• E-mail
• Print
• Comment
• Font Size
• Digg
• del.icio.us
• Discuss article

Carbohydrate-Induced Hypertriglyceridaemia Among West Indian Diabetic & Non Diabetic Subjects After Ingestion of Three Local Carbohydrate Foods

Posted on: Saturday, 5 March 2005, 03:00 CST

Background & objective: Studies suggest that the link between postprandial hyperglycaemia and cardiovascular risk in type 2 diabetes mellitus might be related to postprandial hypertriglyceridaemia and the increased levels of the highly atherogenic small and dense low density lipoprotein (LDL) particles. In this study we therefore aimed to determine which of the three popular carbohydrate foods has the highest potential of increasing postprandial triglyceride levels in type 2 diabetic patients and in healthy non diabetic individuals.

Methods: All subjects were studied on three different occasions seven days apart after an overnight fast. On each day of study, anthropometric indices were measured and after collecting fasting blood sample, subjects consumed bread, roti or rice within 10 min and water taken as wished. Subsequently, 7 ml of venous blood samples were collected at 60, 90, 120 and 150 min for insulin, glucose and lipids determinations.

Results: The diabetic and non diabetic healthy subjects had similar baseline body mass index, insulin, triglyceride, total and LDL-cholesterol. The mean percentage triglyceride increase after ingestion of the test foods was highest with bread and lowest with rice irrespective of diabetic status or ethnicity, and despite similar baseline triglyceride, insulin and body mass index levels, the diabetic patients of East Indian origin had comparatively higher incremental triglyceride levels for the three test foods than those of African origin.

Interpretation & conclusion: Contrary to anecdotal perception, the commercially prepared whole wheat bread has the highest propensity to induce hypertriglyceridaemia especially among diabetic patients of East Indian origin.

Key words Carbohydrate-induced * cardiovascular risk * hypertriglyceridaemia * primary health care * type 2 diabetes

Many reports on poor glycaemic control in patients with type 2 diabetes mellitus in the developing countries suggest increased risk of type 2 diabetic complications such as cardiovascular disease (CVD) in these patients1-4. Though type 2 diabetes is a known risk factor for CVD, role of postprandial hyperglycaemia in CVD risk in controversial5. An earlier study showed that 2 h postprandial glucose concentration is closely associated with cardiovascular and all-cause mortality in type 2 diabetes6. However, results of a large clinical trial have demonstrated that better control of postprandial glycaemia was beneficial in reducing CVD risk7. The link between postprandial hyperglycaemia and CVD risk in type 2 diabetes appears to be related to postprandial hypertriglyceridaemia and the increased levels of highly atherogenic small and dense low density lipoprotein (LDL) particles8-10. A recent review of studies on dietary carbohydrate (fat/carbohydrate ratio compositions) that is most likely to induce hypertriglyceridaemia and its net effect on CVD risk brought to focus the central issue of the type of dietary carbohydrate that has the least potential of inducing hypertriglyceridaemia11. This is an important public health issue especially in developing countries such as Trinidad and Tobago where carbohydrate constitutes about 70 per cent of daily dietary intake of type 2 diabetic patients12,13. The recent interlaboratory report of the glycaemic index of different carbohydrate diets in different populations is a commendable attempt at documenting the glycaemic indices of all popular carbohydrate foods in different ethnic groups 14. However, it is important to note that in many multi-ethnic populations such as in Trinidad and Tobago, which comprised mainly of people of African (40.8%) and East Indian (40.7%) ethnic groups 15, different carbohydrate foods are prepared according to ethnic cultural orientation. It therefore becomes necessary that an assessment of postprandial hyperglycaemic and hypertriglyceridaemic excursions of the' various commonly consumed carbohydrate foods should be done to aid in dietary recommendations to type 2 diabetic patients. In this regard, based on the report of the three most popular carbohydrate foods among type 2 diabetic patients at the primary care setting in Trinidad13, we attempted to determine which of the three local dietary carbohydrate foods has the least potential of increasing postprandial triglyceride levels in type 2 diabetic patients and in healthy non-diabetic individuals.

