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Human Nutrition and Metabolism
Research Communication

The Degree of Fat Saturation Does Not Alter Glycemic, Insulinemic or Satiety Responses to a Starchy Staple in Healthy Men

Human Nutrition Unit, School of Molecular and Microbial Biosciences, The University of Sydney, NSW 2006, Australia

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

	ABSTRACT

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Inclusion of fat reduces the glycemic response to a carbohydate meal, although the effect of different types of fat on glycemic, insulinemic and satiety responses is unclear. Ten healthy men received 50-g carbohydrate portions of mashed potato with isoenergetic amounts of butter (saturated fatty acid), Sunola oil (monounsaturated fatty acid) or sunflower oil (PUFA) and two 50-g glucose loads on separate days. Capillary blood was collected at regular intervals for 2 h. Satiety ratings were assessed by use of a rating scale. The glycemic index (GI), insulin index (II) and satiety index (SI) scores were calculated. Energy intakes from a meal consumed ad libitum at 2 h and for the remainder of the day were quantified. The GI values ranged from 68 ± 8 to 74 ± 10 and the II values ranged from 113 ± 10 to 122 ± 17, but there was no effect of fat type. SI scores and subsequent energy intake did not differ among the test meals. Substitution of unsaturated fats for saturated fatty acids had no acute benefits on postprandial glycemia, insulin demand or short-term satiety in young men.

KEY WORDS: • fat • glycemic index • insulin index • satiety • saturation

Dietary recommendations have emphasized the importance of a high carbohydrate, low fat diet for the prevention of chronic diseases linked to insulin resistance including obesity, diabetes and coronary heart disease (1,2). There is increasing evidence, however, that the quality of fat in the diet may be more important than the absolute quantity in avoiding so-called lifestyle diseases (3,4). In clinical studies, replacement of saturated fat with unsaturated fat has beneficial effects on serum lipid profiles and risk of heart disease (5). Several studies, summarized by Hu et al. (5), also suggest that a higher proportion of unsaturated fat, compared with saturated and trans-fat, may be beneficial for glucose homeostasis and insulin sensitivity, although other studies have not confirmed these findings (6–8).

Foods that are high in carbohydrates and saturated fat, such as potato chips, crisps, cakes and biscuits, make up a substantial proportion of total carbohydrate intake in Western countries. The substitution of saturated fatty acids with unsaturated fats in these foods may improve the overall nutritional quality but the effect on the postprandial glycemia and insulin demand is unclear. Although many studies in humans have documented the acute effect of added fat on glucose and insulin responses (9–13), the effect of fat type is inconsistent (14–17). Studies in animals have shown that the insulinotropic potency of individual fatty acids is decreased dramatically with chain length and degree of unsaturation (18).

High fat diets are also implicated in weight gain because of their high energy density. Whether the substitution of "unhealthy" saturated fatty acids with "healthier" unsaturated fats reduces passive overconsumption of fat has not been established. Two studies have shown that a high intake of PUFA suppresses energy intake (19) and fat intake (20) compared with saturated fatty acids (SFA) and monounsaturated fatty acids (MUFA). Studies in animal models, however, suggest that margarines high in PUFA and MUFA are less satiating than those high in SFA (21).

The lack of consensus among previous findings prompted us to assess, through the use of standardized glycemic index methodology (22), the acute effects of fats differing in degree of saturation (butter, Sunola and sunflower oil) on the postprandial glucose, insulin and appetite responses to a starchy staple. The two hypotheses addressed were that 1) the acute glycemic and insulin response to a 50-g carbohydrate portion of mashed potato with added butter (SFA) would be greater than the response to a similar meal with added Sunola oil (MUFA) or sunflower oil (PUFA), and 2) postingestive satiety ratings and suppression of food intake would be greater for a mashed potato meal with added PUFA than with added SFA or MUFA.

