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Muesli with 4 g oat β-glucans lowers glucose and insulin responses after a bread meal in healthy subjects

Abstract

Objective:

To evaluate the impact of an extruded muesli product based on β-glucan-rich oat bran on postprandial glycaemia and insulinaemia.

Subject/Design:

The study is divided in two series. Blood glucose and serum insulin responses were studied after subjects consuming test meals including a serving of muesli with 3 g (series 1) and 4 g (series 2) of β-glucans, respectively. The muesli was a component in a single serving packet with muesli and yoghurt. This was served together with white wheat bread in the morning after an overnight fast. The compositions were standardized to contain 50 g available carbohydrates. As a reference meal a serving packet without β-glucans was included. The study was performed at Applied Nutrition and Food Chemistry, Lund University, Sweden. Nineteen and thirteen healthy volunteers with normal body mass index were recruited for series 1 and 2, respectively.

Results:

Muesli with 3 g of β-glucans, included in a mixed bread meal, gave no significant differences in glycaemic response compared to a reference meal without muesli and β-glucans. In contrast, muesli with 4 g of β-glucans significantly (P<0.05) lowered the glucose and insulin responses compared to the reference meal.

Conclusions:

Muesli enriched with 4 g of β-glucans reduces postprandial glucose and insulin levels to a breakfast based on high glycaemic index products. A total of 4 g of β-glucans from oats seems to be a critical level for a significant decrease in glucose and insulin responses in healthy people.

Introduction

A major challenge of nutrition science is in the combat of diet-related disorders. In particular, the global pandemic of type 2 diabetes and pre-diabetic states goes hand in hand with a global pandemic of obesity, with the majority of the type II diabetics also suffering from obesity. Dietary measures that could facilitate weight maintenance, and improve insulin sensitivity are thus of interest in the prevention of the insulin resistance syndrome.

The postprandial glucose level after carbohydrate consumption is known to induce hormonal and metabolic responses with potential influence on health. In this respect food, characterized by a low glycaemic response (low glycaemic index (GI) foods), has been found to induce benefits on certain risk factors for chronic diseases, such as type II diabetes, cardiovascular disease and obesity. A low-GI diet may improve management of diabetes by lowering early postprandial hyperglycaemi and decreasing risk for postabsorptive hypoglycaemia (Brand et al., 1991; Wolever et al., 1992; Järvi et al., 1995; Gilbertson et al., 2001). By inducing low insulin levels (Björck et al., 2000) and increased insulin sensitivity (Wolever et al., 1992; Frost et al., 1996, 1998; Järvi et al., 1999) a low-GI diet also affects the risk for other metabolic diseases associated with the insulin resistance syndrome, for example, cardiovascular disease (Wannamethee et al., 2005). A recent examination of the Framingham Offspring Study showed that diets with lower GI are associated with lower insulin resistance, and a reduced risk of developing the insulin resistance syndrome (McKeown et al., 2004). Epidemiological evidence are also at hand indicating a preventive role of a low glycaemic response (Salmerón et al., 1997a, 1997b) and of grains and cereal fibre (Meyer et al., 2000) against development of type 2 diabetes. Further, a negative correlation was found between serum high-density lipoprotein cholesterol, another predictor of cardiovascular disease, and GI of the diet (Frost et al., 1999). Epidemiological studies have also found a preventive role of low-GI diet in relation to cardiovascular disease (Liu et al., 2000, 2001), whereas van Dam et al. (2000) did not find such a correlation.

With respect to obesity that has reached to epidemic proportions, the efficacy of low-fat diets has been questioned in recent years and instead the hypothesis has been focused on the intake of high-GI foods (Ludwig, 2000; Brand-Miller et al., 2002; Pawlak et al., 2002). Various studies have demonstrated positive acute effect of low-GI food, for example, increased satiety in healthy subjects (Granfeldt et al., 1994; Liljeberg and Björck, 1998; Östman et al., 2005) and decreased voluntary food intake in obese subjects (Ludwig, 1999). Further medium- to long-term studies in obese subjects are at hand, for example, the findings that a low-GI diet reduced fasting insulin levels in parallel to a weight loss in obese women in a 12-week study (Slabber et al., 1994), or that the body weight of obese children decreased more after a low-GI diet compared to a standard reduced fat diet in a 15-month study (Spieth et al., 2000) In the EURODIAB Complications Study of nearly 3000 adults with type I diabetes, consumption of lower GI diet was found to be related to lower measures of intra-abdominal fat mass and total body fat (waist-to-hip ratio and waist circumference) independently of carbohydrate, fat or fibre intake (Toeller et al., 2001). In the most recent WHO report, ‘Diet nutrition and the prevention of chronic diseases’ (FAO/WHO, 2003), the preventive potential of low-GI diets in relation to obesity and diabetes was graded as ‘possible’.

