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Commonwealth Scientific and Industrial Research Organization (J.B., M.N., P.M.C.), Human Nutrition, Adelaide SA 5000, Australia; Department of Physiology (J.B.), University of Adelaide, Adelaide SA 5000, Australia; and Department of Primary Industries (C.T.), Primary Industries Research Victoria, Werribee VIC 3030, Australia
Address all correspondence and requests for reprints to: J. Bowen, Commonwealth Scientific and Industrial Research Organization, Human Nutrition, P.O. Box 10041 BC, Adelaide SA 5000, Australia. E-mail: jane.bowen{at}csiro.au.
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Abstract |
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Objective: The objective of the study is to compare the acute effect of different proteins and carbohydrates on indicators of appetite and appetite regulatory hormones.
Design: This is a randomized cross-over study of four orally consumed preloads followed by blood sampling (+15, 30, 45, 60, 90, 120, 180 min), then a buffet meal.
Setting: The study was carried out in an outpatient clinic.
Patients and Other Participants: Nineteen overweight (body mass index 32.1 ± 0.9 kg/m2) men participated.
Interventions: Liquid preloads (1 MJ) contained whey (55 g), casein (55 g), lactose (56 g), or glucose (56 g).
Main Outcome Measures: Plasma ghrelin, cholecystokinin (CCK), insulin, glucose and amino acids, gastric emptying rate (plasma paracetamol), appetite rating (visual analog scale), and ad libitum energy intake were the main outcome measures.
Results: Energy intake was 10 ± 3% higher after the glucose preload compared with lactose and protein preloads (P < 0.05), which were predicted by ghrelin at 120 min (P < 0.05). CCK was 71 ± 6% higher 90 min after the protein preloads compared with glucose and lactose (P < 0.05), which predicted appetite at 180 min (P < 0.05). There was a small increase in branched chain amino acids after the whey preload compared with casein (P < 0.01), but this was independent of appetite and energy intake.
Conclusion: Acute appetite and energy intake are equally reduced after consumption of lactose, casein, or whey compared with glucose, which was consistent with differences in plasma ghrelin. Higher CCK responses after proteins correlated with satiety but did not affect energy intake.
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Introduction |
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Both carbohydrate and protein type appear to have different effects on satiety. Glycemic index (GI) ranks carbohydrate-containing foods based on postprandial glycemia. Low GI foods are thought to increase satiety by prolonging the availability of glucose in the postabsorptive state and by producing a lower insulin response; however, this association remains controversial (5). Higher satiety and lower ad libitum energy intake was observed after whey protein consumption compared with casein in lean subjects (6). The authors proposed this was a consequence of faster gastric emptying of whey (7).
Gastrointestinal hormones involved in appetite regulation could mediate the differences in satiety between proteins and carbohydrates. Ghrelin is an orexigen that is mainly released from the stomach (8) in response to feedback from either the intestine or a postabsorptive site (9). Plasma concentration rises before meals and decreases within 15–20 min of food consumption (10). Administration of ghrelin is associated with increased food intake in humans (11). The dynamics of ghrelin during the postabsorptive phase (i.e. return to preprandial concentration) and effects on subsequent meal size are poorly understood. Few studies have investigated the effect of macronutrients on postprandial ghrelin (12, 13, 14).
Cholecystokinin (CCK) regulates the rate of nutrient delivery from the stomach to the small intestine, and secretion is stimulated by presence of duodenal protein and fat (15). The secretion of gastrointestinal hormones such as ghrelin may be affected by gastric emptying rate. For example, a rapid emptying rate reduces time for gastric digestion and releases chyme that requires extensive small intestinal digestion (16). Consequently luminal contents will move further distally in the small intestine, and this may prolong the stimuli for changes in satiety hormones. In addition to regulating gastric emptying, CCK is also associated with satiation in animals (17) and humans (18).
The aim of this study was to compare the effects of two proteins, which differ in their rate of gastric emptying (whey, fast; casein, slow), with two carbohydrates, which differ in GI (glucose, high; lactose, low), on appetite and food intake in overweight men. Additionally, we investigated whether differences in satiety were related to postprandial plasma ghrelin, CCK, glucose, insulin, amino acids, and the rate of gastric emptying. The study was performed in men to avoid the effects of menstrual cycle on appetite (19). Additionally, eating behavior (20) and circulation of satiety hormones (21) are different in lean and obese subjects. Because dietary strategies that may optimize satiety are most applicable to overweight subjects, we selected overweight subjects for this study.
