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LETTER TO THE EDITOR |
Department of Medicine
University Hospital–Innenstadt
Munich
Germany
E-mail:baerbel.otto{at}med.uni-muenchen.de
Department of Medicine
University Hospital–Grosshadern
Munich
Germany
Dear Sir:
Depending on the type of macronutrient, differences in postprandial ghrelin secretion have been shown in lean and obese humans (1–3). In their recently published study, Blom et al (4) compared the effect of a high-protein breakfast (25% lower than baseline; lowest values at 120 min) with that of a high-carbohydrate meal (18% lower than baseline; lowest values at 60 min) on the postprandial ghrelin response. These differences in postprandial ghrelin response in 15 healthy men were suggested to be influenced by the release of other gut satiety peptides such as cholecystokinin, glucagon, glucose-dependent insulinotropic polypeptide, and glucagon-like peptide 1 (4). Lower ghrelin concentrations after meals were correlated with the stimulation of glucose-dependent insulinotropic polypeptide and glucagon concentrations. These interesting postprandial associations between gut peptides may also help our interpretation of changes in ghrelin concentrations after a high-fat meal and may explain the lower postprandial ghrelin response that is known to occur in obese subjects (3). In most of the studies on this topic, the lowest ghrelin concentration after a fat load was found at the end of the test period (usually 180 min; 1–3). Romon et al (5) recently compared ghrelin concentrations after a high-fat meal (79% of energy from fat, 3% of energy from carbohydrate, and 18% of energy from protein) with those after a high-carbohydrate meal (81% of energy from carbohydrate, 1% of energy from fat, and 18% of energy from protein) in 17 obese women over a longer period of 10 h. Ghrelin changes after fat intake were characterized by an initial significant decrease (lowest value at 180 min), which was followed by a slower return to baseline than was seen with the high-carbohydrate meal (5).
In contrast with these data in women (5), our group (6) found a prolonged suppression of plasma ghrelin concentrations (7.0 ± 1.2%; P 
0.005) after a fat-enriched fluid meal (87% of energy from fat, 7% of energy from carbohydrates, and 6% of energy from protein) over 4 h in a subgroup analysis of 10 obese men. As Romon et al (5) had found in obese women, our group (6) found a rather slow increase in ghrelin: ie, 6 and 8 h after the meal, ghrelin concentrations still tended to be suppressed, at 5.6 ± 3.7% (P = 0.093) and 5.3 ± 2.7% (P = 0.074), respectively. Insulin concentrations should not be considered responsible for the prolonged ghrelin decrease, because plasma concentrations of insulin showed only a marginal increase after a high-fat meal (5). Elevated plasma triacylglycerols after fat ingestion also are unlikely to be the reason for the prolonged drop, because intravenous lipid infusion did not influence ghrelin concentrations (7). On the other hand, we know that cholecystokinin is released from the gut in response to food intake, when its release is stimulated by the absorption of amino acids or fatty acids (4, 8, 9). Cholecystokinin release depends on the duodenal lipid dose (9). In addition, peripheral interactions of ghrelin and cholecystokinin have been described in rats (10).
On the basis of the recent findings of Blom et al (4) with respect to ghrelin release after a high-protein meal, we hypothesize that the release of gastroenteropancreatic peptides (especially cholecystokinin and glucagon-like peptide 1) may also play a role in the prolonged suppression that is followed by a slow increase of ghrelin concentrations after a high-fat meal. To clarify mechanisms and find possible implications in the pathophysiology of obesity, further studies should be planned to investigate the postprandial associations between ghrelin and gastroenteropancreatic peptide release.
ACKNOWLEDGMENTS
None of the authors had a personal or financial conflict of interest with the study of Blom et al.
REFERENCES
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