The GI concept and health

According to WHO recommendations the optimal diet to maintain health (except for children under two) comprises at least 55% total energy from a variety of carbohydrate sources. Cereals with high starch content provide the main source of carbohydrates worldwide.

In recent decades a dramatic increase in the prevalence and incidence of type 2 diabetes, cardiovascular disease (CVD) and obesity has occurred in many parts of the world. Important risk factors for the development of type 2 diabetes and CVD are obesity, physical inactivity and an energy dense diet, high in saturated fatty acids and low in dietary fibre.  There is also the possibly that high intake of foods eliciting a high glycemic response - high glycemic index foods - also has a deleterious effect on these conditions.

The glycemic index (GI) concept has been introduced to enable comparison of foods based on their glycemic effect. It provides a standardised comparison for the 2 hour postprandial glucose response of a carbohydrate with that of white bread or glucose. The GI of cereal products has been determined and been shown to vary considerably. Differences can be due to botanical origin of the starch (as this determines the structural type of the starch granule) and subsequent food processing (which determines the extent of starch gelatinisation, particle size and the integrity of the plant cell wall). The potential beneficial or deleterious effects of starchy foods in the diet will therefore depend on the carbohydrate characteristics of the product eaten and how it has been processed.

Current data and gaps in knowledge

Data indicates that a diet characterised by a low GI may reduce insulin resistance and may decrease the risk of development of type 2 diabetes and cardiovascular disease. However, the underlying mechanisms are not completely understood and require further study. Moreover, the beneficial effects (for example on glucose tolerance) appear to be mediated short-term and possibly even from one meal to the other, i.e. the second-meal effect. 

Other areas where differences in the postprandial glucose profile may be of physiological significance include satiety, weight maintenance and cognitive function. Data regarding the satiating capacity in relation to GI features are, however, not consistent.  Interestingly, data at hand suggests that low GI foods reduce the accumulated food intake in obese children, facilitates weight loss and improves glucose metabolism in obese hyperinsulinaemic women. Very little information is present regarding the potential impact of postprandial glycemic level on cognitive function and mental performance.

The determinants of postprandial glucose excursions are numerous and include the amount and nature of the carbohydrates ingested, the rate of gastric emptying, the rates of intraluminal carbohydrate digestion and of intestinal glucose absorption, the entero-pancreatic hormonal response, and specific postabsorptive metabolic changes.

Better knowledge of the factors controlling postprandial glucose metabolism could lead to new measures for the attenuation of postprandial glycemia, which could subsequently reduce the impact of hyperglycemia on the pathogenesis of diabetes and cardiovascular disease.

GI and food choices

In 1997, The FAO/WHO expert consultation on dietary carbohydrates (FAO Food and Nutrition papers, 1998, Carbohydrates in human nutrition) recommended the use of GI when making food choices, particularly in subjects with impaired glucose tolerance. Diabetic associations in Australia and Europe supported this view, whereas the American Diabetic Association has been less supportive of the concept.  One criticism has been the limited number of food choices.  Indeed there is a shortage of low GI alternatives for breakfast, bread and snack foods. 

Recently a GI table of more than one thousand products was published (Foster-Powell et al., Am J Clin Nutr 2002). The GI features of a food should however, not be considered in isolation: other nutritional properties, such as fat content and nutrient composition, should also be taken into account.

The limited choice of low GI products presents an opportunity for the food industry to explore and develop, producing more low GI foods. The FAO/WHO expert consultation recommended that the processing chosen to produce starchy food should be optimised to preserve the nutritional properties of starch. More low GI products, high in dietary fibre and low in energy density should also be made available for consumers.

Another aspect of starchy foods that should also be taken into account is the proportion of starch resistant to digestion.  Even if this type of starch is not included in the glycemic response (and in the determination of the GI) low GI starchy foods frequently contain starch that is resistant to digestion. An increase of the proportion of low GI foods could thus result in an increased flux of undigested carbohydrates reaching the colon for fermentation, which may induce beneficial effects on metabolism. Several studies indicate that the colon and the colonic fermentation of carbohydrates play a role in the control of lipid and the postprandial glucose metabolism. To identify the underlying mechanisms further research will be undertaken on this aspect.

Research questions to be addressed

Health benefits of the consumption of slow release starchy foods.


. What are the long and short-term effects of consumption of high versus low GI starchy foods on glucose metabolism and lipid profile?


. To what extent are the GI features of foods related to post-meal satiety and cognitive function?


. What are the effects of fermentation of starchy foods on colonic metabolism and what are health-related consequences?


. To what extent can the health benefits of slow release starchy foods be estimated by use of the GI? Could other factors such as the release profile of glucose, regulation of endogenous glucose production glucose, hormonal responses or the presence of fermentable carbohydrates be of additional importance?


. In what way do the following factors determine the health benefits of high versus low GI starchy foods?

  • food production processes

  • rate and extent of digestion

  • gastrointestinal events (e.g. gastrointestinal transit time and hormones)

  • post-absorptive metabolism (e.g. second-meal phenomena)

  • fermentation

. What are the possibilities for extending the number of low GI starchy foods?


Expected results


. Assessment of "metabolic quality" of starch containing products in healthy volunteers and diabetic patients.


. Techniques for measuring starch digestion and fermentation (partly stable isotope technology based).


. Availability of 13C-labelled starch and food products.


. Health parameters related to industrial starch processing.


. Scientific basis for recommendations for the development of starch based functional foods.


. Definition of the role of the "glycemic index" concept in communication strategies concerning 'healthier' starch products.


GI of cereal products

According to the FAO / WHO (1997), the glycemic index (GI) is defined as "the incremental area"a) under the blood glucose response curve of a 50g carbohydrate portion of a test food expressed as a percent of the response to the same amount of carbohydrate from a standard food taken by the same subject". The reference food can be white bread or glucose. The GI allows the comparison of the glycemic responses over two hours of iso-glucidic portion of food (containing 50g of available carbohydrates).

The GI of a wide variety of foods, particularly cereal foods, has been largely studied and determined ; most of them are compiled in the Foster-Powell and al.'s International table of Glycemic Index (1).

