Vinegar dressing and cold storage of potatoes lowers postprandial glycaemic and insulinaemic responses in healthy subjects



To investigate the effects of cold storage and vinegar addition on glycaemic and insulinaemic responses to a potato meal in healthy subjects.

Subjects and setting:

A total of 13 healthy subjects volunteered for the study, and the tests were performed at Applied Nutrition and Food Chemistry, Lund University, Sweden.

Experimental design and test meals:

The study included four meals; freshly boiled potatoes, boiled and cold stored potatoes (8°C, 24 h), boiled and cold stored potatoes (8°C, 24 h) with addition of vinaigrette sauce (8 g olive oil and 28 g white vinegar (6% acetic acid)) and white wheat bread as reference. All meals contained 50 g available carbohydrates and were served as a breakfast in random order after an overnight fast. Capillary blood samples were collected at time intervals during 120 min for analysis of blood glucose and serum insulin. Glycaemic (GI) and insulinaemic indices (II) were calculated from the incremental areas using white bread as reference.


Cold storage of boiled potatoes increased resistant starch (RS) content significantly from 3.3 to 5.2% (starch basis). GI and II of cold potatoes added with vinegar (GI/II=96/128) were significantly reduced by 43 and 31%, respectively, compared with GI/II of freshly boiled potatoes (168/185). Furthermore, cold storage per se lowered II with 28% compared with the corresponding value for freshly boiled potatoes.


Cold storage of boiled potatoes generated appreciable amounts of RS. Cold storage and addition of vinegar reduced acute glycaemia and insulinaemia in healthy subjects after a potato meal. The results show that the high glycaemic and insulinaemic features commonly associated with potato meals can be reduced by use of vinegar dressing and/or by serving cold potato products.


The Swedish Agency for Innovation Systems (Project No P11900-3 A) and Öresund Starch Profiles (ÖSP).


Today we see a worldwide increase in the prevalence of diseases linked to insulin resistance. Although sedentary lifestyle play a major role, the characteristics of the diet is highly involved in the genesis of the insulin resistance syndrome. One quality parameter of the diet, which is increasingly implicated in relation to the insulin resistance syndrome is the glycaemic index (GI). The GI classifies carbohydrate-rich foods according to their blood glucose raising effect (Jenkins et al, 1981). Several studies have shown beneficial effects with low GI diets in the prevention and treatment of insulin resistance (McKeown et al, 2004) and related diseases, for example, cardiovascular disease (Liu et al, 2000) and type II diabetes (Salmeron et al, 1997a, 1997b).

The GI of carbohydrate foods can be optimised by the modulation of certain food factors affecting the rate of glucose delivery to the blood by, for example, reducing the gastric emptying rate and/or by delaying the digestion and absorption of carbohydrates in the small intestine. This may be achieved by choosing specific raw materials and/or processing conditions that influence the bioavailability of the carbohydrate substrate. Although not a prerequisite, food factors that reduce GI also frequently lead to formation of resistant starch (RS) (Granfeldt et al, 1995; Björck et al, 2000). RS is the starch fraction which is not absorbed in the small intestine of healthy individuals (Asp, 1992) and thus, provide the colonic microflora with a fermentable carbohydrate substrate, which promote colonic production of short-chain fatty acids (SCFAs). Studies indicate that especially butyrate is formed during colonic fermentation of RS (Scheppach et al, 1988). Butyrate is considered to be an important substrate for the colonocytes (Roediger, 1980). Furthermore it is not only associated with benefits in relation to colonic health in general, but also with favourable symptoms in patients with ulcerative colitis (Brouns et al, 2002; Hallert et al, 2003). Several studies have shown increased amounts of RS upon retrogradation of starchy foods, for example, in boiled potatoes after storage in a refrigerator (Englyst & Cummings, 1987; Kingman & Englyst, 1994; Åkerberg et al, 1998). Potato products are generally regarded as high GI foods (Soh & Brand-Miller, 1999; Foster-Powell et al, 2002) and the possibility to simultaneously lower the glycaemic response and increase the RS content offers an interesting way of improving the nutritional value of the potato.