Material & Methods

Selection of patients with type 2 diabetes'. Subjects were selected from a database of 725 type 2 diabetic patients that participated in our recently concluded food frequency survey in two primary care clinics in North-West Regional Health Authority (NWRHA) in Trinidad13. Though all patients had telephone facility, only 60 patients were randomly selected from the computer database and contacted on telephone. Study protocol and objectives of the study were thoroughly explained to them. Fifty six patients eventually expressed interest to participate in the study and visited our laboratory for registration. However, only 38 of the 56 patients finally participated. The study was designed to assess the patients during their normal lifestyle and dietary intake. Thus the patients were instructed to continue on their prescribed medication and/or diet/exercise and normal lifestyle throughout the study period.

Recruitment of non diabetic subjects and screening for diabetes: Posters and flyers were used to enroll apparently healthy subjects within the NWRHA. Oral glucose tolerance test (OGTT) was performed on all individuals which was compulsory to exclude healthy subjects that might have undiagnosed diabetes. Thus, of the 34 individuals who volunteered to participate in the OGTT screening, only 27 (79.4%) satisfied the inclusion criteria (fasting and 2 h postprandial plasma glucose < 7.0 and 11.1 mmol/1 respectively) based on the new diagnostic criteria16. Subjects who satisfied the inclusion criteria were also instructed to be on their routine lifestyle and diet throughout the period.

Test foods: The following three test foods (Table I) were identified carbohydrate foods frequently consumed by type 2 diabetes patients visiting primary care clinics in NWRHA in Trinidad13. Commercially available whole wheat brown bread (Kiss Baking Co Ltd, Trinidad) was served with lettuce and cheese. Each test food (rice and roti) was prepared and administered according to common local cultural practices but using the guidelines of the local Food Composition Tables to calculate the carbohydrate, protein, fat composition and food quantity20. For each test food, none of the additional nutrient (curried chicken, lettuce, cheese or cucumber) contained significant quantity of carbohydrate to raise blood glucose level. It should be noted that the test foods varied in quantity but not in the available carbohydrate content and all the subjects finished all the test foods provided irrespective of quantity.

Study protocol: The study protocol was reviewed and approved by the Faculty of Medical Sciences Ethics Review Committee. Each individual was studied in our laboratory on three different occasions seven days apart in the morning after an overnight (12-14 h) fast. As our Metabolic ward accommodated only four patients at a time, 4 or less patients were studied during any one session but patients consumed different test foods based on their individualised study schedule. During the visit, details of ethnic origin and age were directly ascertained from the subjects and recorded. Waist (cm), at the level of the umbilicus with the patient standing and breathing normally, hip circumferences (cm), were obtained by tape measure while weight (kg), with standard hospital balance, and height (m), with metal rule, were measured (in light clothing, without shoes). After collecting fasting blood sample, subjects as per their study schedule consumed bread, roll or rice (test foods) within 10 min. The diabetic patients took their oral medications. Subsequently, 7 ml of venous blood samples were collected at 60, 90, 120 and 150 min while the subjects were allowed to drink water as wished during the study. The blood samples were preserved in fluorideoxalate in plain tubes and plasma and serum specimens respectively were removed after centrifugation within 30 min of collection and stored at -20C.

Table I. Carbohydrate, protein and fat composition of test foods

Biochemical analysis: Plasma glucose and serum total cholesterol (TC), triglyceride (TG), and high density lipoprotein cholesterol (HDL-C) were measured by enzymatic methods using commercial dry slides kits in multi-channel auto-analyzers (Johnson & Johnson Vitros 250, Ortho-Clinical Diagnostics Inc., Rochester NY 14626, USA). LDL cholesterol (LDL-C) was calculated using Friedwald equation21. Serum insulin levels were determined by enzyme linked immunoabsorbent assay (ELISA) using commercial ELISA kits (Mercodia Insulin ELISA, Mercodia AB, Uppsala, Sweden). The detection limit of the assay was less than ImU/l and intra- and inter-assay coefficients of variation (CV) of the assay were 3.7 and 6.4 per cent respectively.