The GI of cereal products varies greatly within the same food category and also between different cereal food categories. These variations can be due to different parameters affecting starch structure like the botanical origin of the starch and the food processing (starch gelatinisation), but also by the other food components of the products like lipids, proteins, type of sugar, fiber, organic acids, anti-nutrients...

The following graph shows the GI values of different types of cereal foods.

a) GI is the incremental area under the blood glucose response curve (IAUC) after subtracting the fasting level

References :

1 Foster-Powell K, Holt SH, Brand-Miller JC : International table of glycemic index and glycemic load values: 2002. Am J Clin Nutr 76: 5-56.

Botanical origin

Among the parameters linked to the botanical origin of the starch, the amylose/amylopectin ratio is one of the most influential parameters impacting the Glycemic Index of starchy foods. Amylose is less available for amylolytic attack than amylopectin due to its structure, this ratio has therefore an impact on the subsequent glycemic response and consequently on the GI of foods : the higher the amylose / amylopectine ratio, the lower the GI for the same type of food.

Thus, the legumes having a higher amylose content than cereals or tubers, have a lower GI. Moreover, this ratio can vary greatly even within the same plant species depending on the genotype of the variety. For example, in rice, some genotypes of sweet rice contain no amylose, while long grain rice has a starch profile of 25% amylose and 75% amylopectin (1). Likewise, waxy varieties of barley have only 3% amylose while high amylose barley genotypes can contain as much as 44% amylose (2). Thus, it has been shown that a low amylose rice has a GI of 83, whereas an high amylose rice has a GI of 50 (3).

Fig 1. Ratio of amylose/amylopectin of plants from different botanical origins: higher amylose content tends to induce lower glucose response.

Moreover, other botanically-related parameters are of importance, such as the physical environment of the starch granule. Indeed, in some species such as the legumes, the starch is enclosed in the plant cell-wall, which limits its access to hydrolytic enzymes.

The maturity of the foodstuff also impacts the associated GI of the food. For example, it has been observed that new potatoes result in a relatively lower GI than mature ones. Likewise, bananas become more readily digestible upon maturation.

References :

1 Goddard MS, Young G, Marcus R. :The effect of amylose content on insulin and glucose responses to ingested rice. Am J Clin Nutr 1984 Mar;39(3):388-92.

2 Akerberg-A, Liljeberg-H, Bjorck-I. : Effects of amylose/amylopectin ratio and baking conditions on resistant starch formation and glycaemic indices. Journal of Cereal Science. 28(1). July, 1998. 71-80.

7 Foster-Powell K, Holt SH, Brand-Miller JC : International table of glycemic index and glycemic load values: 2002. Am J Clin Nutr 76: 5-56.

Food processing

The food processing leading to physico-chemical transformation of the starch has an impact on the starch digestibility and consequently on the glycemic response.

Starch is usually not consumed in its native state, which is insoluble in water and only slowly accessible to amylase because of hindrance caused by hydrogen bonds between the glucose chains. However when heated in the presence of water, hydrogen bonds are disrupted and the starch granules absorb water and swell. The gelatinisation steps lead to the formation of a starch paste, in which the state of utmost disorganization is favorable to amylase access (1).

(from Bornet F. 1993 Carbohydrate Polymers 21:195-203)

Some food processes can increase the GI of foodstuffs, e.g. the one leading to starch gelatinisation. Thus, the starch in raw potato, which is highly resistant to digestion (87% RS) because it is encapsulated in granules, becomes almost totally digestible (1.2% RS) when the potato is processed (boiled), and which leads to a GI close to 100 (2). Englyst et al. (3) also demonstrated that among 23 processed cereal products, biscuits have the lowest gelatinisation index and the lowest GI, due to the process by which they are made, which keeps the starch granules partially intact.

The major parameters influencing the GI of a starchy food are the water content of the dough and the baking temperature. Indeed the higher these parameters, the more gelatinised the starch will be. The starch will thus be more available to amylolysis and the postprandial blood glucose levels will be higher.

Other technological parameters can also be of importance, for example, the pressure in the extrusion process, which also leads to the gelatinisation of starch. Many studies have assessed the influence of food processing of wheat, corn, rice or potato products on the subsequent metabolic response and it has been observed that the more processed the food is, the higher the glycemic response will be (4, 5).

References :

1 Lang V, Danone Vitapole, France : Development of a range of industrialized cereal-based foodstuffs, high in slowly digestible starch. Starch in food : structure, function and applications, edited by Ann-Charlotte Eliasson (2004).

2 Garcia-Alonso A.: Effect of processing on potato starch: In vitro availability and glycaemic index. Starch. [print] 52(2-3). March, 2000. 81-84.

3 Englyst-K-N, Vinoy-S, Englyst-H-N, Lang-V. :Glycaemic index of cereal products explained by their content of rapidly and slowly available glucose. Br J Nutr. 2003 Mar;89(3):329-40.

4 Ross SW, Brand JC, Thornburn AW, Truswell AS: Glycemic Index of processed wheat products.. Am J Clin Nutr 1987; 46:631-5

5 Brand JC, Nicholson PL, Thorburn AW, Truswell AS. : Food processing and the glycemic index. Am J Clin Nutr. 42(6):192-61, 1985 Dec

GI and insulin resistance 

Intervention studies have compared the effect of replacement of sucrose or fructose by starch. They show no effect on insulin sensitivity. Two studies have reported a decrease in insulin sensitivity when giving sucrose up to 30% of total caloric intake in replacement of starch (Reiser 1979, 1981).On the contrary, 3 studies show no effect of these changes (Bantle 1986, 1993, Peterson 1986). Thus no clear effect could be shown, but the starch used in these studies was not always low GI starch .

More studies comparing really high GI and low GI diets on insulin resistance are necessary.