	MATERIALS AND METHODS

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Eleven healthy, nonsmoking men with a mean age of 21.9 ± 0.8 y (range 18–26 y) were recruited by advertisement from the student population of the University of Sydney. The BMI (mean ± SD) of the subjects was 21.5 ± 0.7 kg/m² (range 18.5 ± 24.5 kg/m²). The subjects’ usual diet was assessed by use of a modified version of a previously validated semiquantitative food frequency questionnaire (23) to estimate total daily energy intake (kJ) and proportions of carbohydrate, protein and fat (including SFA, MUFA and PUFA). None of the subjects was a restrained eater or dieter [mean score 3.4 ± 0.9; i.e., 10 for Factor I (cognitive restraint)] on the three-factor eating restraint questionnaire (24) and none had suffered any serious illness or history of obesity, type 2 diabetes, gastrointestinal disease or surgery, or was taking medication known to influence appetite or gastrointestinal motility. The study complied with the Helsinki Declaration of 1975 as revised in 1983 and the protocol was approved by the Institutional Ethics Committee. Subjects gave written informed consent.

The study included three test meals consisting of 50-g carbohydrate portions (307 g) of mashed potato (i.e., 61 g instant mashed potato prepared with 246 g water) with equivalent-energy quantities of Sunola (30 g) or sunflower (30 g) oil or butter (36.5 g). Instant mashed potato was chosen because it is a familiar, high carbohydrate, high glycemic index (GI) food (average GI = 88) (25) in which the fat content can be easily manipulated. The nutrient composition of the mashed potato and the added fats was calculated with the manufacturer’s data. Sunola oil contained mainly MUFA (80%), sunflower oil mainly PUFA (64%) and butter predominantly SFA (69%). The total energy content of the test foods was 2054 kJ. Protein, carbohydrate and fat accounted for 3, 42 and 55%, respectively, of the energy provided by the test foods. The test foods were prepared the day before and placed in individual bowls, covered and refrigerated overnight. They were heated in a standard microwave oven for 2 min on the morning of the test.

The reference food was 50 g of glucose (Glucodin powder, Boots Healthcare, North Ryde, NSW, Australia) dissolved in 500 mL of water. The glycemic and insulin responses to the reference food were tested on two separate occasions in each subject.

Each subject underwent five tests on separate days, in random order, separated by at least 2 d. Each subject was tested at the same time of the day and under similar conditions, thus acting as their own controls. Subjects were instructed to maintain regular activity patterns, to abstain from consuming alcohol on the day before testing and to avoid eating a meal based on legumes the night before a test. On test days, subjects attended the laboratory after a 10- to 12-h overnight fast. Upon arrival, they were asked to complete a short questionnaire assessing recent food and alcohol intake, body weight and fasting hunger ratings, and two fasting blood samples (-10 and 0 min) were collected. Subjects were then instructed to consume the test foods with 250 mL of water at an even rate over 12 min. Subjects were not aware of the type of fat in each meal and were unable to detect the difference when questioned.

At -10, 0 and at 15, 30, 45, 60, 90 and 120 min after ingestion of the test or reference foods, fingerprick blood samples (1.0 mL) were taken from warmed hands by use of an automatic lancet (Safe-T-Pro; Boehringer Mannheim Australia, Castle Hill, NSW). Blood samples were collected in 1.5-mL microcentrifuge tubes previously coated with heparin (10 IU heparin sodium salt; Sigma Chemical Co., St. Louis, MO), freeze dried and immediately centrifuged at 12,500 x g for 1 min. Plasma was pipetted into chilled tubes and stored at -20°C until assay (<1 mo).

Immediately before each blood sampling, subjective ratings of satiety were assessed by use of an equilateral seven-point category rating scale (RS) (26) with which ratings could range from -3 RS units = extremely hungry to +3 RS units = extremely full, with variations in the degree of hunger and fullness in between and 0 RS units = no particular feeling. At 120 min, subjects were offered a standard preweighed meal containing quantities of food in excess of what they were expected to eat. The subjects were instructed to consume the meal ad libitum and the total amount eaten (g) was measured covertly. Before leaving the laboratory, subjects were asked to keep a weighed food record for the remainder of the day.