Statistical analysis: The results were expressed as mean SE. The Statistical Package for the Social Sciences (SPSS Inc., 233, Chicago IL, USA) software was used in all analyses. The incremental area under the glucose/time \curve (IAUGC) for the three test foods were calculated using a computer Calculator Software (supplied by TMS Wolever, Department of Nutritional Sciences, University of Toronto, Toronto, Ontario M5S 3E2 Canada), based on the method of Wolever et al22. The glycaemic index of the test foods was calculated from the known literature values using the method of Wolever and Jenkins19 (Table I). Postprandial triglyceride increase was calculated as the per cent difference between 2.5 h and fasting triglyceride divided by the fasting triglyceride values. For statistical purposes only, all triglyceride data were log-transformed to normalise data distribution. Comparisons of mean glucose, insulin and lipid values between subjects were performed using Students' ttests. Analysis of variance (ANOVA, Post Hoc tests) was employed for multiple comparisons of incremental glucose and triglyceride values for the test foods while paired-sample T-test was used to compare the fasting and 2.5 h triglyceride levels for each of the test foods. P < 0.05 was considered statistically significant.

Table II. Clinical characteristics and anthropometric indices of the diabetic and non diabetic subjects

Table III. Differences in glucose, insulin and lipid levels before and after test foods

Table IV. Fasting and postprandial glycaemfa after ingesting the test foods in diabetic and non diabetic subjects of the two ethnic groups

Results

A total of 38 patients with type 2 diabetes (15 males, 23 females) and 27 non diabetic subjects (9 males, 18 females) participated in the study (Table II). Forty two (65%) participants were of East Indian ethnic group (26 diabetics, 16 non diabetics) while 23 were of the African ethnic group (12 diabetics, 11 non diabetics). The patients had mean diabetes duration of 9.9 yr and the majority (95%) were treated with oral hypoglycaemic agents. Though the diabetic patients were older than the healthy subjects, both groups had similar body mass index and waist circumferences (Table II). Mean fasting insulin, TG and LDL-C levels were similar in diabetic and non diabetic subjects, 10 (26%) diabetic patients and 1 (4%) non diabetic subject had fasting hypertriglyceridaemia (TG > 2.26 mmol/1, Table II). Consequently, following the ingestion of bread, but not rice or roti, the 2.5 h TG levels became significantly higher in diabetic subjects than in non diabetic subjects (P<.05, Table III). Although all the diabetic patients, irrespective of ethnic group, had similar baseline glucose, TC, and LDL-C levels before the consumption of the test foods, patients of East Indian ethnic group had significantly higher baseline TG (and 9 of 10 patients with fasting liypertriglyceridaemia) than those of African origin (P<0.01, Table IV). Patients of East Indian origin had significantly higher levels of 2.5 h TG and lower levels of HDL- C respectively following the ingestion of the test foods compared to patients of African ethnic group (P< 0.01, Table IV). While bread induced the highest TG increase in diabetic and non diabetic subjects, rice has the least potential to induce TG increase in both the groups. Although there were no significant relationships between incremental glucose and triglyceride after ingesting bread and roti in diabetic and non diabetic subjects, a significant correlation was found in all diabetic patients and those of East Indian origin after ingesting rice (Table V).