References :

Reiser S, Powell AS, Schofield DJ, Panda P, Ellwood K, Prather E. Isocaloric exchange of dietary starch and sucrose in humans. Effect on fasting blood insulin, glucose, glucagons and insulin response to a sucrose load. Am J Clin Nutr, 1979 ; 49 : 832-839

Reiser S, Bohn E, Hallfrisch J, Michaelis O, Keeney M, Prather E. Serum insulin and glucose in hyperinsulinic subjects fed three different levels of sucrose. Am J Clin Nutr, 1981; 49 : 832-839

Bantle JP, Laine DC, Thomas JW. Metabolic effects of dietary fructose and sucrose in type I and II diabetic subjects. Jama, 1986; 256: 3241-3246

Bantle JP, Swanson JE, Thomas W, Laine DC. Metabolic effects of dietary sucrose in type II diabetic subjects. Diabetes Care, 1993; 16 : 1301-1305

PetersonDB, Lambert J, Gerring S, Darling P, Carter RD, Jelfs R, Mann JL. Sucrose diet of diabetic patients_just another carbohydrate? Diabetologia 1986; 29:216-220

GI and risk of development of type 2 diabetes

Prospective studies have found no relationship between total carbohydrate intake and risk of diabetes.

Two studies have assessed the risk of diabetes according to the content of mono- or di-saccharides of the diet.

. One (Janket et al.) found no effect of total mono or disaccharides.

. The other, (Meyer et al.) found an increased risk of type 2 diabetes of 30% after consumption of 25.8 g/d glucose (compared to 14 g/d), and of 27% after consumption of 30 g /d fructose (compared to 16 g/d) whereas high consumption of sucrose (51 g/d vs 31 g/d) decreased diabetes risk by 19%.

These two studies have found no effect of GI.

Studies from Salmeron et al. (1997a and b) found an increase risk of diabetes for the highest glycemic load (5th of the distribution) and a negative correlation with the consumption of cereals at breakfast (due to the effect of fiber). The glycemic load takes into account the GI of food and the quantity of carbohydrates.

More studies have shown an effect of low GI regimen on the control of type 1 and type 2 diabetes.

Thus, a review of the literature does not draw a clear conclusion about the relationship between the development of type 2 diabetes and the GI of food. However, studies where mono or di saccharides are replaced by low GI foods are still lacking.

References :

Janket SJ, Manson JE, Sesso H, Buring JE, Liu SE. A prospective study of sugar intake and risk of type 2 diabtes in women. Diabetes Care, 2003, 26: 1008-1015

Meyer KA, Kushi LH, Jacobs DR, Slavin J, Sellers TA, Folson AR. Carbohydrates, dietary fiber, and incident type 2 diabetes in older women. Am J Clin Nutr, 2000; 71 : 921-930

Salmeron J, Ascherio A, Rimm EB, Colditz GA, Spiegleman D, Jenkins DJ, Stampfer MJ, Wing AL, Willett WC. Dietary fiber, glycemic load, and risk of NIDDM in men . Diabetes Care , 1997 a; 20:545-550

Salmeron J, Manson JE, Stampfer MJ, Colditz GA, , Wing AL, Willett WC. Dietary fiber,glycemic load, and risk of NIDDM in women . Jama , 1997 b; 277:472-477

GI and risk of development of cardiovascular disease

Many studies have been conducted on the effect of low GI vs high GI diet on plasma lipoproteins and metabolic syndrome. These studies do not involve healthy subjects, but obese diabetic, dyslipidemic subjects.

They have shown a favourable effect of low GI diets on these parameters (Wolever, 1992, Fontvielle 1998, Jenkins 1987, Bouche 2002).

A negative relationship between HDL cholesterol, GI and glycemic load has been found (Ford, 2001).

Prospective studies on cardiovascular risk have been conducted. Van Dam (2000) found no effect of GI or glycemic load on myocardial infarction, whereas an effect was demonstrated in the American nurses study (Liu, 2000)

Therefore, no definitive conclusion can be drawn on the influence of GI on cardio-vascular risk, but a relationship between glycemic load and lipoprotein profile seems to exist especially in overweight patients.

References :

Wolever, TM, Jenkins DJ, Vuskan V, Jenkins AL, Buckley GC, Wong GS, Josse RG. Beneficial effect of low glycemic index diet in type 2 diabetes. Diabet Med,1992, 9 : 451-458

Fontvielle AM, Rizkalla SW, Penformis A, Acosta M, Bornet FR, Slama G. The use of low glycemic index foods improves metabolic control of diabetic patients over five weeks. Diabet Med , 1992;9 : 44-450

Jenkins DJ, Wolever TM, Kalmusky J, Guidici S, Giordano C, Patten R, Wong GS, Bird JN, Hall M, Buckley G. Low glycemic index indiet hyperlipidemia : use of traditional starchy foods. Am J Clin Nutr. 1987; 46:66-71

Bouche C, Riskalla S, Luo J, Vidal H, Veronese A, Pacher N, Fouquet C, Lang V, Slama G. Five-week, low glycemic index diet decreases total fat mass and improves plasma lipid profile in moderately overweight non diabetic men. Diabetes Care 2002;25:822-828

Ford ES,Liu. Glycemic index and serum high-density liprotein cholesterol concentration among us adult. Arch Intern Med, 2001;161 : 572-576

Van Dam RM, Visscher AW, Feskens EJ, Verhoef P, Kromhout D. Dietary glycemic index in relation to metabolic risk factors and incidence of coronary heart disease : the Zutphen study. Eur J Clin Nutr , 2000 ; 54 : 726-731

Liu S, Willett WC, Stampfer MJ, Holmes MD, Hu FB, Franz M, Sampson L, Hennekens CH, Manson JE. A prospective study of dietary glycemic load, carbohydrate intake, and risk of coronary heart disease in us women. Am J Clin Nutr, 2000, 71 : 1455-1471

Second meal effect

This concept means that the metabolism of a meal is dependent of the metabolism of the previous meal. Before the second meal, subjects are not in a fasting state and parameters such as glycemia, insulinemia, free fatty acid level, triglycerides, lipid and carbohydrate oxidation have not returned to the basal state (state before the 1st meal). We have shown that after a high-energy breakfast (compared to a low energy one), free fatty acid levels were lower before the second meal and lipid balance was more positive for this meal (Martin 2000).

