Gastroenterology

Gastroenterology

Volume 126, Issue 2, February 2004, Pages 432-440
Gastroenterology

Clinical-alimentary tract
Independent influences of body mass and gastric volumes on satiation in humans

https://doi.org/10.1053/j.gastro.2003.11.007Get rights and content

Abstract

Background & Aims: We assessed the association of body mass and gastric volumes (fasting and postprandial) with satiation and postprandial symptoms. Methods: Healthy obese and nonobese subjects underwent measurement of caloric intake at maximum satiation; postprandial symptoms were measured with visual analogue scales 30 minutes after a meal. Gastric volume during fasting and after 300 mL of Ensure was measured with technetium-99m single-photon emission computed tomography imaging. We used multiple regression analysis to assess the associations among variables. Results: Among 134 participants (81 women and 53 men), the median age was 26 years (range, 12–58 years), and the median body mass index was 24 kg/m2 (range, 17–48 kg/m2). Increased body mass index, but not height, was associated with delayed satiation (P < 0.003, adjusted for sex). Overweight and obese subjects ingested, on average, 225 ± 57 more kilocalories (945 ± 239 kJ) at maximum satiation compared with normal weight individuals. Increased fasting gastric volume was not associated with body mass index or height, but it was significantly associated with delayed satiation (P = 0.001, adjusted for body mass index and sex). An increase of 50 mL in the fasting gastric volume was associated with 114 ± 32 kcal (479 ± 134 kJ) more ingested at maximum satiation. Increased body mass index was associated with lower fullness scores 30 minutes after a meal (P = 0.0012, adjusted for sex and volume of Ensure ingested). In contrast, scores of postprandial bloating and pain were higher with increased body mass index (both P < 0.05, adjusted for sex and volume of Ensure ingested). Conclusions: Greater body mass index and fasting gastric volume are associated with reduced satiation. Increased body mass index or height was not associated with greater gastric volumes.

Section snippets

Data source

Data from this study were from healthy volunteers from the local community who participated in studies performed at the General Clinical Research Center at the Mayo Clinic, Rochester, Minnesota, from July 2000 to November 2002. Exclusion criteria included pregnant or breast-feeding women, prior abdominal surgery other than appendectomy or tubal ligation, positive symptoms on an abridged bowel disease questionnaire, present or previous chronic gastrointestinal illness, systemic disease, or use

Study population

We evaluated 134 healthy subjects (81 women and 53 men). Data on BMI were missing in only 1 man. The median age was 26 years (IQR, 19–35 years; range, 12–58 years), and the median BMI was 24 kg/m2 (IQR, 22–29 kg/m2; range, 17–48 kg/m2). The number of participants in each BMI category is shown in Table 1.

Male sex and increased body mass index are associated with delayed satiation

With drinking at a constant rate, satiation was independently affected by sex (P < 0.0001) and BMI (P = 0.003). Figure 2 shows the Kaplan-Meier curves with the proportion of subjects who

Discussion

Three main observations arise from this study. First, increased BMI is associated with a delayed onset of satiation and reduced fullness 30 minutes after a meal. Second, gastric volume during fasting significantly influences time and, hence, caloric intake to reach maximum satiation. Third, increased BMI is not associated with increased gastric volume.

The observed association between BMI and satiation does not seem to be related to differences in height. In adolescents, the association between

Acknowledgements

We thank Dr. Joseph A. Murray for helpful comments and Cindy Stanislav for secretarial support.

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    Supported in part by nursing support available through General Clinical Research Center grant RR00585 (Physiology Core) from the National Institutes of Health (NIH). M.C. is supported by grants R01-DK54681 and K24-DK02638 from the NIH. S.D.-A. was supported by the Falk Fellowship for Clinical Research Training at the Mayo Foundation.

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