Table V. Incremental glucose and triglyceride levels and the relationship between incremental glucose and triglyceride in different subject groups after ingestion of test foods

Discussion

The finding that commercially available whole wheat brown bread elicited the highest postprandial TG increase amongst the three test foods in both diabetic and non diabetic subjects is interesting. There is a general perception that whole wheat brown bread has high fibre content and is therefore good for diabetic patients. The present finding casts serious doubt on the preference of this popular whole wheat brown bread among the diabetic patients considering its potentials to induce hypertriglyceridaemia, which carries increased cardiovascular risk". Though high carbohydrate and reduced fat (or cholesterol) diet has been generally advised to diabetic patients, diets that replaced fat with high carbohydrate have been consistently found to worsen some plasma lipid profile23. This warrants the need to identify the dietary carbohydrate food in each local population that has the least potential of inducing postprandial hypertriglyceridaemia. The present study showed that rice prepared and eaten according to diabetic patients' self reported format, has the least potential of increasing postprandial triglyceride levels as well as postprandial hyperglycaemia. Previous studies have shown that plasma triglyceride in diabetes was related to hyperglycaemia and control of postprandial glucose excursion reduced the postprandial triglyceride increase24,25. It is rather surprising that analysis of our data did not show any significant relationships between increase in postprandial glucose and triglyceride after ingesting roti or bread, two test foods with highest postprandial glucose excursion. It could be related to the small sample size in our study, which would have reduced the statistical power of the analysis.

The finding that the diabetic patients of East Indian ethnic group had comparatively higher levels of postprandial triglyceride and lower levels of HDLC indicated greater CVD risk in this ethnic group. The relatively higher postprandial hypertriglyceridaemia might be related to the fact that 9 of the 10 patients with fasting hypertriglyceridaemia were of East Indian origin In this population, the prevalence of diabetes is higher in people of East Indian origin compared with people of African origin26,27. In Trinidad, it is perceived that frequent consumption of roti, a popular dietary carbohydrate food among people of East Indian origin, has some relation with higher diabetes prevalence in this ethnic group. The analysis of the results of this ethnic group showed that ingestion of bread and rice respectively resulted in the highest and lowest triglyceride increase. On the contrary, we found that the correlation coefficients between incremental glucose and triglyceride in patients of East Indian origin, and indeed in all subjects groups, were lowest after the ingestion of roti. However, it should be noted that apart from ethnicity, factors such as anthropometrie indices, age, duration of diabetes and gender influence metabolic responses to foods". For example, it has been demonstrated that body mass index, fasting TG and insulin are the best predictive factors for carbohydrate-induced hypertriglyceridaemia28. Further the amount of simple sugars contained in each carbohydrate test food was not determined in the present study considering that high simple sugars in carbohydrate diet stimulate fatty acid synthesis and consequently determines the levels of plasma triglyceride after carbohydrate meals29. Similarly, fasting hypertriglyceridaemia as seen in the diabetic patients and overproduction or reduced clearance of VLDL-triglyceride after meals might have influenced the postprandial triglyceride levels30. Probably extension of the study duration beyond 2.5 h would have provided a better discrimination between diabetic and non diabetic subjects eventhough 2 h glycaemia after a standard oral glucose tolerance test (75 g glucose) has been shown to be closely related to the level of glycaemia after a standardised meal31. American Diabetes Association has suggested that a measurement of plasma glucose 2 h after a start of a meal is practical and generally approximates the peak value in patients with diabetes32. However, it should be acknowledged that additional physiological information regard ing total postprandial TG response would have been provided if serum TG levels at 60, 90 and 120 min were also measured. Perhaps, this would have assisted in evaluating the recent report of gender dimorphism in TG responses to meals, which has been shown to be higher in men than women33.

In conclusion, the results of the present study showed that mean percentage triglyceride increase after ingestion of the test foods was highest with bread and lowest with rice irrespective of diabetic status or ethnic group of the subjects, and despite similar anthropometrie indices, the diabetic patients of East Indian ethnic group had comparatively higher incremental triglyceride levels for the test foods than patients of African origin indicating a greater CVD risk in this group of patients.

Acknowledgment

The authors acknowledge the financial support provided by the Dean's Research Award Grant, University of the West Indies, Trinidad and Dr G. Davis for clinical assistance, Joanna Owen and Keisha Lewis for technical assistance and nursing staff of Lifestyle Disease Clinics, Arima and Chaguanas for their cooperation and professional assistance.