References :

Martin A, Normand S, Sothier M, Peyrat J, Louche-Pelissier C, Laville M. Is advice for breakfast consumption justified? Results from a short-term dietary and metabolic experiment in young healthy men. Br J Nutr. 2000 Sep;84(3):337-44.


The satiating efficiency of food products in the post-prandial phase can be divided into two phases: satiation and satiety. Satiation refers to the process that causes a stop in intake during a meal. Satiety is the feeling of fullness after a meal, and has been defined as the suppression of further food intake after eating has ended (1). The mechanism behind satiety is complex and not fully understood, and probably several factors are involved. The period of eating usually occurs during a short time and therefore the mechanism for satiation is often explained by factors that arise during eating, such as orosensory and cognitive influence, gastric distention, and secretion of some gut hormones (2). One theory is that a rise in body temperature is linked to the termination of a meal (3). Instead, the suggested mechanisms associated with satiety include changes in the concentration of blood glucose, insulin, amylin, and gut hormones(2 15). Macronutrients, i.e. protein, carbohydrate and fat, have different satiating capacities. Fat has been shown to have the poorest satiating capacity, whereas both protein and carbohydrates have been shown to have better satiating capacity than fat (2, 4). Also differences in carbohydrate quality seem to have implications for satiety. Thus, low-GI starchy foods generally tend to be more satiating than high-GI foods (5-7). The mechanism is not clear-cut, and may involve other factors than the course of glycemia and insulinemia per se, such as the release of different satiety signals (5).

References :

1. Livingstone, B.E., P.J. Robson, and R.W. Welch, Methodological issues in the assessment of satiety. Scandinavia Journals of Nutrition/Näringsforskning, 2000. 44: p. 98-103.

2. Feinle, C., D. O'Donovan, and M. Horowitz, Carbohydrate and satiety. Nutr Rev, 2002. 60(6): p. 155-69.

3. Erlanson-Albertson, C., Appetite regulation and uncoupling proteins. Scandinavia Journals of Nutrition/Näringsforskning, 2000. 44: p. 108-110.

4. Westerterp-Plantenga, M.S., Satiety and 24h diet-induced thermogenesis as related to macronutrient composition. Scandinavia Journals of Nutrition/Näringsforskning, 2000. 44: p. 104-107.

5. Bjorck, I. and H. Elmstahl, Glykemiskt Index Metabolism och mättnadsgrad. Scandinavian Journal of Nutrition, 2000. 44(3): p. 113-117.

6. Liljeberg, H.G.M., C.H. Lönner, and I.M.E. Björck, Sourdough fermentation or addition of organic acids or corresponding salts to bread improves nutritional properties of starch in healthy humans. Journal of Nutrition, 1995. 125: p. 1503-1511.

7. Liljeberg, H.G., A.K. Akerberg, and I.M. Bjorck, Effect of the glycemic index and content of indigestible carbohydrates of cereal-based breakfast meals on glucose tolerance at lunch in healthy subjects. Am J Clin Nutr, 1999. 69(4): p. 647-55

Weight maintenance

Weight maintenance is the ability to maintain a stable weight after a regimen period.

Cognitive function/mental performance

The research regarding the physiological impact of low- versus high-GI foods and/or diets has mainly been focused on metabolic variables and risk factors, whereas the effects on other physiological parameters such as e.g. memory and cognitive functions have been investigated only to a minor degree. However, glucose is the main fuel for the brain and a number of studies have demonstrated positive effects on cognitive function after having a glucose drink or breakfast vs. not having breakfast (1-7), indicating the importance of glucose for mental performance. Low blood glucose levels, even if not in the hypoglycaemic range, have further been shown to have a negative influence on cognitive function (8).

Usually, low-GI foods result in a smaller rise in blood glucose in the early post-prandial phase compared with high-GI foods. Instead, low-GI foods normally maintain a higher blood glucose level in the late postprandial phase. It could therefore be hypothesised that, from the perspective of providing fuel to the brain, high-GI foods have advantages in the early post-prandial phase whereas the low GI foods are to be preferred in the late post-prandial period by maintaining a net increment in blood glucose until the next meal. Consequently, there are findings that suggest that even small increases in blood glucose may have a positive effect on brain function (8). It is not known which level of glucose in circulating blood is necessary to reach maximal cognitive function, and it could also be that low GI foods have the capacity to reach critical levels immediately after meal. Knowledge of the extent to which memory and cognitive function are affected by the course of glycemia and insulinemia in the post-prandial phase is an important area for research. Within the present EUROSTARCH project, psychological methods capable of measuring working memory (short term memory) and vigilance (also known as attention) are adopted with the purpose of studying the dynamics of cognitive function over the entire post-prandial period. The capacity of working memory is limited and in the working memory test, the span of the system is determined repeatedly during the whole post-prandial period. In the vigilance test the ability to maintain attention is measured during the late post-prandial period.

References :

1. Pollitt, E. and R. Mathews, Breakfast and cognition: an integrative summary. Am J Clin Nutr, 1998. 67(4): p. 804S-813S.

2. Benton, D., D.S. Owens, and P.Y. Parker, Blood glucose influences memory and attention in young adults. Neuropsychologia, 1994. 32(5): p. 595-607.

3. Benton, D. and P.Y. Parker, Breakfast, blood glucose, and cognition. Am J Clin Nutr, 1998. 67(4): p. 772S-778S.

4. Martin, P.Y. and D. Benton, The influence of a glucose drink on a demanding working memory task. Physiol Behav, 1999. 67(1): p. 69-74.

5. Messier, C., et al., Dose-dependent action of glucose on memory processes in women: effect on serial position and recall priority. Brain Res Cogn Brain Res, 1998. 7(2): p. 221-33.

6. Scholey, A.B., S. Harper, and D.O. Kennedy, Cognitive demand and blood glucose. Physiol Behav, 2001. 73(4): p. 585-92.

7. Hall, J.L., et al., Glucose enhancement of performance on memory tests in young and aged humans. Neuropsychologia, 1989. 27(9): p. 1129-38.