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Subjects and Methods |
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Twenty men were recruited by public advertisement and one withdrew before the study commenced. All subjects were weight stable, nonsmokers, unrestrained eaters (assessed by a validated three-factor eating questionnaire) (22), and did not have medical conditions that affect gastrointestinal motility or appetite. The study was approved by the Commonwealth Scientific Industrial Research Organisation Human Ethics Committee. All subjects gave informed, written consent to participate.
Experimental protocol
Subjects attended the clinic on four occasions with 7 d between visits. On each occasion, subjects arrived after fasting overnight and refraining from exercise, paracetamol, and alcohol for 24 h. Subjects’ weight and height were measured (Mettler scales, model AMZ14; A&D Mercury, Kinomoto, Japan) in light clothing. Body mass index (BMI) was calculated as weight (kilograms) divided by height (meters2). A cannula was inserted into a lower arm vein, and a fasting blood sample was taken (–15 min). Subjects then completed a validated visual analog scale (VAS) questionnaire to assesses nausea, hunger, thirst, satiation, desire to eat, and amount of food that could be eaten (23). Opposing extremes of each feeling were described at either end of 100-mm horizontal lines and subjects drew a vertical line on the scale to indicate how they felt. The liquid preload was consumed at 0900 h (time 0). Subjects were asked to finish the beverage in 5 min, and the beverage was followed by 1500 mg paracetamol (GlaxoSmithKline, Ermington, Australia) dissolved in 100 ml water. Postprandial plasma paracetamol concentration is a validated, indirect marker for the rate of liquid and semisolid gastric emptying (24). Subsequent blood samples and VAS measurements were collected 15, 30, 45, 60, 90, 120, and 180 min after time 0. Subjects were then given a buffet-style lunch. Each subject served their own meals from designated portions of the buffet foods and ate until satisfied. After 30 min, subjects departed the clinic.
Dietary protocol
Preloads (1 MJ) were made from water (100 g), milk (1% fat; 200 g), artificially sweetened chocolate syrup (50 g), and either whey protein isolate (55 g; Murray Goulburn, Brunswick, Australia), calcium caseinate (55 g, Murray Goulburn), glucose (60 g; GI = 100; Glucodin, Boots Healthcare, North Ryde, Australia) or lactose (56 g; GI = 43; Ace Chemical Company, Adelaide, Australia) (Table 1
). The preloads did not contain dietary fiber and were controlled for energy, energy density, palatability, and consistency.
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Biochemistry
Blood for serum was collected in tubes with no additives and allowed to clot at room temperature for 30 min. Blood for plasma was collected in sodium fluoride/EDTA (1 g/liter) tubes containing aprotinin (500 KIU/ml blood; Roche, Basel, Switzerland) and stored on ice. Blood for plasma amino acid analysis was collected in tubes containing EDTA and heparin at 0, 30, 60, 90, and 120 min. Serum and plasma were isolated by centrifugation for 10 min at 2000 x g (5 C) (Beckman GS-6R centrifuge; Beckman Coulter, Fullerton, CA) within 1 h of collection and aliquots were stored at –80 C.
Total ghrelin in unextracted plasma was measured by competitive RIA (Phoenix Pharmaceuticals, Belmont, CA); the detection limit was 70 pg/ml and interassay variation was 5.5%. CCK was analyzed by competitive RIA (Euro-diagnostica, Malmo, Sweden) using an antiserum raised against CCK-8 with cross-reactivity to CCK-33; the detection limit of the assay was 0.3 pmol/liter and interassay variation was 14%. CCK was extracted using ethanol; plasma was mixed with an equal part of 96% ethanol, vortexed for 10 sec, left to stand at room temperature for 10 min, and then centrifuged at 1700 x g for 15 min. The decanted supernatant was evaporated to dryness using a speed-vac concentrator (Savant, Farmingdale, NY) at 37 C, then reconstituted to original plasma volume with assay buffer. Serum paracetamol (acetaminophen) was measured using an enzymatic kit (Cambridge Life Sciences, Cambridgeshire, UK) adapted for a Cobas Bio centrifugal analyser (Roche Diagnostics, Basel, Switzerland). Serum insulin was measured using a enzyme immunoassay kit (Mercodia, Uppsala, Sweden). Plasma glucose was determined using an enzymatic kit (Hoffmann-La Roche Diagnostics, Basel, Switzerland) and control sera on a Hitachi 902 Automatic Analyzer (Roche Diagnostics).