The glycaemic response of a starchy food is influenced by its rate of intestinal absorption, which in turn is influenced by its gross matrix structure (Granfeldt et al., 1991; Liljeberg et al., 1992; Tovar et al., 1992), the starch crystallinity (Granfeldt et al., 1995a, 2000, 1995b) and food components such as certain organic acids (Liljeberg and Björck, 1998; Liljeberg et al., 1995) or viscous dietary fibre (Holm and Bjorck, 1992; Fairchild et al., 1996; Liljeberg et al., 1996).

Current dietary recommendations emphasize generous amounts of carbohydrate foods and dietary fibre in the diet. The daily recommendation for dietary fibre intake in Sweden is 25–35 g. Soluble fibre has generated considerable interest because of its potential to moderate the rate of the postprandial glucose delivery to the blood (Nutall, 1993) and of its capacity to affect cholesterol metabolism (Brown et al., 1999). Water-soluble, gel-forming fibre in the form of guar gum, and β-glucans added to glucose solution or mixed with food reduce the expected rise in blood glucose and insulin concentration both in diabetics (Tappy et al., 1996; Jenkins et al., 2002) and healthy subjects (Jenkins et al., 1977; Fairchild et al., 1996; Liljeberg et al., 1996). In long-term control studies, various soluble fibres have been shown to reduce low-density lipoprotein cholesterol such as psyllium (Anderson et al., 1995), β-glucans (Önning et al., 1999; Kerckhoffs et al., 2003), guar gum (Aro et al., 1981) and leguminous fibre (Simpson et al., 1981). Further, oat bran concentrate has been found to improve long-term control of diabetes (Pick et al., 1996). The active component in oats is refereed to be β-glucans.

This mechanism for reducing glycaemic response and cholesterol may be utilized in the formulation of functional food. However, when used commercially, many factors, for example, cost and taste are of importance. In a recent study by Jenkins et al. (2002) it was concluded that β-glucans may be useful as a functional food component for reducing postprandial glycaemia, without changing the palatability of the product. In particular, there is a need to develop new low-GI food alternatives among the cereal products and many of the current bread and muesli-type products are characterized by high GI.

The purpose of the present paper was to study the effects on postprandial glycaemia and insulinaemia of an extruded muesli product based on a β-glucan–enriched oat bran as a major ingredient. Two levels of β-glucans, 3 or 4 g, were included in a breakfast based on muesli/yoghurt and white bread, and tested in healthy subjects. A similar meal without β-glucans was used as reference. The Ethics Committee of the Faculty of Medicine at Lund University approved the study.

Materials and methods

Experimental design

The present study is divided in two series: with the test meal including a serving of muesli with 3 and 4 g of β-glucans, respectively. The muesli was a component in a single serving packet with muesli and yoghurt. The effect of this serving packet with muesli/yoghurt on blood glucose and insulin responses after a bread breakfast meal was studied. As a reference meal a serving packet without β-glucans was included.

Series 1

Test meal, including 3 g β-glucans

The test meal and the reference meal were provided by (Skånemejerier, Malmö, Sweden). The test meal consisted of a serving packet with vanilla yoghurt and muesli with 3 g β-glucans besides that a sandwich with white wheat bread, cheese and butter were included. The muesli consisted of flakes made from oat bran (OatWell, Swedish Oat Fiber/Crea Nutrition, Väröbacka, Sweden), dried fruit (3.1 g), wheat germ, corn flakes, malt extract and salt. The amount of oat bran flakes was adjusted to contain 3 g of β-glucans. The reference meal was the same as the test meal, except for the oat bran flakes in the muesli. The content of available carbohydrates in the muesli was compensated for more bread in the reference meal. The compositions were standardized to contain 50 g available carbohydrates (Table 1).

Table 1 Composition of the test meal and the reference meal, series 1

Subjects

Nineteen healthy, non-smoking volunteers, 13 women and 6 men, took part in the study. Their average age was 37.5±15.2 years (mean±s.d.) and their mean body mass index 22.4±0.6 (mean±s.d.). The night before every test breakfast, the subjects were requested to eat a standardized late-evening meal, based on 2–3 slices of white wheat bread. After 10 pm, the subjects were allowed to drink only water. The reference and test breakfast meals were served randomized after an overnight fast. The tests were performed approximately 1 week apart and commenced at the same time in the morning. All meals were consumed steadily and finished within 12–14 min. Water (150 ml) and 150 ml tea or coffee was served with each meal. The test subjects were allowed to choose between these drinks and retained the same drink through the study.