References

1. Chugh KS, Kumar R, Sakhuja V, Pcrcira BJ, Gupta A. Nephropathy in type 2 diabetes mellitus in third world countries-Chandigarh study, lnt J Artif Organs 1989; 12 : 299-302.

2. Erasmus RT, Sinha AK. Assessment of long-term glycacmic control in diabetic patients attending Port Moresby General Hospital. P N G Med J 1995; 38 : 16-9.

3. Ismail IS, Nazaimoon WM, Mohamad WB, Lctchuman R, Singaraveloo M, Pendek R, el al. Sociodemographic determinants of glycaemic control in young diabetic patients in peninsular Malaysia. Diabetes Res din Pract 2000; 47 : 57-69.

4. Ezcnwaka CE, Offiah NV. Differences in glycemic control and cardiovascular risk in primary care patients with type 2 diabetes in West Indies, Clin Exp Med 2001; 1 : 91-8.

5. Parkin CG, Brooks N. Is postprandial glucose control important? Is it practical in primary care setting? Clin Diabetes 2002; 20 : 71-6.

6. de Vcgt F, Dekker JM, Ruhe HG, Stehouwer CD, Nijp\els G, Bouter LM, et al. Hyperglycaemia is associated with allcause and cardiovascular mortality in the Hoorn population: the Hoorn study. Diabetologia 1999; 42 : 926-31.

7. Stratum IM, Adler AI, Neil HA, Matthews DR, Manley SE, Cull CA. at al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ 2000; 321 : 405-12.

8. Haffner SM, Mykkanen L, Stern MP, Paidi M, Howard BV. Greater effect of diabetes on LDL size in women than in men. Diabetes Care 1994; 17 : 1164-71.

9. Groot PHE, van Stiphout WA, Krauss XH, Jansen H, van ToI A, van Ramshorst E, et al. Postprandial lipoprotein metabolism in normolipidemic men with and without coronary artery disease. Arterioscler Thromb 1991; 11: 653-62.

10. Patsch JR, Miesenbock G, Hopferwieser T, Muhlberger V, Knapp E, Dunn JK, et al. Relation of triglyceride metabolism and coronary artery disease. Studies in the postprandial state. Arterioscler Thromb 1992; 12: 1336-45.

11. Hellerstein MK.Carbohydrate-induced hypertriglyceridemia: modifying factors and implications for cardiovascular risk. Ciiri- Opin Lipidol 2002; 13 : 33-40.

12. Wolcver T, Ramdath D. The use of Caribbean foods in the management of diabetes mellitus. West Indian Med J 1997; 46(Suppl 1) : 21-3.

13. Ezenwaka CE, Kalloo R, Davis G. Self reported dietary carbohydrate pattern among diabetic patients in primary care setting in Trinidad. West Indian Med J2003; 52 (Suppl. 1): 22.

14. Wolever TM, Vorster HH, Bjorck I, Brand-Miller J, Brighenti F, Mann Jl, et al. Determination of the glycaemic index of foods: interlaboratory study. Ew J Clin Niitr20Q3; 57 : 475-82.

15. Republic of Trinidad and Tobago. Office of the Prime Minister. Central Statistical Office. Population and Housing Census vol. II: Age Structure, Religion, Ethnic Group, Education, Port of Spain: Central Statistical Office; 1998.

16. Glucose tolerance and mortality: comparison of WHO and American Diabetes Association Diagnostic criteria. The DECODE Study Group. European Diabetes Epidemiology Group. Diabetes Epidemiology: Collaborative analysis of Diagnostic criteria in Europe. Lancet 1999; 354 : 617-21.

17. Ramdath DD, Isaacs RLC, Ramdhaine N, Wolever TMS. Glycaemic index of commonly eaten Caribbean staples. West Indian Med J 2001; 50 (Suppl. 2) : 26.

18. Indar-Brown K, Norenberg C, Madar Z. Glycemie and insulinemic responses after ingestion of ethnic foods by NIDDM and healthy subjects. Am J Clin Nutr 1992; 55 : 89-95.