8. Donohoe, R.T. and D. Benton, Cognitive functioning is susceptible to the level of blood glucose. Psychopharmacology (Berl), 1999. 145(4): p. 378-85.

Rate of gastric emptying

One function of the stomach is to grind food to smaller particles, mix it with digestive juices and deliver it slowly and at a controlled rate to the small bowel where it can be absorbed. The emptying of the stomach is a highly co-ordinated physiological response to the presence of food. The stomach has three distinct muscular regions (the fundus, the antrum and the pylorus) which act in concert with each other and with the duodenum to empty the solid, the liquid and the oil phase of a meal.

The rate at which the stomach empties its contents is important since it has significant metabolic consequences. For example, gastric emptying influences the rate of absorption of nutrients and drugs by controlling its delivery to the small bowel. In addition, there is increasing evidence that parameters such as glycemic index are closely correlated with the rate of gastric emptying.

Delayed gastric emptying

Gastric emptying can be delayed ("gastroparesis") for several reasons. Nearly any disease or condition that produces neuromuscular dysfunction of the gastrointestinal tract may also cause gastroparesis. However, aside from medication-induced delayed gastric emptying, the most common disorders include diabetes, postsurgical gastroparesis and delayed gastric emptying without apparent cause or so-called idiopathic gastoparesis.

Symptoms of delayed gastric emptying

Symptoms of delayed gastric emptying include nausea, vomiting, early satiety, bloating, belching, dyspepsia or gastroesophageal reflux.

Measurement of gastric emptying rate

A variety of methods have been developed to measure gastric emptying. The radioscintigraphic technique is currently the established procedure to measure the gastric emptying rate of both liquids and solids simultaneously. A test meal radiolabelled with a gamma emitting radionuclide is administered to the patient and a gamma camera, positioned over the abdomen, monitors the transit of the meal through the gastro-intestinal tract.

Ultrasound scanning can be used to measure the gastric volume as a function of time. Changes in the calculated volumes have been correlated with gastric emptying measured by scintigraphy.

Impedance techniques are based on the principle that following the ingestion of a liquid with low electrical conductivity, the impedance of the epigastric region increases, followed by a gradual decrease to the baseline as the fluid is emptied from the stomach. The time-course of this decline in impedance reflects the duration of gastric emptying.

Magnetic resonance imaging provides high-resolution three-dimensional images of the stomach and allows not only measurement of gastric emptying, but also measurement of gastric secretion and evaluation of contraction patterns.

The non-invasive carbon-labelled breath test is an indirect but elegant means to measure gastric emptying. A 13C labelled medium-chain fatty acid (octanoic acid) is bound to a solid meal. After ingestion and delivery to the duodenum, the octanoic acid is quickly absorbed and metabolized in the liver to labelled CO2 which is exhaled and measured in the breath. The rate at which labelled CO2 appears in the breath is a measure for the rate of gastric emptying. Similarly, gastric emptying of fluids can be measured using 13C-glycine or 13C-acetate.


Maughan RJ, Leiper JB. Methods for the assessment of gastric emptying in humans: an overview. Diabetic medicine 1996: 13:S6 S10

Hornbuckle K, Barnett JL. The diagnosis and work-up of the patient with gastroparesis. J Clin Gastroenterol 2000, 30:117 124.

Ghoos YF, Maes BD, Geypens BJ, Mys G, Hiele MI, Rutgeerts PJ, Vantrappen G. Measurement of gastric emptying rate of solids by means of a carbon-labeled octanoic acid breath test. Gastroenterology 1993; 104:1640 1647.

Mourot J, Thouvenot P, Couet C, Antoine JM, Krobicka A, Debry G. Relationship between the rate of gastric emptying and glucose and insulin responses to starchy foods in healthy adults. Am J Clin Nutr 1988; 48:1035 1040.


gastroparesis a slight degree of paralysis of the muscular coat of the stomach

fundus the bottom or lowest part of the stomach

antrum the pyloric end of the stomach, partially shut off during digestion from the fundus

pylorus the muscular tissue surrounding and controlling the outlet of the stomach to the duodenum

duodenum the first part of the small intestine, about 25 cm or 12 fingerbreadths (hence the name) in length

idiopathic referring to a disease of unknown cause

bloating abdominal distention from swallowed air or intestinal gas from fermentation

eructation belching

dyspepsia impaired gastric function due to some disorder of the stomach, characterized by epigastric pain, burning or nausea

scintigraphy a diagnostic procedure employing administration of a radioactive substrate with an affinity for the organ of tissue of interest, followed by determination of the distribution of the radioactivity by an external detector

radionuclide nuclide that exhibits radioactivity

ultrasound a diagnostic procedure based on the measurement of the reflection or transmission of high frequency (> 30,000 Hz) waves

Carbohydrate digestion and intestinal glucose absorption

Carbohydrate digestion

Amylose and amylopectin are hydrolyzed by salivary and pancreatic α-amylase. Salivary α-amylase is inactivated in the acid environment of the stomach. Αlpha-amylase can hydrolyze the α-1,4-glycosidic bonds that are present in amylose and amylopectin ,but not the α-1,6-glycosidic linkages at the branching sides in amylopectin. Glucose oligosaccharides containing uncleaved α-1,6-glycosidic bonds are the so-called α-limit dextrins. After starch hydrolysis by α-amylase the remaining products, maltose, maltotriose and the α-limit-dextrins, are hydrolyzed into glucose by the brushborder enzyme complexes sucrase-isomaltase and maltase-glucoamylase . Alpha amylase, sucrase-isomaltase, and maltase-glucoamylase are so-called α-glucosidases. By inhibition of intestinal α-glucosidases the digestion of carbohydrates to absorbable monosaccharides can be delayed.

Glucose absorption

Glucose enters the enterocytes by active transport mediated by the sodium-glucose cotransporter (SGLT-1). The energy is provided by the sodium gradient across the brush-border membrane, maintained by the enzyme Na+-K+ -ATPase in the basolateral membrane. Glucose leaves the intestinal cells down its concentration gradient via the glucose transporter (GLUT2). In vitro studies as well as in vivo studies suggest that guar, a viscous fiber, impairs disaccharide hydrolysis and glucose absorption. It seems to reduce the diffusion rate in the unstirred layer.