Series 2

Test meal, including 4 g β-glucans

The test meal in series 2 consisted of a serving packet with vanilla yoghurt and muesli with 4 g β-glucans besides that a sandwich with white wheat bread, cheese and butter was included. The muesli consisted of flakes made from oat bran (OatWell), dried fruit (3.1 g), wheat germ, corn flakes, malt extract and salt. The amount of oat bran flakes was adjusted to contain 4 g of β-glucans. The test meal in series 2, thus consisted of exactly the same ingredients as the test meal in series 1 with the exception that more oat fibre flakes were included in the muesli, to an amount containing 4 g β-glucans. The reference meal was the same as the test meal, except for the muesli. The content of available carbohydrates in the muesli was compensated for more bread in the reference meal. The compositions were standardized to contain 50 g available carbohydrates (Table 2).

Table 2 Composition of the test meal and the reference meal, series 2

Subjects

Thirteen healthy, non-smoking volunteers, eight women and five men, took part in the study. Their average age was 37.5±3.6 years (mean±s.d.) and their mean body mass index 22.4±0.6 (mean±s.d.). The night before every test breakfast, the subjects were requested to eat a standardized late evening meal, based on 2–3 slices of white wheat bread. After 10 pm, the subjects were allowed to drink only water. The reference and test breakfast meals were served randomized after an overnight fast. The tests were performed approximately 1 week apart and commenced at the same time in the morning. All meals were consumed steadily and finished within 12–14 min. Water (150 ml) and 150 ml tea or coffee was served with each meal. The test subjects were allowed to choose between these drinks and retained the same drink through the study.

Sampling and analysis

The subjects arrived in the laboratory in the morning after an overnight fast. A fasting blood sample was taken before the meal was served. After the breakfast, blood samples were taken at 15, 30, 45, 70, 95 and 120 min for analysis of glucose and at 15, 30, 45, 95 and 120 min for analysis of insulin.

Blood glucose concentrations were determined with a glucose oxidase peroxidase reagent and serum insulin concentrations were determined with an enzyme immunoassay kit (Mercodia AB, Uppsala, Sweden).

The Ethics Committee of the Faculty of Medicine at Lund University approved the study.

Statistical analysis

The areas under the curves (AUCs) (0–95 and 0–120 min) were determined for blood glucose and serum insulin (GraphPad Prism ver. 3.0; GraphPad Software, San Diego, CA, USA). GI and II (insulinaemic index) were calculated from the AUCs with each subject being their own reference. All areas below the baseline were excluded from the calculations. Values are presented as mean±s.e.m. All statistical calculations were performed in Minitab Statistical Software (release 13 for Windows; Minitab Inc., State College, PA, USA). Significances were evaluated with the general linear model (analysis of variance) followed by Tukey's multiple comparisons test. Values of P<0.05 were considered significant.

Results

Series 1

When the muesli/yoghurt with 3 g β-glucans was included in the mixed bread-based meal no significant differences were seen in the glycaemic response (Figure 1), except for at one time point, 15 min, where the blood glucose level was significantly lower after the test meal with the oat bran flakes, comparing to the reference meal (P<0.05). A reduction of the incremental area under curve (0–95 min) by 17.6% was obtained compared to the reference meal, although it was not significant (Table 3).

Figure 1
figure1

Mean incremental blood glucose responses in healthy subjects following ingestion of breakfast meals; a test meal with wheat bread, yoghurt and muesli with oat bran flakes containing 3 g of β-glucans () and a reference meal with white wheat bread, yoghurt and muesli without oat bran flakes (▪). Values with different letters are significantly different (P<0.05).

Table 3 Fasting values, postprandial glucose and insulin areas, series 11

The postprandial insulin response was significantly lower at two time points, 15 and 30 min, after the test meal, compared to the reference meal (P<0.05, Figure 2). No significant difference was seen between the insulin areas after the two meals, although a reduction of 12.6% could be observed for the first 95 min (Table 3).

Figure 2
figure2

Mean incremental serum insulin responses in healthy subjects following ingestion of breakfast meals; a test meal with wheat bread, yoghurt and muesli with oat bran flakes containing 3 g of β-glucans () and a reference meal with white wheat bread, yoghurt and muesli without oat bran flakes (▪). Values with different letters are significantly different (P<0.05).

Series 2

When muesli with 4 g β-glucans was served with the white bread the glycaemic responses were significantly lower during the first 70 min period, compared to the reference meal without muesli (P<0.05, Figure 3). In the late-postprandial phase, the glucose response after the reference meal decreased faster than after the test meal with muesli; and at 95 min the glucose response was significantly higher after the test meal, compared to the reference meal (P<0.05, Figure 3). The area under the glucose curve after the test meal was significantly lower than after the reference (P<0.05, Table 4).