19. Wolever TM, Jenkins DJ. The use of the glycemie index in predicting the blood glucose response to mixed meals. Am J Clin Nutr 1986; 43 : 167-72.

20. Food Composition Tables for Use in the English-speaking Caribbean, 2nd ed. Revised, The Caribbean Food and Nutrition Institute, Specialized Centre of the Pan American Health Organization and World Health Organization (PAHO/ WHO), Mona, Kingston 7, Jamaica 1998.

21. Friedwald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma without use of the preparative ultracentrifuge. Clin Chem 1972; 18: 499-502.

22. Wolever TM, Jenkins DJ, Jenkins AL, Josse RG. The glycemic index: methodology and clinical implications. Am J Clin Nutr 1991; 54 : 846-54.

23. Parks EJ, Hellerstein ME. Carbohydrate-induced hypertriacyl glycerolemia: historical perspective and review of biological mechanisms. Am J Clin Nutr 2000; 71: 412-33.

24. Howard BV. Lipoprotein metabolism in diabetes mcllitus. J Lipid Res 1987; 28 : 613-28.

25.Hanefeld M, Fischer S, Schulze J, Spengler M, Wargenau M, Schollberg K, et al. Therapeutic potentials of Acarbose as a first- line drug in NIDDM insufficiently treated with diet alone. Diabetes Care 1991; 14 : 732-7.

26. Miller GJ, Beckles GL, Maude GH, Carson DC, Alexis SD, Price SG, et al. Ethnicity and other characteristics predictive of coronary heart disease in a developing community: principal results of the St James Survey, Trinidad, lnt J Epidemiol 1989; 18: 808-17.

27. Miller GJ, Maude GH, Beckles GL. Incidence of hypertension and non-insulin dependent diabetes mellitus and associated risk factors in a rapidly developing Caribbean community: the St James survey, Trinidad. J Epidemiol Community Health 1996; 50 : 497-504.

28. Parks EJ, Rutledge JC, Davis PA, Hyson DA, Schneeman BO, Kappagoda CT. Predictors of plasma triglyceride elevation in patients participating in a coronary atherosclerosis treatment program. J Cardiopulm Rehabil 2001; 21: 73-9.

29. Hudgins LC, Hellerstein MK, Seidman CE, Neese RA, Tremaroli JD, Hirsch J. Relationship between carbohydrateinduced hypertriglyceridemia and fatty acid synthesis in lean and obese subjects. J lipid Res 2000; 41 : 595-604.

30. Mitlendorfcr B, Sidossis LS. Mechanism for the increase in plasma triacylglycerol concentrations after consumption of short- term high-carbohydrate diets. Am J Clin Nutr 2001; 73 : 892-9.

31. Wolever TM, Chiasson JL, Csima A, Hunt JA, Palmason C, Ross SA, et al. Variation of postprandial plasma glucose, palatability, and symptoms associated with a standardized mixed test meal versus 75 g oral glucose. Diabetes Care 1998; 21 : 336-40.

32. American Diabetes Association. Postprandial blood glucose. Diabetes Care 2001; 24 : 775-8.

33.Couillard C, Bergeron N, Prud'homme D, Bergeron J, Trcmblay A, Bouchard C, et al. Gender difference in postprandial lipaemia: importance of visceral adipose tissue accumulation. Arterio Thromb Vase Biol 1999; 19 : 2448-55.

Chidum E. Ezenwaka & Risha Kalloo

Unit of Pathology & Microbiology, Faculty of Medical Sciences, The University of the West Indies, St Augustine, Trinidad

Received December 17, 2003

Reprint requests: Dr Chidum Ezenwaka, Unit of Pathology & Microbiology, Faculty of Medical Sciences

The University of the West Indies, St Augustine, Trinidad

e-mail: ezenwaka@tstt.net.tt or ezcnwaka@yahoo.com

Copyright Indian Council of Medical Research Jan 2005

Source: Indian Journal of Medical Research

More News in this Category