Plasma glucose concentrations were measured in duplicate by use of a Roche Hitachi 912 automatic centrifugal spectrophotometric analyzer (Boehringer Mannheim, GmbH, Mannheim, Germany) employing a glucose hexokinase/glucose-6-phosphate dehydrogenase method (Roche Diagnostic Systems, Frenchs Forest, Australia). The mean intraassay and interassay CV were both <5%. Plasma insulin was measured by use of a commercial antibody-coated tube radioimmunoassay kit (Coat-a-Count; Diagnostic Products Corporation, Los Angeles, CA). The mean intraassay and interassay CV were both <5%. Cumulative changes in plasma glucose, insulin and satiety responses were quantified as the incremental area under the 120 min response curve (AUC) and the GI, insulin index (II) and satiety index (SI) were calculated as previously described (26). When individual GI or II scores differed from the mean by >2 SD, they were considered outliers and were excluded from the final analysis.

Dietary energy and macronutrient intakes were calculated by use of Food Works Professional Edition Version 3.00 software (Xyris Software, Highgate Hill, Qld, Australia). Energy (kJ) and macronutrient (% protein, % fat and % carbohydrate) data were based on the Australian food composition tables and manufacturers’ data.

Results are given as means ± SEM. Two-way ANOVA was performed by use of SPSS for Windows Release 11.0.0 (Standard Version, Chicago, IL). With 10 subjects, the study had >80% power to discriminate a 1 SD difference between meals at significance level P < 0.05.

	RESULTS

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
The study protocol was well tolerated. Of the 11 subjects recruited, 10 completed the study. The GI values of the meals ranged from 68 ± 8 to 74 ± 10 and were lower than the reference food (glucose) (P = 0.04) (Fig. 1A). However, fat type did not affect the GI (Fig. 1A, inset) or the II values (Fig. 1B, inset). The mean II values for the three test meals were all disproportionately greater than their corresponding GI values.

View larger version (23K): [in this window] [in a new window]   FIGURE 1 Incremental changes in plasma glucose (A) and insulin (B) concentrations in young men after consumption of a mashed potato meal with added butter (SFA), Sunola (MUFA) oil or sunflower (PUFA) oil compared with glucose. Values are means, n = 10. The insets show the glycemic index (A) and insulin index (B) of the meals. Values are means ± SEM, n = 10. Fat type did not affect the variables, P > 0.05.

	DISCUSSION

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Although the addition of fat increased insulinemia, the degree of fat saturation in a mashed potato meal had no biologically important effect on acute glycemic, insulinemic and satiety responses in young healthy men. These findings suggest that substitution of "healthy" fats for saturated fatty acids will not improve acute postprandial hyperglycemia and insulinemia nor reduce passive overconsumption of energy-dense meals.

Previous studies have produced conflicting findings. Gatti et al. (14) reported a reduction in the postprandial glucose responses to white bread after the addition of olive oil (MUFA) and corn oil (PUFA), but not butter (SFA). There is no effect of fat type on the insulin response. In contrast, Pederson et al. (15) found no differences in glucose responses to meals containing rapeseed oil (MUFA), sunflower oil (PUFA) or palm oil (SFA), whereas the early insulin response is lower after the PUFA meal. Joannic et al. (16) reported that both glycemia and peak insulin response are significantly lower with a meal containing PUFA compared with MUFA. Finally, Brynes et al. (17) found no significant differences in the incremental glucose or insulin AUC responses to a meal with added olive oil (MUFA), corn oil (PUFA) or butter (SFA). Our findings are consistent with those of Brynes et al. (17).

The contrast in findings among studies may be related to methodology, including the use of venous versus capillary blood, the timing of blood samples and the type and amount of fats and carbohydrates studied. The use of standard GI methodology in the present study allowed the detection of rapid changes in glycemic and insulinemic responses while minimizing the variation between responses to the foods arising from day-to-day variation in glucose tolerance.

The absence of differences in the present study results was not likely related to testing an insufficient quantity of fat. Pedersen et al. (15) used a smaller amount of fat (15 g) and Gatti et al. (14) used a similar amount (30 g) but detected differences. In those studies, only specific time points were significantly different, not the overall response as determined by the AUC. Furthermore, in some instances, the responses to the different fats were compared not to each other but to a carbohydrate meal alone (14).