Another factor that can be exploited to improve glycaemia and insulinaemia to starchy foods is addition of organic acids, such as acetic acid (Ebihara & Nakajima, 1988). Both Brighenti et al (1995) and Liljeberg and Björck (1998) found a significant lowering of the glycaemic responses in healthy subjects when adding acetic acid, in the form of vinegar, to starchy meals. Furthermore, vinegar addition to a test meal composed of a white bagel, butter and orange juice was shown to improve acute postprandial insulin sensitivity in insulin resistant subjects (Johnston et al, 2004), as measured using the procedure by Matsuda and DeFronzo (1999).

In the present study, the effect of cold storage of potatoes (8°C, 24 h) and/or addition of vinegar (28 g/292 g potatoes) on acute blood glucose and insulin responses to a potato meal was investigated in healthy subjects. Furthermore, the impact of cold storage on the yield of RS was measured using an in vitro method.

Subjects and methods

Chemical analysis

Potentially available starch was analysed in the test products according to Holm et al (1986). Total starch content was determined in freshly boiled and boiled and cold stored potatoes with the method by Björck and Siljeström (1992). Further, in vitro RS content was analysed in freshly boiled and boiled and cold stored potatoes according to Åkerberg et al (1998) with the exception that incubation was performed at 37°C instead of 40°C (Fredriksson et al, 2000).

Subjects and meals

In all, 13 healthy volunteers (10 women and three men) aged 19–32 y, with normal body mass indices (22.5±2.1 kg/m2; mean±s.d.) and without drug therapy participated in the study. Potatoes of the cultivar Sava (a firm winter potato variety) were bought from a local farmer. Tubers of approximately the same size (128±18 g, mean±s.d.) were chosen so that each meal consisted of three potatoes. The potatoes were peeled, weighed and boiled in 1 l of water for 21–30 min to reach the same eat consistency. Furthermore, they were cut into four pieces and either served freshly boiled or after cold storage at 8°C for 24 h. In addition, cold stored potatoes previously boiled were served with a vinaigrette sauce including 28 g white vinegar (6% acetic acid, Druvan, Eslöv, Sweden) and 8 g olive oil (Zeta, Di Luca & Di Luca AB, Stockholm, Sweden). In all, 28 g vinegar corresponded to 28 mmol acetic acid. White wheat bread, baked according to Liljeberg and Björck (1994) was used as a reference. All meals, containing 50 g available starch, were consumed over 12 min and served with 250 ml water and 150 ml coffee/tea. The meals were served in random order at the same time in the morning after an over-night fast. The tests were performed approximately one week apart and commenced at the same time in the morning.

Blood analyses

Capillary blood samples were taken prior to the meal (0) and at 15, 30, 45, 60, 90 and 120 min after the meal for analysis of glucose and after 15, 30, 45, 90 and 120 min for analysis of serum insulin. Glucose concentrations in whole blood were determined with a glucose oxidase peroxidase reagent and serum insulin concentrations were determined on an integrated immunoassay analyzer, CODA™ Open Microplate System (Bio-Rad Laboratories, Hercules, CA, USA) using an enzyme immunoassay kit (Mercodia Insulin ELISA, Mercodia AB, Uppsala, Sweden). Approval of the study was given by the Ethics Committee of the Faculty of Medicine at Lund University.

Calculations and statistical methods

For each subject and test meal, the incremental postprandial areas under the curves for glucose and insulin were calculated (Graph Pad Prism, version 3.0; Graph Pad Software, San Diego, CA, USA). All areas below baseline were excluded. The glycaemic and insulinaemic indices were calculated from the 90 and 120 min incremental blood glucose and insulin areas, respectively, by using white wheat bread as a reference (GI/II=100/100). Statistical analyses were performed with incremental areas as well as for concentrations of blood glucose and insulin at each time point. Values are presented as mean±s.e.m. All statistical analyses were performed with 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.


