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Reply to C Otto et al

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Dear Sir:

In their comments, Otto et al support our hypothesis that attenuation and delay of ghrelin responses may be mediated through changes in gut peptides, such as glucose-dependent insulinotropic peptide and glucagon-like peptide 1 (GLP-1). Otto et al suggest that gut hormones may help explain the well-recognized attenuated postprandial ghrelin response that is found in obese subjects but not in normal-weight subjects. This notion is supported by data on obese women from studies by Romon et al (2) and by the data on obese women cited by Otto et al in their letter.

Within the scope of the increasing prevalence of obesity, it is important to understand the physiologic mechanisms of hunger and satiety and, specifically, the differences in these mechanisms between lean and obese subjects. Such knowledge may be used for the development of functional foods or dietary interventions to help obese persons manage their weight. However, it will be extremely difficult to design studies without limitations that may hamper straightforward conclusions. For example, our data were obtained by comparing subjects who were given high percentages of protein (30% of energy) with the same subjects given a normal or regular high-protein meal (12–15% of energy). In addition, a more general problem is that a diet with a high protein content should be compared with an isoenergetic control diet. Protein calories should be compensated for in the control diet, either from the carbohydrate or fat fraction or from a combination of the 2 fractions. Each of these possibilities may affect the outcome differently. In addition, comparisons should be made between lean and obese subjects—in other words, between different subjects—or weight-reduction studies should be performed.

Otto et al suggest using a fat load to investigate gut hormone responses. We recently performed a human intervention trial including both lean [body mass (BMI; in kg/m²): 21.2 ± 1.5; n = 10) and obese (BMI: 29.7 ± 1.9; n = 10) men; each group was given a breakfast containing 54% of energy as fat, 41% of energy as carbohydrate, and 5% of energy as protein, and we studied the effects on plasma ghrelin and cholecystokinin (CCK) responses. In that study, we did not observe a difference in ghrelin or in CCK response after such a fat load between lean and obese subjects (WJ Pasman et al, unpublished results, 2005). These data therefore do not support a role for fat in a prolonged suppression of ghrelin.

The role of the gut peptide GLP-1 in ghrelin responses was more directly studied by intravenously infusing GLP-1. These results, recently published elsewhere (3), showed that total ghrelin concentrations were correlated with both GLP-1 (–0.58; 95% CI: 0.81, –0.18) and glucose-dependent insulinotropic peptide (–0.63; 95% CI: –0.84, –0.27) during GLP-1 infusions; they were also correlated, but less so, with CCK (–0.50; 95% CI: –0.77, –0.08). Glucose-dependent insulinotropic peptide correlated strongly with insulin and CCK under these conditions. Unfortunately, these studies were performed only in lean men, and therefore we currently do not know whether these correlations exist in obese men as well.

In the latter study, GLP-1 was infused to lower the gastric emptying rate (3). Direct effects of GLP-1's interaction with ghrelin therefore cannot be excluded and should be studied by, for example, infusing GLP-1 but not in combination with a meal. Moreover, studies that vary the gastric emptying rate by using various other mechanisms may further elucidate these interactions. Most likely, the roles of the various receptors for these gut hormones in the brain and on nerves such as the vagus nerve and other target tissues are important, and these roles should be investigated. We agree that more of these studies, using a variety of techniques explaining pathophysiologic changes occurring in obesity, are needed.

ACKNOWLEDGMENTS

None of the authors had a conflict of interest.

REFERENCES

1. Blom WA, Lluch A, Stafleu A, et al. Effect of a high-protein breakfast on the postprandial ghrelin response. Am J Clin Nutr 2006;83:211–20.[Abstract/Free Full Text]
2. Romon M, Gomila S, Hincker P, Soudan B, Dallongeville J. Influence of weight loss on plasma ghrelin responses to high-fat and high-carbohydrate test meals in obese women. J Clin Endocrinol Metab 2006;91:1034–41. Epub 2005 Dec 29.[Abstract/Free Full Text]
3. Blom WA, Lluch A, Vinoy S, Stafleu A, van den Berg R, Holst JJ, Kok FJ, Hendriks HF. Effects of gastric emptying on the postprandial ghrelin response. Am J Physiol Endocrinol Metab 2006 Feb;290(2):E389–95.

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