Figure 3
figure3

Mean incremental blood glucose responses in healthy subjects following ingestion of breakfast meals; a test meal with wheat bread, yoghurt and muesli with oat bran flakes containing 4 g of β-glucans () and a reference meal with white wheat bread and yoghurt without muesli (▪). Values with different letters are significantly different (P<0.05).

Table 4 Fasting values, postprandial glucose and insulin areas, series 21

The early postprandial insulin response (45 min) was significantly lower after the test meal with muesli compared to the reference meal (P<0.05, Figure 4). The area under the insulin curve was significantly lower than after the reference meal (P<0.05, Table 4).

Figure 4
figure4

Mean incremental serum insulin responses in healthy subjects following ingestion of breakfast meals; a test meal with wheat bread, yoghurt and muesli with oat bran flakes containing 4 g of β-glucans () and a reference meal with white wheat bread and yoghurt without muesli (▪). Values with different letters are significantly different (P<0.05).

Discussion

The muesli/yoghurt product containing 4 g of β-glucans from oat bran in a serving significantly reduced glycaemic and insulinaemic areas as well as levels at specific time points after a bread meal, whereas 3 g of β-glucans did not reach statistical significance regarding effects on metabolic responses although a tendency was seen to lower responses even with this lower β-glucans level. The oat barn used in series 1 and 2 was manufactured in the same way. The reduction in postprandial area (0–90 min) (% of reference meal) was doubled when 1 g more of β-glucans was present in the muesli/yoghurt portion (17.6 and 35.5%, respectively with 3 and 4 g β-glucans). Few previous studies have been carried out with β-glucan–rich oat fractions on high-GI food in healthy subjects. With oat gum (80% β-glucans) the glucose response has been shown to decrease almost 60% when 14.4 g was added to a glucose drink (50 g glucose) (Braaten et al., 1991) or 40% when 11 g was added to a wheat porridge (60 g of available starch) (Wood et al., 1990). Compared to the present study, higher amounts of β-glucans were used (12 and 9 g, respectively). In the present study we seem to have found a critical level, 4 g of β-glucans, for a significant decrease in glucose and insulin responses after a 50 g carbohydrate portion, in healthy people. We have previously shown that the naturally occurring levels in commercially available oat breakfast products like porridge or flaked cereals do not affect glucose and insulin responses (Granfeldt et al., 1994, 1995b). Thus, both a portion of oat flakes, and of oat porridge (50 g available carbohydrates) containing approximately 2.5 g β-glucans gave equally high glucose and insulin responses as white wheat bread. Whereas a portion of barley porridge containing 6.8 g β-glucans made from barley genotypes with elevated contents of β-glucans (17.5 g/100 g) significantly decreased postprandial glycaemia (Liljeberg et al., 1996) compared to white wheat bread. Reductions in postprandial glucose have also been seen in diabetics. Tappy et al. (1996) showed a decrease of 60% in glycaemic response after 35 g carbohydrate load with 6 g β-glucans, and in a more recent study by Jenkins et al. (2002) a reduction in glycaemic response by 12, 27 and 31%, respectively were seen with 3.7, 6.2 and 7.3 g β-glucans. Thus, increasing the dose of β-glucans successively reduced the glucose response, which also was seen in the current study.

The mechanism for a lowering postprandial glycaemia with β-glucans is probably related to an increased luminal viscosity, leading to a prolongation of carbohydrate digestion and absorption (Battilana et al., 2001). β-glucan is a source of viscous dietary fibre that preferably is found in oat and barley. However, in a recent study Biörklund et al. (2005) found a decrease in postprandial glucose and insulin response in hypercholesterolaemic subjects, after 5 g of β-glucans from oats but not from the same amount of β-glucans from barley. The authors hypothesized that both the lower molecular weight and the lower solubility of the barley β-glucans compared to oat β-glucans resulted in a lower viscosity in the barley product, which probably would influence the difference in glucose response between the food products containing oat and barley β-glucans. Not only is the origin of importance for the viscosity, a degradation of β-glucans may occur during food processing. Åman et al. (2004) showed an enzymatic degradation of β-glucan during baking, although the mean molecular weight of β-glucan in oats was retained in, for example, oat flakes and oat porridge. Variation in raw materials, processing conditions or ingredients may modify the physicochemical properties of β-glucan-like viscosity, molecular weight and solubility (Beer et al., 1997) and in this way influences the physiological properties. To maintain the functional nutritional attributes of β-glucan, it is important that the processing of oat kernels to oat bran, with an elevated concentration of β-glucan, does not damage the polymeric β-glucan structure. These factors require careful attention during processing, if β-glucan properties are to be maintained or improved in the final food application until consumption. Therefore, in vitro models should be used, for the assessment of the physiological properties of viscous dietary fibres.