The RS content was determined in vitro in freshly boiled, and in boiled and cold stored potatoes (8°C, 24 h). The amount of RS was significantly higher in the cold stored potatoes compared with the freshly boiled ones (Table 1).

Table 1 RS and available starch contents in freshly boiled and boiled and cold stored potatoes

No statistical difference was seen in GI or II values whether calculated from areas at 90 or 120 min postprandially (Tables 2 and 3). The GI (120 min) of freshly boiled potatoes was 168, which is very high (Table 2). The GI was significantly lower for cold potatoes with vinaigrette and fell within the same range as that of the white wheat bread reference. II values (120 min) were significantly lower for cold potatoes (134), and cold potatoes with addition of vinaigrette (128) compared with freshly boiled potatoes (185) (Table 3). The meal containing cold potatoes with addition of vinaigrette sauce resulted in significantly lower blood glucose responses at 15–45 min and at 90 min after the meal, compared with freshly boiled potatoes (Figure 1). Cold stored potatoes and white bread displayed significantly lower blood glucose responses at 15–30 min. White bread induced significantly lower insulin response than freshly boiled potatoes at 30–45 min postprandially (Figure 2).

Table 2 Acute postprandial blood glucose areas and GI values at 90 and 120 min in 13 healthy subjects after carbohydrate equivalent portions of white bread and potatoes served freshly boiled or boiled and cold stored with and without addition of a vinaigrette sauce
Table 3 Acute postprandial serum insulin areas and II values at 90 and 120 min in 13 healthy subjects after carbohydrate equivalent portions of white bread and potatoes served freshly boiled or boiled and cold stored with and without addition of a vinaigrette sauce
Figure 1

Mean blood glucose responses in healthy subjects after a breakfast with equicarbohydrate amounts of white wheat bread (▪), freshly boiled potatoes (), boiled potatoes stored at 8°C for 24 h () and boiled potatoes stored at 8°C for 24 h with addition of a vinaigrette sauce (♦). Values are means (n=13) with bars indicating s.e.m. Values with different letters are significantly different (ANOVA followed by Tukey's multiple test, P<0.05).

Figure 2

Mean serum insulin responses in healthy subjects after a breakfast with equicarbohydrate amounts of white wheat bread (▪), freshly boiled potatoes (), boiled potatoes stored at 8°C for 24 h () and boiled potatoes stored at 8°C for 24 h with addition of a vinaigrette sauce (♦). Values are means (n=13) with bars indicating s.e.m. Values with different letters are significantly different (ANOVA followed by Tukey's multiple test, P<0.05).


The present study showed that cold storage of boiled potatoes generated appreciable amounts of RS. Further, the possibility to substantially decrease glycaemic and insulinaemic responses to a potato meal was explored and found to be practically viable. Boiled potatoes are generally known to cause high GI's and II's, independent of variety and/or cooking method (Soh & Brand-Miller, 1999; Foster-Powell et al, 2002). Since potatoes are one of the staple foods in western countries, it is of interest to find methods to lower the accessibility of starch, hence lowering the glycaemic impact after a meal. In this study, two methods to reduce the rate of starch delivery to the blood were tested; cold storage and vinegar addition. Several studies have shown a decrease in starch availability, and in most cases also a subsequent increase in RS, when boiled potatoes are stored in a refrigerator, as evaluated in vitro (Englyst & Cummings, 1987; Kingman & Englyst, 1994; Åkerberg et al, 1998; Garcia-Alonso & Goni, 2000). Cold storage of potatoes has also been demonstrated to affect starch bioavailability in vivo. Consequently, Englyst and Cummings (1987) reported a dramatic increase in starch malabsorption with up to 12% of the starch passing indigested to the ileostomy effluent. Further, studies by Kanan et al (1998) demonstrated a 69% reduction of the GI following cold storage of boiled potatoes as calculated from the GI-values given in the international GI-tables (Foster-Powell et al, 2002). The increase in RS in the studies mentioned above is within the range of 1–4 times amounting to up to 7% RS (starch basis) after cold storage. Mainly amylose has been suggested to be involved in the formation of RS in, for example, autoclaved cereal starches (Berry, 1986). However, in boiled potatoes, also retrograded amylopectin seems to play a role (Englyst & Cummings, 1987). Differences in thermal processing conditions may explain why either amylose or amylopectin are involved in the formation of RS, but also the botanical origin of the starch plays an important role. Amylopectin from potato retrograde to a higher extent than cereal amylopectin following storage at 6°C for 2 or 4 days, which has been attributed to the longer outer chains in the case of potato amylopectin (Fredriksson et al, 1998). For many starchy foods, a reduction in GI is accompanied by a higher RS content. However, the lowered available starch content per se does not explain the lowered GI (Jenkins et al, 1987; Wolever, 1990; Raben et al, 1994; Björck et al, 2000).