Plasma amino acid analysis was performed for samples after the whey and casein treatments. Plasma was diluted with internal standard solution (nor-leucine) and placed in a Centricon YM-10 ultra filtration device, vortexed, and centrifuged for 25 min at 5200 rpm (10 C). The filtrate was diluted with HPLC buffer, and the amino acids were separated using a cation exchange HPLC column in the lithium form (Shodex CXpak amino acids column) and quantified after post column derivatization with ninhydrin (26).
Biochemical analyses were performed after study completion, and all samples for individuals were analyzed in the same assay.
Statistical analysis
Results are presented for 19 subjects and are expressed as means ± SE (SEM) except for subject characteristics (SD). No differential effects between whey and casein were identified for any parameters, so data for both preloads are presented as a mean, called "protein" (except amino acid data).
The distance between the left end of the VAS scale and each mark was measured (millimeters). The change in rating from baseline was calculated. Reliability analysis was performed (Cronbach’s alpha) to assess inter-item correlation of all VAS questions. By factor analysis the reliability of all questions (
= 0.59) was improved by excluding nausea and thirst ( = 0.73), confirmed by Pearson correlation (two-tailed, P < 0.01). Accordingly, an overall "appetite" measure was calculated as the mean response to "amount that could be eaten", "desire to eat", "hunger", and "satiation".
Total area under the curve (AUC) for glucose, insulin, ghrelin, CCK, paracetamol, and amino acids was calculated using the trapezoidal equation (27). AUCs were compared using one-way ANOVA.
ANOVA with repeated measures was used to determine the effects of the treatment and time (minutes) with the treatment order, BMI, and fasting insulin and glucose included as covariates. Where ANOVA showed a statistically significant main effect, Tukey’s post hoc tests were performed to compare group differences. Relationships between appetite and energy with other variables (BMI, weight, AUC, and fasting, peak, and nadir concentrations) were examined using multiple linear regressions. Statistical analysis was performed using SPSS 11.5 for Windows (SPSS Inc., Chicago, IL). Differences are considered significant if P < 0.05.
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Results |
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Nineteen subjects completed this study with a mean BMI of 32.1 ± 3.7 kg/m2 (range, 26.8–40.4), fasting glucose concentration of 110 ± 1 mg/dl (range, 93–141 mg/dl), and aged 53.3 ± 6.1 yr (range, 41–63 y). Inclusion of one subject with elevated fasting blood glucose concentration (141 mg/dl) did not affect outcomes or significance and, therefore, was included in data analysis. There were no differences in the fasting values of any parameters between treatments.
Energy intake, appetite, and ghrelin
Ad libitum energy intake after the glucose treatment was 493 ± 141 kJ and 541 ± 190 kJ greater than after the protein and lactose preloads, respectively (P < 0.05; Table 2). There was no treatment effect on macronutrient composition of the intake (data not shown).
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). After the protein and lactose preloads, the nadir concentration remained stable for 1 h before returning to the preprandial concentration. After the glucose preload, ghrelin returned to baseline levels within 1 h of the nadir and then exceeded this level in the next hour.
There was no treatment effect for appetite or ghrelin AUC (Table 2).
Paracetamol and CCK
Paracetamol increased after consumption of all preloads (Fig. 2). There was a significant time by treatment effect (P < 0.01); plasma levels were lower 90 min after the protein preloads compared with both carbohydrate preloads (Fig. 2). Paracetamol AUC was also lower for the protein treatments compared with both carbohydrates (P < 0.01; Table 1)
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). AUC for the protein treatments was also greater than AUC for the carbohydrate treatments (P < 0.01; Table 2). Glucose, insulin, and amino acids
There was a time (P < 0.0001) and time by treatment effect for plasma glucose (P < 0.01; Fig. 3). The glucose preload produced a higher peak glucose concentration (P < 0.01) and AUC (P < 0.01; Table 2) compared with the lactose treatment, confirming the difference in their glycemic indices. Postprandial insulin peaked at 45 min and returned to baseline concentration by 120 min (time effect; P < 0.01; Fig. 3) independent of treatment. There was a time by treatment effect between whey and casein preloads for branched chain (P < 0.01), but not for total plasma amino acids (Fig. 3).