Also long-term effects of β-glucans may improve glucose metabolism. Thus, in a crossover study with moderately hypercholesterolaemic men and women, a modest amount of β-glucans (5–7.5 g) during 5 weeks was shown to have beneficial effects on glucose and insulin responses after a glucose challenge (Hallfrisch et al., 1995), suggesting benefits on glucose tolerance. β-glucans are indigestible in the small intestine but are fermented by bacteria in the colon. With respect to glucose tolerance there is evidence in support of mechanism involving colonic fermentation of indigestible carbohydrates. Accordingly, in a recent overnight study (Granfeldt et al., 2004) we showed that an evening meal containing high levels of indigestible carbohydrates (resistant starch and soluble dietary fibre) substantially reduced GI and II of white bread determined at a subsequent breakfast meal compared to an evening meal of white wheat bread. Further, in a follow up study (Nilsson et al., 2006) the same evening meal, boiled barley kernels, gave significantly lower blood glucose response to a white wheat bread breakfast, compared to evening meals with white wheat bread or spaghetti with added wheat bran. A high fermentative activity in the colon may increase the colonic production of short-chain fatty acid including propionic acid, which has been implemented as a moderator of hepatic glucose metabolism (Venter et al., 1990).

The results of the present study show that a muesli/yoghurt product containing 4 g of β-glucans reduces postprandial glucose and insulin levels to a mixed bread-based breakfast.

The present work further demonstrates that 4 g of β-glucans from oats, with retained physicochemical properties, seems to be a critical level for a significant decrease in glucose and insulin responses, in healthy people. In general, oat products available on the market do not contain sufficient quantities of β-glucan to achieve appreciable health effects of this type, which opens for tailoring and production of new functional food products. However, as the origin processing parameters and food matrix may influence the physiological effects of the β-glucans, new low-GI products need to be carefully evaluated for their physiological effects before entering the market. This may have been evaluated in this study with an in vitro approach considering the physiological viscosity.

References

  1. Åman P, Rimsten L, Andersson R (2004). Molecular weight distribution of beta-glucan in oat-based foods. Cereal Chem 81, 356–360.

    Article  Google Scholar 

  2. Anderson JW, O'Neal DS, Riddell-Mason S, Floore TL, Dillon DW, Oeltgen PR (1995). Postprandial serum glucose, insulin, and lipoprotein responses to high- and low-fiber diets. Metabolism 44, 848–854.

    CAS  Article  Google Scholar 

  3. Aro A, Uusitupa M, Voutilainen E, Hersio K, Korhonen T, Siitonen O (1981). Improved diabetic control and hypocholesterolaemic effect induced by long-term dietary supplementation with guar gum in type 2 (insulin-independent) diabetes. Diabetologia 21, 29–33.

    CAS  Article  Google Scholar 

  4. Battilana P, Ornstein K, Minehira K, Schwarz J, Acheson K, Schneiter P et al. (2001). Mechanisms of action of beta-glucan in postprandial glucose metabolism in healthy men. Eur J Clin Nutr 55, 327–333.

    CAS  Article  Google Scholar 

  5. Beer MU, Wood PJ, Weisz J, Fillion N (1997). Effect of cooking and storage on the amout and molecular weight of (1 → 3)(1 → 4)-β-D-glucan extracted from oat products by an in vitro digestion system. Cereal Chem 74, 705–709.

    CAS  Article  Google Scholar 

  6. Biörklund M, van Rees A, Mensink RP, Önning G (2005). Changes in serum lipids and postprandial glucose and insulin concentration of beverages dose-controlled trial. Eur J Clin Nutr 59, 1272–1281.

    Article  Google Scholar 

  7. Björck IME, Liljeberg HGM, Östman EM (2000). Low glycaemic-index foods. Br J Nutr 83, S149–S155.

    Article  Google Scholar 

  8. Braaten JT, Wood P, Scott FW, Riedel KD, Poste L, Collins W (1991). Oat gum lowers glucose and insulin after an oral glucose load. Am J Clin Nutr 53, 1425–1430.

    CAS  Article  Google Scholar 

  9. Brand J, Colagiuri S, Crossman S, Allen A, Roberts D, Truswell S (1991). Low-glycemic index foods improve long term glycemic control in NIDDM. Diabetes Care 14, 95–101.

    CAS  Article  Google Scholar 

  10. Brand-Miller JC, Holt SH, Pawlak DB, McMillan J (2002). Glycemic index and obesity. Am J Clin Nutr 76, 281S–285S.

    CAS  Article  Google Scholar 

  11. Brown L, Rosner B, Willett WW, Sacks FM (1999). Cholesterol-lowering effects of dietary fiber: a meta-analysis. Am J Clin Nutr 69, 30–42.