Studies have shown that per unit energy, fat has a weaker effect on satiety than protein and carbohydrate (27) and high fat foods normally have a high energy density (28). Foods that are high in fat therefore tend to have a greater capacity to promote passive overconsumption, leading to weight gain and obesity, and this has been demonstrated in both lean (29) and obese (30) subjects. Data relating to the effects of different types of fat on appetite are limited. Lawton et al. (19) reported that a mixed meal containing safflower oil (PUFA) decreases nutrient intake at a subsequent meal, reduces postingestive ratings of motivation to eat and suppresses total test-day energy intake more than meals containing equivalent-energy amounts of either Trisun-80 oil (MUFA) or manufactured sheanut oil (SFA). In contrast, Kamphuis et al. (20) found that obese subjects eat less fat, but not energy, at a test meal enriched with linoleic acid [an (n-6) PUFA] compared with oleic acid [an (n-9) MUFA]. Our findings of no differences in SI scores or energy and macronutrient intakes at a subsequent meal consumed ad libitum contrasted with these previous reports. Differences in the experimental design may explain the discrepancy. It is possible that the amount of fat in our test food (30 g) was not enough to exert the same effects as those observed by Lawton et al. (19) using 80 g of fat. Furthermore, there was a longer delay until the meal consumed ad libitum in the previous study (4 h versus 2 h). This may have allowed measurement of potential differences in the postabsorptive effects of the different fats. Nevertheless, when food intake was assessed over the remainder of the day, we still found no differences in energy or macronutrient intake. The young men participating in our study probably have the greatest capacity to regulate energy intake in response to energy manipulation (27) and our observations may not be applicable to other study groups.

Previous studies have shown that the presence of fat reduces the postprandial glycemic response but not the insulin response to a carbohydrate load (9,31). This disproportionately high insulin response may be a mechanism by which insulin resistance develops with long-term consumption of high fat diets (9,31,32). Our findings may therefore have been altered if differences in dietary fat saturation were chronic or if the subjects were insulin resistant. However, it is not yet clear whether the type of fat has a long-term effect on insulin sensitivity. Short-term isoenergetic supplementation of a standard diet with fatty acids of varying degrees of saturation does not affect either insulin secretion or insulin sensitivity (33). In longer studies, however, diets higher in MUFA have been shown to improve insulin sensitivity as long as total fat intake is <37% energy (7).

Our study did not address the mechanisms by which the presence of fat augments postprandial glucose and insulin responses. These may include altered hepatic extraction of blood glucose (13), increased viscosity of the intestinal contents and a delay in gastric emptying, thus delaying the rate of carbohydrate digestion and absorption from the gut (9,13). The reduction in the blood glucose response and the potentiation of the insulin response in the presence of fat may be mediated by the incretin hormones gastric inhibitory polypeptide and glucagon-like peptide-1 (34) and by cholecystokinin (35). The lack of differences between the potato meals with added SFA, MUFA and PUFA in our study suggests that, irrespective of the degree of saturation, fat exerts its effects through similar mechanisms.

In conclusion, the degree of fat saturation did not influence the glycemic, insulinemic or satiety responses to a carbohydrate meal in young men. Contrary to the favorable effects of unsaturated fats on serum lipid profiles, these findings indicate that substitution of a high intake of saturated fatty acids with a high intake of unsaturated fats has no acute benefits for postprandial hyperglycemia, insulin demand or short-term satiety. Potential differences in carbohydrate and fat storage and oxidation in humans as a function of fat type should be the subject of further study.

	FOOTNOTES

 
² Abbreviations used: AUC, area under the curve; GI, glycemic index; II, insulin index; MUFA, monounsaturated fatty acids; RS, rating scale; SFA, saturated fatty acids; SI, satiety index.

Manuscript received 20 January 2003. Initial review completed 25 February 2003. Revision accepted 1 May 2003.

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TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 

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