Techniques to monitor carbohydrate digestion in vivo

13C-labelled carbohydrates

13C, a stable isotope of carbon, can be used to study the digestion, absorption and metabolism of carbohydrates in vivo. Stable isotopes of an element have the same number of protons, but a different number of neutrons. Stable isotopes are not radioactive. After hydrolysis of ingested 13C-enriched starch, 13C-glucose is absorbed, oxidized and exhaled as 13CO2. 13CO2 is also produced in the colon during fermentation of undigested 13C-enriched starch and partly excreted in breath.

Some plants, for example, - like corn, teff, millet and cane sugar, - contain carbohydrates that are naturally enriched in 13C. 13C-enriched carbohydrates can also be obtained by growing plants in a 13C-enriched atmosphere.

13CO2 breath test

13CO2 in breath samples can be quantified using isotope ratio mass spectrometry. The 13CO2 -starch breath test can be used to evaluate the digestion and fermentation of various 13C-starch preparations. Using mathematical models it might be possible to distinguish between 13CO2 produced by oxidation of absorbed glucose from the small intestine and that produced by fermentation in the colon.


The 13C-enrichment of plasma glucose can be analyzed in blood samples that are collected after intake of naturally labeled 13C-starch. Measurement of 13C-glucose in plasma allows more specific study of the bioavailability of starch than does the total blood glucose response. The total blood glucose is not a very accurate reflection of the intestinal glucose absorption, due to several physiological processes. The blood glucose in the venous system is supplied with carbohydrates from the intestinal tract, but also with endogenously produced glucose. Furthermore, glucose is continuously taken up by the tissues, mainly the muscle and the brain, as an energy supply. Therefore, the venous blood glucose concentration is the result of the influx of glucose into the circulation (exogenous and endogenous glucose) and glucose removal from the circulation.

Dual isotope method

By administering two substrates labeled with stable isotopes (D-[6,6-2H2]glucose and 13C-starch) it is possible to estimate the systemic appearance rates of both hepatic and starch-derived (intestinal) glucose. In the dual isotope method D-[6,6-2H2]glucose (deuterium labelled) glucose is infused continuously to be able to determine the rate at which glucose appears in the systemic circulation from exogenous (intestinal) and endogenous (mainly hepatic) sources. After a steady state is reached, in which the deuterium enrichment of the glucose in the systemic circulation stays constant, 13C-labelled carbohydrates are ingested. Distinction between endogenous and exogenous glucose is possible based on the 13C-enrichment in plasma glucose. Based on the rate of appearance of glucose and the plasma 13C-glucose concentration, fluxes of plasma glucose derived from both endogenous sources and the intestine can be calculated. Thus, using the dual isotope method intestinal carbohydrate digestion and glucose absorption can be quantified.

Entero-pancreatic hormones

Postprandial glucose concentrations are influenced by several hormones secreted by the pancreas and the intestine.

In response to the postprandial rise in glucose concentration, the pancreas increases its secretion of insulin and suppresses the release of glucagon, thereby limiting hepatic glucose production and promoting the uptake of glucose by muscle and fat tissue. Increased insulin levels effectively deposit a large proportion of glucose into these tissues, if receptor sensitivity to insulin is normal. The degree of postprandial hyperglycemia is controlled by the balance between glucose influx and glucose removal. When glucose removal exceeds glucose release, plasma glucose returns to fasting levels.

Gastrointestinal hormones that play an important role in the control of postprandial glucose homeostasis are the incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP).

GLP-1 is secreted from the intestinal L-cells mainly located in the distal small intestine and colon. GLP-1 stimulates insulin secretion, decreases the secretion of glucagons, delays gastric emptying and has appetite-inhibiting properties.

The release of GIP is elicited by nutrient and neurohumoral stimulation from proximal regions of the small intestine. GIP is secreted from the intestinal K-cells, which exhibit the highest density in the proximal small intestine. Carbohydrate and fat intake stimulate GIP release. GIP potentiates glucose-induced insulin secretion and maximizes energy storage.

Starch resistant to digestion

Most of the starch, which is ingested, is digested in the small intestine and absorbed as glucose. However, some starch can escape digestion and arrive in the large intestine where it is usually fermented producing short chain fatty acids, other organic acids such as lactic acid, and gases (see more in "fermentation"). This fraction of the starch is called "resistant starch". Indeed it has been defined in 1992 (Asp, 1992) as "the sum of starch and products of starch degradation not absorbed in the small intestine of healthy individuals". It represents around 2-3% of the total starch of most of the starchy foods, however the fraction of RS may be much higher in some cases. Indeed, RS are usually classified in 3 categories:

RS1 is physically inaccessible, usually due to an encapsulation in intact cell walls. Typical examples are RS from pulses (beans, chickpeas, lentils.).

RS2 are raw starches naturally highly resistant to mammalian -amylase such as banana, raw potato or high amylose starches.

RS3 are present in starchy foods or pure starches treated by hydrothermic processes then retrograded (crystallization of amylose then amylopectin at temperatures from ambient to freezing (-20°C) temperatures in non dehydrated starchy products). A classical example of appearance of RS in a food is the cooked rice or potatoes that is maintained in a fridge for several hours (or days) where small amount of RS is generated.

In the recent reviews, a forth category (RS4) has been described which includes heavily chemically modified starches.

RS can then be found in "natural" foods or can be incorporated in foods as an ingredient, usually to improve their techno-functional characteristics and/or organoleptic properties. Several RS2 and RS3 are now commercially available from the main starch producers.

The interest for RS started more than 10 years ago when the fermentation profile of RS was shown to be rich in butyrate. This short chain fatty acid is the main nutrient of colonic cell and protects the colon from a number of diseases such as colon cancer. More recently RS has been described as a prebiotic polysaccharide which is supposed to beneficially affect the host by selectively stimulating the growth of one or a limited number of bacteria (bifidobacteria and/or lactobacilli) in the colon.