The mechanism by which organic acids reduce glycaemia and insulinaemia to, for example, white bread and rice (Liljeberg & Björck, 1998; Sugiyama et al, 2003) is not fully understood. In the case of acetic acid, the magnitude of reduction in glycaemia may be as much as 35%, depending on the level of acetic acid. Brighenti et al (1995) suggested that the acetic acid caused an inhibition of the amylases whereas others have found evidence of a delay in gastric emptying rate (Liljeberg & Björck, 1998). The studies mentioned above have been performed in healthy subjects. In a recent study, vinegar added to a meal with a bagel, butter and orange juice was shown to improve postprandial insulin sensitivity in insulin resistant subjects (Johnston et al, 2004). Furthermore, lactic acid has also been shown to induce metabolic benefits in humans (Liljeberg et al, 1995; Östman et al, 2002a). In a recent feeding study with obese hyperinsulinaemic rats, the insulin demand was reduced at an oral glucose tolerance test performed at the end of a dietary period with wheat bread baked in the presence of lactic acid (Östman et al, 2005). It seems to be a prerequisite that lactic acid is present during heat treatment of the starch in order to produce a lowered GI, possibly by introducing an amylolytic barrier (Östman et al, 2002b). Thus, different organic acids seem to have the capacity to modulate acute glycaemia although through different mechanisms. Several studies have been performed to evaluate the potential effects of acetic acid on glucose metabolism. Acetic acid has thus been shown to suppress disaccharidase activity in Caco-2 cells (human colonic carcinoma cells) (Ogawa et al, 2000) and to activate gluconeogenesis and induce glycogenesis in the rat liver after a fasting state (Fushimi et al, 2001). Although it has been established that the presence of acetic acid in a meal delays the gastric emptying rate and thus reduce postprandial glycaemia (Ebihara & Nakajima, 1988; Liljeberg & Björck, 1998), more studies are needed to elucidate to what extent other physiological mechanisms also may be involved and affect glucose metabolism.

In the present study, vinegar was mixed with olive oil to a vinaigrette sauce. In a study by Liljeberg & Björck (1998), white vinegar corresponding to 18 mmol/50 g available carbohydrates was served to white wheat bread together with 8 g olive oil. The GI and II of the vinegar supplemented white bread meal were calculated to 64 and 65, respectively. Adding vinegar alone (18 mmol/50 g available carbohydrates) appears to be less effective in modulating glycaemia to white bread (Östman et al, 2005), and the corresponding GI and II's were 89 and 103, respectively.

In the present study, the combination of cold storage and addition of a vinaigrette sauce substantially reduced GI for the boiled potatoes with 43% and II with 31%, respectively. Cold storage per se tended to reduce GI (26%) although the effect did not reach statistical significance. However, cold storage per se did significantly reduce II with 28%. As a comparison, in a study by Östman et al (2005), addition of 28 mmol white vinegar to white bread decreased GI significantly with 23% and II with 22% when calculated at 90 min.