    CAS  Article  Google Scholar 

  12. Fairchild RM, Ellis PR, Byrne AJ, Luzio SD, Mir MA (1996). A new breakfast cereal containing guar gum reduces postprandial plasma glucose and insulin concentrations in normal-weight human subjects. Br J Nutr 76, 63–73.

    CAS  Article  Google Scholar 

  13. FAO/WHO (2003). Report: Diet, nutrition and the prevention of chronic diseases: report of a joint WHO/FAO expert consultation. WHO Technical Report Series 916.

  14. Frost G, Keogh B, Smith D, Akinsanya K, Leeds A (1996). The effect of low-glycemic carbohydrate on insulin and glucose response in vivo and in vitro in patients with coronary heart disease. Metabolism 45, 669–672.

    CAS  Article  Google Scholar 

  15. Frost G, Leeds A, Trew G, Margara R, Dornhorst A (1998). Insulin sensitivity in women at risk of coronary heart disease and the effect of a low glycemic diet. Metabolism 47, 1245–1251.

    CAS  Article  Google Scholar 

  16. Frost G, Leeds AA, Doré CJ, Madeiros S, Brading S, Dornhorst A (1999). Glycaemic index as a determinant of serum HDL-cholesterol concentration. Lancet 353, 1045–1048.

    CAS  Article  Google Scholar 

  17. Gilbertson HR, Brand-Miller JC, Thorburn AW, Evans S, Chondros P, Werther GA (2001). The effect of flexible low glycemic index dietary advice versus measured carbohydrate exchange diets on glycemic control in children with type 1 diabetes. Diabetes Care 24, 1137–1143.

    CAS  Article  Google Scholar 

  18. Granfeldt Y, Wu X, Björck I (2004). Determination of the glycemic index (GI); some methodological aspects. Eur J Clin Nutr 60, 104–112.

    Article  Google Scholar 

  19. Granfeldt YE, Björck IME, Hagander B (1991). On the importance of processing conditions, product thickness and egg addition for the glycaemia and hormonal responses to pasta: a comparison with bread made from ‘pasta ingredients’. Eur J Clin Nutr 45, 489–499.

    CAS  PubMed  Google Scholar 

  20. Granfeldt YE, Drews A, Björck IME (1995a). Arepas made from high-amylose corn flour produce favourably low glucose and insulin responses in healthy humans. J Nutr 125, 459–465.

    CAS  PubMed  Google Scholar 

  21. Granfeldt YE, Eliasson A-C, Bjorck I (2000). An examination of the possibility of lowering the glycemic index of oat and barley flakes by minimal processing. J Nutr 130, 2207–2214.

    CAS  Article  Google Scholar 

  22. Granfeldt YE, Hagander B, Björck IM (1995b). Metabolic responses to starch in oat and wheat products. On the importance of food structure, incomplete gelatinization or presence of viscous dietary fibre. Eur J Clin Nutr 49, 189–199.

    CAS  PubMed  PubMed Central  Google Scholar 

  23. Granfeldt YE, Liljeberg HGM, Drews A, Newman R, Björck IME (1994). Glucose and insulin responses to barley products: influence of food structure and amylose-amylopectin ratio. Am J Clin Nutr 59, 1075–1082.

    CAS  Article  Google Scholar 

  24. Hallfrisch J, Scholfield DJ, Behall KM (1995). Diets containing soluble oat extracts improve glucose and insulin responses of moderately hypercholosterolemic men and women. Am J Clin Nutr 61, 379–384.

    CAS  Article  Google Scholar 

  25. Holm J, Bjorck I (1992). Bioavailability of starch in various wheat-based bread products: evaluation of metabolic responses in healthy subjects and rate and extent of in vitro starch digestion. Am J Clin Nutr 55, 420–429.

    CAS  Article  Google Scholar 

  26. Holm J, Björck IME, Drews A, Asp N-G (1986). A rapid method for the analysis of starch. Starch/Stärke 38, 224–226.

    CAS  Article  Google Scholar 

  27. Jenkins AL, Jenkins DJA, Zdravkovic U, Wursch P, Vuksan V (2002). Depression of the glycemic index by high levels of beta-glucan fiber in two functional foods tested in type 2 diabetes. Eur J Clin Nutr 556, 622–628.

    Article  Google Scholar 

  28. Jenkins DJ, Leeds AR, Gassull MA, Cochet B, Alberti GMM (1977). Decrease in postprandial insulin and glucose concentrations by guar and pectin. Ann Intern Med 86, 20–23.

    CAS  Article  Google Scholar 

  29. Järvi AE, Karlström BE, Granfeldt YE, Björck IME, Asp N-G, Vessby BOH (1999). Improved glycemic control and lipid profile and nomalized fibrinolytic activity on a low-glycemic index diet in type 2 diabetic patients. Diabetes Care 22, 10–18.