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The strongest predictor of energy intake was ghrelin at 120 min (adjusted r2 = 0.055, P = 0.024). Inclusion of peak insulin concentration in the regression model decreases the adjusted r2 value from 0.055 to 0.037 (P = 0.130). Fasting glucose was the strongest predictor of ghrelin at 0 min (adjusted r2 = 0.141, P = 0.001), 120 min (adjusted r2 = 0.134, P = 0.001), and 180 min (adjusted r2 = 0.127, P = 0.001). The strongest predictor of appetite at 180 min was CCK at 90 min (adjusted r2 = 0.055, P = 0.029), and the strongest predictor of appetite AUC was CCK AUC (adjusted r2 = 0.047, P = 0.048).
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Discussion |
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The glucose preload resulted in an earlier return of ghrelin to the preprandial concentration and higher ad libitum energy intake (+500 kJ) compared with all other treatments. This suggests that ghrelin may be involved in mediating the variable satiety responses observed after consumption of dietary carbohydrates with differing GI (28). Consistent with this, earlier findings suggest that the rapid postprandial decrease in ghrelin after oral glucose loads (29) is dependent on subsequent changes in plasma insulin (30), which would vary depending on GI. Only one other study has explored the effect of different carbohydrates ("simple", 121 g maltodextrin; "complex", 102 g maltodextrin and 12 g exopolysaccharide) on postprandial plasma ghrelin (31). In that study, ghrelin AUC was lower after the complex carbohydrate preload, and this correlated with lower appetite AUC (31), although the glycemic response to both preloads was similar. We also observed that ghrelin and appetite ratings remained suppressed after the lactose preload despite a similar insulin response to the glucose treatment. Indeed, ghrelin remained low even after insulin returned to baseline concentration. Our results, and others (31, 32), indicate that there are additional factors that are involved in regulating the ghrelin response to ingestion of different carbohydrates. Our assessment of gastric emptying and CCK do not give further insight into possible candidates.
The prolonged postprandial suppression of ghrelin after consumption of both dietary proteins may partly explain the association between dietary protein and higher satiety, compared with carbohydrates (1, 2, 3). Recently, another study also found that ghrelin remained suppressed for 3 h after consumption of a high protein, mixed meal, whereas it remained below baseline for 1 h after high fat and moderate carbohydrate isoenergetic meals (33). Previous studies investigating the effect of protein on ghrelin regulation in humans provide conflicting results. Erdmann et al. (12) found that plasma ghrelin increased after consumption of a high protein test food (1260 kJ; turkey meat), yet concentration decreased after carbohydrate (1090 kJ; bread, butter, marmalade) and fat (2520 kJ kcal; cream). Similarly, plasma ghrelin concentration did not change after consumption of pork and chicken (13, 14). Differences in the caloric load, macronutrient composition, form, and energy density between test foods in these studies may confound the results. The reduction in ghrelin we observed after all treatments coincided with an elevation in insulin. Again, however, insulin does not explain the prolonged suppression of ghrelin between 120–180 min when insulin had returned to baseline concentration. The regulation of ghrelin during this late postprandial phase appears to be important, as it was associated with effects on appetite and ad libitum energy intake.
Animal studies have recently shown that infusion of CCK blocks the orexigenic effect of ghrelin in the arcuate nucleus and reduces food intake (34, 35), but this relationship has not been described in humans. We observed a prolonged elevation in plasma CCK after consuming proteins, but not after either carbohydrate in overweight men. This confirms a similar effect of duodenal infusion (36) of protein and carbohydrate on CCK in lean subjects. We suggest an inverse interaction between CCK and ghrelin, which diminishes the orexigenic effect of ghrelin, may contribute to the higher satiety associated with proteins compared with carbohydrates. Indeed, we found that CCK at 90 min correlated with lower appetite ratings. What is not consistent with this proposition is the equally low ghrelin after the lactose preload despite a low CCK. Nevertheless, an interaction between CCK and ghrelin may influence satiety and the inter-meal interval.