Health claims on RS are not yet allowed in Europe but some RS may obtain this type of claim in the future.

To know more on Resistant starch :

Asp N.G. (Suppl. Editor). 1992. Resistant starch - Proceedings from the 2nd plenary meeting of EURESTA: EUROPEAN FLAIR CONCERTED ACTION No.11(COST 911) Physiological implications of the consumption of resistant starch in man. Eur. J. Clin. Nutr. 46(S2), S1-S148.

Asp N.G., van Amelsvoort J.M.M., Hautvast J.G.A.J. 1996. Nutritional implications of resistant starch. Nutr. Res. Rev. 9, 1-31.

Champ M., Kozlowski F., Lecannu G. (2001) In vivo and in vitro methods for resistant starch measurement. In : Dietary fibre. Eds: B.V. McCleary and L. Prosky, Blackwell Science, Oxford. pp.106-119.

Topping D.L., Fukushima M., Bird A.R. 2003. Resistant starch as a prebiotic and symbiotic: state of the art. Proc. Nutr. Soc., 62, 171-176.

Contact : Dr. Martine Champ, INRA/CRNH, Nantes (France),


Components of the diet that fail to be digested will pass to the colon where they may be fermented by bacteria. Colonic fermentation of resistant starch and other non-digestible carbohydrates (NDC) produces a number of products that could play important roles in metabolic and physiological processes. Although fermentation yields gaseous products, it is the short chain fatty acids that are of principal interest in this context. The volatile fatty acids (VFA) acetic, propionic and butyric acids are of prime importance, although lactic acid production may also be of significance in early life [1]. VFA can be produced within the body (endogenous) as well as by colonic fermentation (exogenous production). Oxidation of exogenous VFA provides an energy salvage mechanism of undigested dietary components. In marginal diets this can represent a significant proportion of energy intake. Theoretically, starch fermentation will release acetic, propionic and butyric acids in the approximate molar ratio 3:1:1, although factors including NDC structure and bacterial composition will influence this. However this ratio is never observed in the circulation. Because of its pivotal role in intermediary metabolism, endogenous acetate production is far greater than that of the other VFA. Also, butyric and propionic acids are preferentially utilised prior to entry into the general circulation, thereby altering the relative concentrations of VFA in the circulation. Butyric acid is the preferred fuel of the coloncyte. It has trophic effects on the colonic epithelium, and is now recognised as an anti-inflammatory agent, downregulating inflammatory cytokine expression. Butyric acid has also been shown to increase differentiation and apoptosis in animal and human colon cancer cell models. Much will be oxidised in the colonocyte. A smaller flux enters the portal circulation and a portion is oxidised in the liver. An even smaller portion enters the general circulation. Butyric acid concentration may remain undetectable in the bloodstream unless it has been produced recently by colonic fermentation. In contrast, propionic acid is usually detectable in the circulation as much escapes oxidation in the colonocyte and reaches the liver where it can be oxidised. Alternatively, propionate can enter anabolic pathways, including gluconeogenesis. Similarly, acetate enters the portal circulation. Some will enter anabolic pathways in the liver, such as lipogenesis, and some will enter the general circulation to be oxidised by other tissues, such as muscle. Thus acetate is always detectable in the circulation. With greatly variable production and consumption, VFA are in constant flux, necessitating powerful techniques to quantify their production rates. The application of stable isotope technology within the EUROSTARCH project provides such a tool [2].


1. Edwards CA and AM Parrett (2002) Intestinal flora during the first few months of life: new perspectives. British Journal of Nutrition 88: S11-S18

2. Pouteau E, Vahedi K, Messing B, Flourié B, Nguyen P, Darmaun D & M Krempf (1998) Production rate of acetate during colonic fermentation of lactulose: a stable isotope study in humans American Journal of Clinical Nutrition 68: 1276-1283

Role of colonic fermentation in the control of lipid metabolism

The non-digestible carbohydrates that escape absorption in the small intestine are degraded by bacterial fermentation in the large bowel. This process of fermentation yields gases (H2, CH4 and CO2) and short chain fatty acids (SCFAs) mainly acetate, propionate and butyrate. SCFAs are of major importance in understanding the physiological function of dietary fiber.

Butyrate is metabolized by colonocytes, whereas propionate and acetate are transported through the portal vein to the liver. Most propionate is metabolized by hepatocytes and only colonic acetate rapidly appears in the systemic blood in millimolar concentrations.

Obesity and insulin resistance are commonly associated with high free fatty acid (FFA) concentrations in plasma leading to lipotoxicity and metabolic disorders. In the liver, FFA interfere with insulin suppression of hepatic glucose production. In peripheral glucose-dependent cells, lipotoxicity or high plasma FFA concentration inhibits insulin action on glucose transport through cell membranes, and enhances peripheral insulin-resistance. Therefore, lowering elevated FFA would reduce insulin resistance.

Previous observations have shown that plasma acetate derived from ethanol consumption inhibits lipolysis from adipose tissue and decreases plasma FFA. Acetate production by bacterial fermentation of indigestible carbohydrates in the human colon could represent another possibility of reducing plasma FFA and preventing or reversing insulin resistance. To test this hypothesis, the effect of lactulose (a non absorbable disaccharide) intake on fatty acids metabolism in insulin resistant obese patients was assessed by the determination of acetate production, plasma glycerol appearance rate and FFA concentrations using a stable isotope dilution method. After an oral dose of lactulose, an increase of 50% of total acetate production rate and a significant increase of plasma acetate concentration were observed whereas the glycerol turnover and FFA concentrations in plasma significantly decreased by 30 and 35%. The decrease in FFA concentration and glycerol turnover was inversely correlated to the rate of acetate production.

These results showed, in insulin resistant obese subjects, a short-term decrease in FFA after lactulose ingestion related to a decrease of lipolysis in close relationship with an increase of acetate production. Thus, a highly fermented carbohydrate can reduce lipotoxicity via an anti-lipolytic mechanism mediated by acetate.