    Article  Google Scholar 

  30. Järvi AE, Karlström BE, Granfeldt YE, Björck IME, Vessby BOH, Asp N-GL (1995). The influence of food structure on postprandial metabolism in patients with non-insulin-dependent diabetes mellitus. Am J Clin Nutr 61, 837–842.

    Article  Google Scholar 

  31. Kerckhoffs DA, Hornstra G, Mensink RP (2003). Cholesterol-lowering effect of β-glucan from oat bran in midly hypercholesterolic subjects may decrease when β-glucan is incorporated into bread and cookies. Am J Clin Nutr 78, 221–227.

    CAS  Article  Google Scholar 

  32. Liljeberg HGM, Björck IME (1998). Delayed gastric emptying rate may explain improved glycaemia in healthy subjects to a starchy meal with added vinegar. Eur J Clin Nutr 52, 368–371.

    CAS  Article  Google Scholar 

  33. Liljeberg HGM, Granfeldt YE, Björck IME (1992). Metabolic response to starch in bread containing intact kernels versus milled flour. Eur J Clin Nutr 46, 561–575.

    CAS  PubMed  PubMed Central  Google Scholar 

  34. Liljeberg HGM, Granfeldt YE, Björck IME (1996). Products based on a high fiber barley genotype, but not on common barley or oats, lower postprandial glucose and insulin responses in healthy humans. J Nutr 126, 458–466.

    CAS  Article  Google Scholar 

  35. Liljeberg HGM, Lönner CH, Björck IME (1995). Sourdough fermentation or addition of organic acids or corresponding salts to bread improves nutritional properties of starch in healthy humans. J Nutr 125, 1503–1511.

    CAS  PubMed  Google Scholar 

  36. Liu S, Manson JE, Stampfer MJ, Holmes MD, Hu FB, Hankinson SE et al. (2001). Dietary glycemic load assessed by food-frequency questionnaire in relation to plasma high-density-lipoprotein cholesterol and fasting plasma triacylglycerols in postmenopausal women. Am J Clin Nutr 73, 560–566.

    CAS  Article  Google Scholar 

  37. Liu S, Manson JE, Stampfer MJ, Hu FB, Giovannucci E, Colditz GA et al. (2000). A prospective study of whole-grain intake and risk of type 2 diabetes mellitus in US women. Am J Public Health 90, 1409–1415.

    CAS  Article  Google Scholar 

  38. Ludwig DS (2000). Dietary glycemic index and obesity. J Nutr 130, 280S–283S.

    CAS  Article  Google Scholar 

  39. Ludwig DS MJ, Al-Zahrani A, Dallal GE, Blanco I, Roberts SB (1999). High glycemic index foods, overeating, and obesity. Pediatrics 103, 1–6.

    Article  Google Scholar 

  40. McKeown NM, Meigs JB, Liu S, Saltzman E, Wilson PWF, Jaques PF (2004). Carbohydrate nutrition, insulin resistance, and the prevalence of the metabolic syndrome in the Framingham offspring cohort. Diabetes Care 27, 538–546.

    Article  Google Scholar 

  41. Meyer KA, Kushi LH, Jacobs Jr DR, Slavin J, Sellers TA, Folsom AR (2000). Carbohydrates, dietary fiber, and incident type 2 diabetes in older women. Am J Clin Nutr 71, 921–930.

    CAS  Article  Google Scholar 

  42. Nilsson A, Granfeldt YE, Östman E, Preston T, Björck IME (2006). Effects of GI and content of indigestible carbohydrates of cereal-based evening meals on glucose tolerance at a subsequent standardised breakfast. Eur J Clin Nutr 60, 1092–1099.

    CAS  Article  Google Scholar 

  43. Nutall F (1993). Dietary fiber in the management of diabetes. Diabetes 42, 503–508.

    Article  Google Scholar 

  44. Önning G, Wallmark A, Persson M, Åkesson B, Elmståhl S, Öste R (1999). Consumtion of oat milk for 5 weeks lowers serum cholesterol and LDL cholesterol in free-living men with moderate hypercholesterolemia. Nutr Metab 43, 301–309.

    Article  Google Scholar 

  45. Östman EM, Granfeldt Y, Persson L, Björck IM (2005). Vinegar supplementation lowers glucose and insulin responses and increases satiety after a bread meal in healthy subjects. Eur J Clin Nutr 59, 983–988.

    Article  Google Scholar 

  46. Pawlak DB, Ebbeling CB, Ludwig DS (2002). Should obese patients be counselled to follow a low-glycaemic index diet? Yes.. Obes Rev 3, 235–243.