There is some evidence to suggest that an increase in plasma free fatty acid (FFA) concentration decreases plasma ghrelin (37) although not consistently observed (38). The preloads in the present study contained a very small amount of fat (<1.0 g), which is unlikely to have substantially increased plasma FFA concentration. Furthermore, an increase in insulin, as was observed after all preloads, suppresses FFA in both lean and obese normoinsulinemic subjects (39). Therefore, independent of the actual effect of increased plasma FFA on ghrelin, it is unlikely to play an important role in postprandial responses in the present study.
The expected difference in energy intake between casein and whey was based on an earlier finding that ad libitum energy intake was 19% lower 90 min after consuming a liquid breakfast preload containing 1.7 MJ and 48 g of whey compared with a similar casein-based preload (6). Postprandial gastric emptying rate was faster and total amino acid concentrations were higher after the whey treatment, although these differences occurred after a subsequent meal (6). We did not observe any differences in appetite or satiety hormones between protein types, perhaps because the interval between the preload and the buffet lunch was longer and not influenced by the consumption of other foods. Thus the postulated faster gastric emptying of whey does not appear to be an important factor in the satiety attributed to some dietary proteins (40). Whey contains high levels of branched chain amino acids (BCAA; leucine, isoleucine, and valine). It has been suggested that these amino acids have a unique metabolic role that may enhance satiety due to extra-hepatic metabolism and interactions with insulin signaling pathways (41). Our findings do not support a role for BCAA in satiety regulation.
Liquid preloads were chosen to avoid the confounding effects of differences in food form and, therefore, facilitate exploration of the effect of macronutrients on postprandial changes in hormones. The disadvantage of liquid preloads is that they do not represent the typical form in which food is generally consumed. Despite this, we did observe a reduction in energy intake that is similar in magnitude to an earlier study comparing proteins and carbohydrates in solid form (–12% ad libitum energy intake) (42). The similar insulin profile after all preloads may have been due to the liquid nature of the preloads and, therefore, explain the lack of an association between ghrelin and insulin in this study. Consumption of high-protein solid meals produces a lower insulin response compared with high-carbohydrate solid meals in healthy subjects (4). Accordingly, the macronutrient effects on satiety hormones that were observed in this study should be confirmed using solid foods.
Although the regression analysis in this study showed significant relationships, the strength of these relationships is weak. This highlights the difficulty of studying appetite given the capacity for behavioral and environmental factors to override physiological regulators of appetite. Further, acute satiety is regulated by other gastrointestinal hormones not assessed in this study, such as peptide YY, glucagon like peptide 1, glucose-dependent inhibitory polypeptide, and oxyntomodulin (43). It should also be noted that we measured total plasma ghrelin, although there are a number of fractions of ghrelin with differing levels of activity and plasma concentration (44). Intact and degraded forms of ghrelin show similar postprandial changes after glucose infusion (45), although this has not been demonstrated in obese subjects. Our group (46) and others (29) have previously found that ghrelin and appetite regulation differ in lean and overweight subjects (21). Therefore, we performed this study in overweight subjects to further explore appetite regulatory mechanisms in this group.
In summary, this study has observed differences in the gastrointestinal hormonal response (CCK and ghrelin) to liquid preloads containing protein (whey or casein), lactose, and glucose in overweight men. We have shown that appetite and energy intake are higher after glucose consumption and this may be mediated by ghrelin. Higher postprandial CCK concentrations after dietary protein provides a possible explanation for the difference in satiety that is established between protein and carbohydrates. Gastric emptying and amino acid absorption do not appear to contribute to acute appetite regulation.
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Acknowledgments |
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Footnotes |
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First Published Online January 24, 2006
Abbreviations: BCAA, Branched chain amino acid; BMI, body mass index; CCK, cholecystokinin; FFA, free fatty acid; GI, glycemic index; VAS, visual analog scale.
Received August 16, 2005.
Accepted January 13, 2006.
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), glucose (
), or lactose (
). For conversion from picograms per milliliter to picomoles per liter for ghrelin, multiply by 0.296. *, Significantly greater than protein and lactose treatments (P < 0.05; time by treatment effect, repeated measures ANOVA with Tukey’s post hoc test).
) or casein (
, Significantly greater than protein (P < 0.01; time by treatment effect, repeated measures ANOVA with Tukey’s post hoc test). 
, Significantly different than casein (P < 0.05; time by treatment effect, repeated measures ANOVA with Tukey’s post hoc test).