differences in insulin sensitivity among these young adults. Indeed, no dietary or anthropometric variables correlated significantly with the M-value.

Fasting plasma glucose was within the normal range (<6.1 mmol/L) in all subjects. Although all SE Asian subjects showed relatively high postprandial hyperglycemia and hyperinsulinemia, 4 of the 10 were judged to be carbohydrate intolerant solely on the basis of a plasma glucose concentration >7.8 mmol/L 2 h after the 75-g carbohydrate load as white bread. More subjects might have been judged intolerant if a 75-g glucose challenge had been given instead of bread. In Australia, women of SE Asian origin have the highest rates of gestational diabetes (21 ). It is likely, therefore, that insulin secretory capacity is already compromised in young Thai and Vietnamese adults.

Asian Indian subjects also appeared to be relatively insulin resistant as judged by HOMA-IR and fasting insulin concentration (glucose clamps were not performed in this group). They displayed marked postprandial hyperinsulinemia after the bread meal (AUC tended to be even higher than that in the SE Asian group; P = NS), but their glucose tolerance was not significantly different from that of the European Caucasian group. The first-phase insulin response was probably better preserved in the Indian subjects because 30-min insulin concentrations were almost twice those in the SE Asian group.

The limitations of our study must be considered. The number of subjects studied is small and their relative leanness and higher educational status means they may not be representative of the general population. Although there were differences in the ratio of men to women in each group, there are no reported effects of gender on either insulin sensitivity or postprandial glycemia (22 –24 ). Differences in fetal nutrition may not be fully accounted for, particularly if subjects were only the first generation of their family born in Australia. There was no evidence to suggest that there were differences in body fat that might explain our findings. BMI, waist circumference and WHR, adjusted for sex, did not differ among most groups (only Arabic Caucasians had a higher WHR than the Chinese). However, we cannot exclude the possibility that a more precise measurement of body fat using dual X-ray absorptiometry or nuclear magnetic resonance may have shown differences among the ethnic groups.

Despite these limitations, few studies have documented insulin sensitivity in young adults using the "gold standard" euglycemic-hyperinsulinemic clamp. Even fewer have assessed several different ethnic groups at the same time. These findings imply that postprandial hyperglycemia and hyperinsulinemia are early "events" and may be important in the pathogenesis of the metabolic syndrome. Dietary guidelines may have to be population specific and take into account predisposition to IR. A high carbohydrate Western diet may have proven benefits for insulin-sensitive Caucasians but may well be disadvantageous to people of SE Asian or Asian Indian origin in whom postprandial hyperglycemia or hyperinsulinemia is a consequence of high carbohydrate intake.

	FOOTNOTES

 
² Abbreviations used: BMI, body mass index; HOMA, homeostasis model assessment; iAUC, incremental area under the curve; IR, insulin resistance; WHR, waist-to-hip ratio.

³ For Commentary on this article see: J Nutr. 132: 2492-2493, 2002

Manuscript received 9 April 2002. Initial review completed 18 April 2002. Revision accepted 20 May 2002.

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This Article Abstract Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Related articles in J. Nutr. Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dickinson, S. Articles by Brand-Miller, J. C. Search for Related Content PubMed PubMed Citation Articles by Dickinson, S. Articles by Brand-Miller, J. C.