Contact: Dr. Veronique Ferchaud-Roucher, CRNH/Inserm U539, Nantes (France)

Pr. Michel Krempf, CRNH/Inserm U539, Nantes (France)

Role of colonic fermentation in control of postprandial glucose metabolism

Carbohydrates may, for different reasons, reach the colon. In cereal products, dietary fibre constitutes a major form of indigestible carbohydrate. However, certain starch fractions, i.e. resistant starch, may also be delivered undigested to the large bowel, thus providing the colonic micro-flora with substrate for fermentation. Examples of resistant starch are physically inaccessible starch enclosed in botanically intact structures e.g. in whole grains, native starch, and retrograded starch. Indigestible carbohydrates, i.e. resistant starch and dietary fibre, reaching the colon increase the fermentative activity in the colon (1). This results in the formation of various microbial metabolites such as short-chain fatty acids (SCFA), mainly acetic-, propionic-, and butyric acid (acetic acid showing highest concentrations), and gases, e.g. carbon dioxide and hydrogen (2,3). It has been proposed that colonically derived SCFAs may have beneficial implications on glucose metabolism. Propionate has thus been shown to affect favourably hepatic carbohydrate metabolism in rats (4) and improve glucose tolerance in man (5). In the present EUROSTARCH project, the capacity of various cereal products to promote a high fermentative activity at the time of a subsequent meal is studied and correlated to glucose tolerance. Different cereal products varying in dietary fibre and/or resistant starch content are served as evening meal, and the glucose tolerance to a subsequent standardised breakfast meal is evaluated along with various fermentation variables (H2 in expired air, SCFA in blood) and blood levels of free fatty acids.

References :

1. Rumessen, J.J., Hydrogen and methane breath tests for evaluation of resistant carbohydrates. Eur J Clin Nutr, 1992. 46 Suppl 2: p. S77-90.

2. Cummings, J.H., et al., Short chain fatty acids in human large intestine, portal, hepatic and venous blood. Gut, 1987. 28(10): p. 1221-7.

3. Cummings, J.H., G.T. Macfarlane, and H.N. Englyst, Prebiotic digestion and fermentation. Am J Clin Nutr, 2001. 73(2 Suppl): p. 415S-420S.

4. Anderson, J.W. and S.R. Bridges, Short-chain fatty acid fermentation products of plant fiber affect glucose metabolism of isolated rat hepatocytes. Proc Soc Exp Biol Med, 1984. 177(2): p. 372-6.

Stable isotope technology

Each of the elements that together comprise organic matter (C, H, O, N & S) possess minor stable isotopes that are present at low concentration throughout nature. They are thus naturally present in the body and in the food that we eat. These minor stable isotopes, such as 13C, are not radioactive and do not present a hazard to the body or in the environment. They have identical biological and chemical properties to their more abundant major isotopes, such as 12C. We can detect them by nature of their differing mass. Generally, we use mass spectrometry to monitor stable isotopes, although optical spectroscopy has been used. Experimental use of stable isotopes in human biology is a very powerful technique, especially in nutrition and metabolic research. These tracers can often be applied in a non-invasive manner. For instance, we can introduce a stable isotope at a level above that present naturally in the diet and follow this as food is digested and passes between body tissues. Within EUROSTARCH we will be exploiting stable isotope technology to increase the availability of 13C-starch for nutritional studies. Specialist forms of mass spectrometry such as compound-specific isotope analysis [1], which will be further developed during Eurostarch, allow us to follow very small quantities of stable isotope tracers in individual compounds, such as glucose and acetic acid. When food is oxidised, much of the 13C is exhaled as breath CO2 which can be readily detected [2]. We are witnessing a revolution in our ability to study and understand nutrition and metabolism as this science and technology develops. Stable isotopes and mass spectrometry are set to become one of the principal tools in the new science of metabolomics.

1. Preston T (1992) The measurement of stable isotope natural abundance variations Plant, Cell and Environment 15 (9): 1091-1097

2. Ghoos Y & WA Coward (1998) Application of stable isotopes in clinical medicine Gut 43 (3): S1-S30

Availability of 13C-starch

Labelling components of the diet with stable isotope tracers provides us with a uniquely powerful tool with which to investigate their nutritional role and metabolic fate. Two basic approaches can be used to label foodstuffs with stable isotope tracers, extrinsic or chemical labelling, and intrinsic or biological labelling. The former technique usually involves introduction of labelled atoms into specific molecules and their incorporation into food. The latter involves providing simple labelled compounds to a plant, (or adding simple organic molecules to animal feed) and letting the natural processes such as photosynthesis produce a full range of products in a manner that is no different from normal food production. Both approaches start with purchasing pure labelled chemicals that have been enriched from natural materials by specialist stable isotope companies [1]. In the case of intrinsic labelling, this may simply be 13C-labelled CO2 gas. Intrinsic labelling is the preferred method when we wish to study the metabolism of a complex macronutrient such as starch which may comprise hundreds of chemical compounds within a very a complex structure typical of a plant cell. An intrinsic label will be distributed evenly through the entire range from fully digestible to non-digestible components. The digestibility of the labelled compounds will reflect the modifications that normally occur during processing, preparation and cooking. In the EUROSTARCH project, we are using intrinsic labelling to prepare 13C-labelled starch for use to investigate the rate of digestion of various preparations, principally of wheat starch. We are exploiting a quantity of 13C-labelled wheat flour that was prepared for the project. During the project we will produce further quantities of 13C-labelled Durum wheat and barley. Here, plants are grown in pots in a large greenhouse until anthesis, when selected plants are transferred to a growth chamber. The plants are held for five days in a strictly controlled environment, with the carbon dioxide in the air being replaced by 13CO2 [2]. They are then returned to the greenhouse until harvest. Common foodstuffs such as bread, pasta or biscuits can be prepared for nutritional experiments using traditional methods. The production of small quantities of other 13C-labelled staple carbohydrates is also under investigation (rice, potatoes etc).

1. See: 

2. Harding M, Coward WA, Weaver LT, Sweet JB & JE Thomas (1994) Labelling wheat flour with 13C Isotopenpraxis 30: 1-8


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