It is concluded that cold storage of potatoes significantly increased RS intake from the potato meal, from 1.7 to 2.5 g. Since the estimated total daily intake of RS in 10 European countries has been estimated to 4.1 g (Dysseler & Hoffem, 1994) a meal consisting of three cold potatoes will provide approximately 60% of the daily intake, which may be advantageous from a health perspective. RS in the form of resistant potato starch has been shown to promote comparatively high yields of butyric acid upon colonic fermentation compared with other sources of indigestible carbohydrates, as judged from butyric acid analysis in human faeces and caecum and colon in pigs, respectively (Cummings et al, 1996; Martin et al, 1998). Cold storage and addition of vinegar also significantly lowered glycaemic and insulinaemic excursions to a potato meal. These effects are noteworthy and could be exploited to lower glycaemic impact of potatoes. However, it should be noted that the pickled potato salad still produced a glycaemic and insulinaemic response of a similar magnitude to that after the white wheat bread reference and it would be interesting to find other processing conditions and/or combinations to achieve a further lowering of the metabolic response.


  1. Asp NG (1992): Resistant starch – Proceedings from the 2nd Plenary Meeting of Euresta – European Flair Concerted Action 11 on Physiological Implications of the Consumption of Resistant Starch in Man. Eur. J. Clin. Nutr. 46, S1.

    Google Scholar 

  2. Berry CS (1986): Resistant starch: formation and measurement of starch that survives exhaustive digestion with amylolytic enzymes during the determination of dietary fibre. J. Cereal Sci. 4, 301–314.

    CAS  Article  Google Scholar 

  3. Björck I, Liljeberg H & Östman E (2000): Low glycaemic-index foods. Br. J. Nutr. 83, S149–S155.

    Article  Google Scholar 

  4. Björck IM & Siljeström MA (1992): In-vivo and in-vitro digestibility of starch in autoclaved pea and potato products. J. Sci. Food Agric. 58, 541–553.

    Article  Google Scholar 

  5. Brighenti F, Castellani G, Benini L, Casiraghi MC, Leopardi E, Crovetti R & Testolin G (1995): Effect of neutralized and native vinegar on blood glucose and acetate responses to a mixed meal in healthy subjects. Eur. J. Clin. Nutr. 49, 242–247.

    CAS  Google Scholar 

  6. Brouns F, Kettlitz B & Arrigoni E (2002): Resistant starch and ‘the butyrate revolution’. Trends Food Sci. Technol. 13, 251–261.

    CAS  Article  Google Scholar 

  7. Cummings JH, Beatty ER, Kingman SM, Bingham SA & Englyst HN (1996): Digestion and physiological properties of resistant starch in the human large bowel. Br. J. Nutr. 75, 733–747.

    CAS  Article  Google Scholar 

  8. Dysseler P & Hoffem D (1994): Estimation of resistant starch intake in Europe. In Proceedings of the concluding plenary meeting of EURESTA, April 1994. European Flair – Concerted Action no. 11 (COST 911) eds N-G Asp, JMM van Amelsvoort, JGAJ Hautvast, Wageningen: European Commission.

    Google Scholar 

  9. Ebihara K & Nakajima A (1988): Effect of acetic-acid and vinegar on blood-glucose and insulin responses to orally-administered sucrose and starch. Agric. Biol. Chem. 52, 1311–1312.

    CAS  Google Scholar 

  10. Englyst HN & Cummings JH (1987): Digestion of polysaccharides of potato in the small intestine of man. Am. J. Clin. Nutr. 45, 423–431.

    CAS  Article  Google Scholar 

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

    CAS  Article  Google Scholar 

  12. Fredriksson H, Björck I, Andersson R, Liljeberg H, Silverio J, Eliasson A-C & Åman P (2000): Studies on α-amylase degradation of retrograded starch gels from waxy maize and high-amylopection potato. Carbohydr. Polym. 43, 81–87.