    CAS  Article  Google Scholar 

  47. Pick ME, Hawrysh ZJ, Gee MI, Toth E, Garg ML, Hardin RT (1996). Oat bran concentrate bread products improve long-term control of diabetes: a pilot study. J Am Diet Assoc 96, 1254–1261.

    CAS  Article  Google Scholar 

  48. Salmerón J, Ascherio A, Rimm EB, Colditz GA, Spiegelman D, Jenkins DJ et al. (1997a). Dietary fibre, glycemic load, and risk of NIDDM in men. Diabetes Care 20, 545–550.

    Article  Google Scholar 

  49. Salmerón J, Manson JE, Stampfer MJ, Colditz GA, Wing AL, Willett WC (1997b). Dietary fibre, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. J Am Med Assoc 277, 472–477.

    Article  Google Scholar 

  50. Simpson HCR, Lousley S, Geekie M, Simpson RW, Carter RD, Hockaday TDR et al. (1981). A high carbohydrate leguminous fibre diet improves all aspects of diabetic control. The Lancet 3, 1–5.

    Article  Google Scholar 

  51. Slabber M, Barnard HC, Kuyl JM, Dannhauser A, Schall R (1994). Effects of a low-insulin-response, energy-restricted diet on weight loss and plasma insulin concentrations in hyperinsulinemic obese females. Am J Clin Nutr 60, 48–53.

    CAS  Article  Google Scholar 

  52. Spieth LE, Harnish JD, Lenders CM, Raezer LB, Pereira MA, Hangen SJ et al. (2000). A low-glycemic index diet in the treatment of pediatric obesity. Arch Pediatr Adolesc Med 154, 947–951.

    CAS  Article  Google Scholar 

  53. Tappy L, Gügolz E, Würsch P (1996). Effects of breakfast cereals containing various amounts of betaglucan fibers on plasma glucose and insulin responses in NIDDM subjects. Diabetes Care 19, 831–834.

    CAS  Article  Google Scholar 

  54. Toeller M, Buyken AE, Heithkamp G, Cathelineau G, Ferriss B, Michel G, Group EICS (2001). Nutrient intakes as predictors of body weight in European people with type 1 diabetes. Int J Obes 25, 1815–1822.

    CAS  Article  Google Scholar 

  55. Tovar J, Granfeldt YE, Björck IME (1992). Effects of processing on blood glucose and insulin responses to starch in legumes. J Agric Food Chem 40, 1846–1851.

    CAS  Article  Google Scholar 

  56. van Dam RM, Visscher AWJ, Feskens EJM, Verhoef P, Kromhout D (2000). Dietary glycemic index in relation to metabolic risk factors and incidence of coronary heart disease: the Zutphen Elderly Study. Eur J Clin Nutr 54, 726–731.

    CAS  Article  Google Scholar 

  57. Venter CS, Vorster HH, Cummings JH (1990). Effects of dietary propionate on carbohydrate and lipid metabolism in healthy volunteers. Am J Gastroenterol 85, 549–553.

    CAS  PubMed  PubMed Central  Google Scholar 

  58. Wannamethee SG, Lowe GDO, Gerald SA, Ann R, Lucy L, Whincup PH (2005). The metabolic syndrome and insulin resistance: relationship to haemostatic and inflammatory makers in older non-diabetic men. Atherosclerosis 181, 101–108.

    CAS  Article  Google Scholar 

  59. Wolever TMS, Jenkins DJA, Vuksan V, Jenkins AL, Buckley GC, Wong GS et al. (1992). Beneficial effect of a low glycaemic index diet in type 2 diabetes. Diabet Med 9, 451–458.

    CAS  Article  Google Scholar 

  60. Wood PJ, Braaten Jan T, Scott FW, Riedel Doreen, Poste LM (1990). Comparisons of viscous properties of oat and guar gum and the effects of these and oat bran on glycemic index. J Agric Food Chem 38, 753–757.

    CAS  Article  Google Scholar 

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Acknowledgements

Sponsorship: Skånemejerier, Malmö, Sweden.

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Correspondence to Y Granfeldt.

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Guarantor: Y Granfeldt.

Contributors: YG contributed to the study design and data analysis. He is also responsible for writing the manuscript. LN contributed to the study design. IB contributed to the study design and to the manuscript.

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Granfeldt, Y., Nyberg, L. & Björck, I. Muesli with 4 g oat β-glucans lowers glucose and insulin responses after a bread meal in healthy subjects. Eur J Clin Nutr 62, 600–607 (2008). https://doi.org/10.1038/sj.ejcn.1602747

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Keywords

  • β-glucan
  • glucose response
  • insulin response
  • functional foods
  • oat bran
  • glucose tolerance

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