    CAS  Article  Google Scholar 

  13. Fredriksson H, Silverio J, Andersson R, Eliasson A-C & Åman P (1998): The influence of amylose and amylopectin characteristics on gelatinization and retrogradation properties of different starches. Carbohydr. Polym. 35, 119–134.

    CAS  Article  Google Scholar 

  14. Fushimi T, Tayama K, Fukaya M, Kitakoshi K, Nakai N, Tsukamoto Y & Sato Y (2001): Acetic acid feeding enhances glycogen repletion in liver and skeletal muscle of rats. J. Nutr. 131, 1973–1977.

    CAS  Article  Google Scholar 

  15. Garcia-Alonso A & Goni I (2000): Effect of processing on potato starch: in vitro availability and glycaemic index. Nahrung. 44, 19–22.

    CAS  Article  Google Scholar 

  16. Granfeldt Y, Drews A & Björck I (1995): Arepas made from high amylose corn flour produce favorably low glucose and insulin responses in healthy humans. J. Nutr. 125, 459–465.

    CAS  Google Scholar 

  17. Hallert C, Björck I, Nyman M, Pousette A, Granno C & Svensson H (2003): Increasing fecal butyrate in ulcerative colitis patients by diet: controlled pilot study. Inflamm. Bowel Dis. 9, 116–121.

    Article  Google Scholar 

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

    CAS  Article  Google Scholar 

  19. Jenkins DJ, Jenkins AL, Wolever TM, Collier GR, Rao AV & Thompson LU (1987): Starchy foods and fiber: reduced rate of digestion and improved carbohydrate metabolism. Scand. J. Gastroenterol. Suppl. 129, 132–141.

    CAS  Article  Google Scholar 

  20. Jenkins DJ, Wolever TM, Taylor RH, Barker H, Fielden H, Baldwin JM, Bowling AC, Newman HC, Jenkins AL & Goff DV (1981): Glycemic index of foods: a physiological basis for carbohydrate exchange. Am. J. Clin. Nutr. 34, 362–366.

    CAS  Article  Google Scholar 

  21. Johnston CS, Kim CM & Buller AJ (2004): Vinegar improves insulin sensitivity to a high-carbohydrate meal in subjects with insulin resistance or type 2 diabetes. Diabetes Care 27, 281–282.

    Article  Google Scholar 

  22. Kanan W, Bijlani RL, Sachdeva U, Mahapatra SC, Shah P & Karmarkar MG (1998): Glycaemic and insulinaemic responses to natural foods, frozen foods and their laboratory equivalents. Indian J. Physiol. Pharmacol. 42, 81–89.

    CAS  PubMed  Google Scholar 

  23. Kingman SM & Englyst HN (1994): The influence of food preparation methods on the in-vitro digestibility of starch in potatoes. Food Chem. 49, 181–186.

    Article  Google Scholar 

  24. Liljeberg H & Björck I (1994): Bioavailability of starch in bread products. Postprandial glucose and insulin responses in healthy subjects and in vitro resistant starch content. Eur. J. Clin. Nutr. 48, 151–163.

    CAS  Google Scholar 

  25. Liljeberg H & Björck I (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 

  26. Liljeberg HG, Lönner CH & Björck IM (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  Google Scholar 

  27. Liu S, Willett WC, Stampfer MJ, Hu FB, Franz M, Sampson L, Hennekens CH & Manson JE (2000): A prospective study of dietary glycemic load, carbohydrate intake, and risk of coronary heart disease in US women. Am. J. Clin. Nutr. 71, 1455–1461.

    CAS  Article  Google Scholar 

  28. Martin LJM, Dumon HJW & Champ MMJ (1998): Production of short-chain fatty acids from resistant starch in a pig model. J. Sci. Food Agric. 77, 71–80.

    CAS  Article  Google Scholar 

  29. Matsuda M & DeFronzo RA (1999): Insulin sensitivity indices obtained from oral glucose tolerance testing: comparison with the euglycemic insulin clamp. Diabetes Care 22, 1462–1470.

    CAS  Article  Google Scholar 

  30. McKeown NM, Meigs JB, Liu S, Saltzman E, Wilson PW & Jacques 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 

  31. Ogawa N, Satsu H, Watanabe H, Fukaya M, Tsukamoto Y, Miyamoto Y & Shimizu M (2000): Acetic acid suppresses the increase in disaccharidase activity that occurs during culture of caco-2 cells. J. Nutr. 130, 507–513.

    CAS  Article  Google Scholar 

  32. Raben A, Tagliabue A, Christensen NJ, Madsen J, Holst JJ & Astrup A (1994): Resistant starch: the effect on postprandial glycemia, hormonal response, and satiety. Am. J. Clin. Nutr. 60, 544–551.

    CAS  Article  Google Scholar 

  33. Roediger WE (1980): Role of anaerobic bacteria in the metabolic welfare of the colonic mucosa in man. Gut 21, 793–798.

    CAS  Article  Google Scholar 

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

    CAS  Article  Google Scholar 

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

    CAS  Article  Google Scholar 

  36. Scheppach W, Fabian C, Sachs M & Kasper H (1988): The effect of starch malabsorption on fecal short-chain fatty acid excretion in man. Scand. J. Gastroenterol. 23, 755–759.

    CAS  Article  Google Scholar 

  37. Soh NL & Brand-Miller J (1999): The glycaemic index of potatoes: the effect of variety, cooking method and maturity. Eur. J. Clin. Nutr. 53, 249–254.

    CAS  Article  Google Scholar 

  38. Sugiyama M, Tang AC, Wakaki Y & Koyama W (2003): Glycemic index of single and mixed meal foods among common Japanese foods with white rice as a reference food. Eur. J. Clin. Nutr. 57, 743–752.

    CAS  Article  Google Scholar 

  39. Wolever TM (1990): The glycemic index. World Rev. Nutr. Diet. 62, 120–185.

    CAS  Article  Google Scholar 

  40. Åkerberg AK, Liljeberg HG, Granfeldt YE, Drews AW & Björck IM (1998): An in vitro method, based on chewing, to predict resistant starch content in foods allows parallel determination of potentially available starch and dietary fiber. J. Nutr. 128, 651–660.

    Article  Google Scholar 

  41. Östman E, Granfeldt Y, Persson L & Björck I (2005): Vinegar supplementation lowers glucose and insulin responses and increases satiety after a bread meal in healthy subjects. The doi-number is: 10.1038/sj.ejcn.1602197.

  42. Östman EM, Liljeberg Elmståhl HG & Björck IM (2002a): Barley bread containing lactic acid improves glucose tolerance at a subsequent meal in healthy men and women. J. Nutr. 132, 1173–1175.

    Article  Google Scholar 

  43. Östman EM, Nilsson M, Liljeberg Elmståhl H, Molin G & Björck I (2002b): On the effect of lactic acid on blood glucose and insulin responses to cereal products: mechanistic studies in healthy subjects and in vitro. J. Cereal Sci. 36, 339–346.

    Article  Google Scholar 

Download references


We thank Lisbeth Persson for invaluable technical assistance.

Author information



Corresponding author

Correspondence to M Leeman.

Additional information

Guarantor: I Björck.

Contributors: ML, EÖ and IB made the design of the study. ML was responsible for collection and analysis of data. ML, EÖ and IB contributed to the writing of the manuscript.

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Leeman, M., Östman, E. & Björck, I. Vinegar dressing and cold storage of potatoes lowers postprandial glycaemic and insulinaemic responses in healthy subjects. Eur J Clin Nutr 59, 1266–1271 (2005).

Download citation


  • potatoes
  • acetic acid
  • vinegar
  • glycaemic index
  • insulinaemic index
  • resistant starch

Further reading