Delayed gastric emptying in the obese: an assessment using the non‐invasive <sup>13</sup>C‐octanoic acid breath test

Jackson, Sarah J.; Leahy, F E; McGowan, AA; Bluck, Leslie J. C.; Coward, W. A.; Jebb, Susan A.

doi:10.1111/j.1462-8902.2004.0344.x

Cited by 104 publications

(92 citation statements)

References 30 publications

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“…Our evidence for inbred strain differences in gastric emptying rate extends the observations of Kirby et al (24) and provides new information on the identity of candidate genes contributing to this phenotype. Our results are similar in magnitude to those observed between lean and obese humans (13%) (22) and are consistent with the effects of known GLP-1 receptor agonists on food intake and gastric emptying (51). The modest effect size on gastric emptying rate in our study is consistent with the typical size of individual genetic contributions to polygenic traits.…”

Section: Discussionsupporting

confidence: 80%

Genetic variation inGlp1rexpression influences the rate of gastric emptying in mice

Kumar¹,

Byerley²,

Vólaufová³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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We demonstrated previously that food intake traits map to a quantitative trait locus (QTL) on proximal chromosome 17, which encompasses Glp1r (glucagon-like peptide 1 receptor), encoding an important modulator of gastric emptying. We then confirmed this QTL in a B6.CAST-17 congenic strain that consumed 27% more carbohydrate and 17% more total calories, yet similar fat calories, per body weight compared with the recipient C57BL/6J. The congenic strain also consumed greater food volume. The current aims were to 1) identify genetic linkage for total food volume in F 2 mice, 2) perform gene expression profiling in stomach of B6.CAST-17 congenic mice using oligonucleotide arrays, 3) test for allelic imbalance in Glp1r expression, 4) evaluate gastric emptying rate in parental and congenic mice, and 5) investigate a possible effect of genetic variation in Glp1r on gastric emptying. A genome scan revealed a single QTL for total food volume (Tfv1) (log of the odds ratio ϭ 7.6), which was confirmed in B6.CAST-17 congenic mice. Glp1r exhibited allelic imbalance in stomach, which correlated with accelerated gastric emptying in parental CAST and congenic B6.CAST-17 mice. Moreover, congenic mice displayed an impaired gastric emptying response to exendin-(9-39). These results suggest that genetic variation in Glp1r contributes to the strain differences in gastric emptying rate.quantitative trait locus; glucagon-like peptide 1 receptor THE GUT HORMONE GLUCAGON-LIKE PEPTIDE 1 (GLP-1) inhibits gastric emptying, reduces postprandial gastric secretion, and may play a physiological role in regulating appetite and energy intake. Systemic administration of GLP-1 in physiological amounts in both humans and animals potently inhibits gastric emptying (9,13,15,31,59,61), and this effect can be blocked by administration of the GLP-1 receptor antagonist exendin (9-39) (21). The mechanism by which GLP-1 inhibits gastric emptying is thought to involve receptors located either in the central nervous system or associated with afferent pathways to the brain stem (9,21,60). In addition to the deceleration of gastric emptying, GLP-1 is involved in regulating satiety, as shown in normal-weight and obese men infused with 33,34). GLP-1 also decreases food intake; by contrast, central administration of the GLP-1 receptor (GLP-1R) antagonist exendin-(9-39) stimulates food intake (14, 54).The GLP-1R is a seven-transmembrane domain receptor belonging to the B family of G-protein-coupled receptors (6, 52). The GLP-1R recognizes GLP-1 specifically and does not show demonstrable binding by related peptides (Ref. 52; for review, see Ref. 6). In rodents, GLP-1 receptor mRNA and high-affinity GLP-1 binding sites have been identified in pancreatic islets, in gastrointestinal tract, in lung, in kidney, in heart, and throughout the brain (7,8,16). The satiety-promoting effects of GLP-1 implicate Glp1r as a physiological gene candidate for ingestive behavior phenotypes (1).Glp1r maps to the peak of a genetic region containing overlapping quantitative trait loci (Q...

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Section: Discussionsupporting

confidence: 80%

Genetic variation inGlp1rexpression influences the rate of gastric emptying in mice

Kumar¹,

Byerley²,

Vólaufová³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…A delayed lag time has also been observed (55)(56)(57)(58) . It has been postulated that disordered GE is not a major factor in the pathogenesis of obesity but secondary to weight gain and may be related to increased gallbladder volume and reduced postprandial gallbladder emptying in obese patients (57) .…”

Section: Gastric Emptying In Obesitymentioning

confidence: 64%

“…It has also been reported in the literature that GE times are longer in the obese population for solid food (55)(56)(57)(58) and for liquids (55,57) . A delayed lag time has also been observed (55)(56)(57)(58) .…”

Section: Gastric Emptying In Obesitymentioning

confidence: 93%

“…GE of liquid is therefore unaffected, as liquification is not necessary and hence GE occurs at the same rate in obese and normal-weight individuals. A further theory that supports delayed GE is that it may actually contribute to obesity rather than be a consequence of obesity (58) . A lack of nutrients in the duodenum resulting from reduced GE means that GI hormones responsible for the regulation of both GE and satiety are not released in high enough concentrations.…”

Section: Gastric Emptying In Obesitymentioning

confidence: 99%

“…It has been postulated that disordered GE is not a major factor in the pathogenesis of obesity but secondary to weight gain and may be related to increased gallbladder volume and reduced postprandial gallbladder emptying in obese patients (57) . It has also been suggested that the delay in GE can be attributed to slower distribution of the meal as a result of a reduction in fundal tone, altered sensitivity of the stretch receptors or a change in antral area and mixing (58) . These changes may be a consequence of increased gastric distension and HF diets.…”

Section: Gastric Emptying In Obesitymentioning

confidence: 99%

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Postgraduate Symposium The role of fat in gastric emptying and satiety: acute and chronic effects

Clegg

Shafat

2009

Proc. Nutr. Soc.

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Dietary fat is an important factor in the aetiology of obesity and the metabolic syndrome. It has been widely debated whether gastric emptying (GE) is altered in obesity. GE times have been reported as both longer and shorter in obese individuals compared with matched lean individuals. However, the general consensus is that GE is accelerated and satiety is lower in obesity.Research has implicated a high-fat (HF) diet in these findings. A single HF meal has a longer GE time than a low-fat meal and can even delay GE of the subsequent meal. However, an HF diet has shown different effects. Feeding a HF diet adapts gastrointestinal function to reduce GE times in comparison with a low-fat diet. Increased GE may lead to decreased satiety and faster onset of subsequent eating episodes. Further results have suggested that consuming an HF diet for 14 d increases the GE rate of HF food but not low-fat food. Consuming HF diets for 2 weeks has also been shown to increase food intake. Decreased satiation following an HF diet may cause increased food intake and a positive energy balance, potentially resulting in a gradual increase in adiposity. Recent results have suggested that gastrointestinal transit is accelerated following only 3 d on a HF diet. The variable GE times reported in obesity may be associated with interactions between the HF diet and obesity and not simply the obese state.

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Current literature in diabetes

2005

Diabetes Metab. Res. Rev.

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Delayed gastric emptying in the obese: an assessment using the non‐invasive ¹³C‐octanoic acid breath test

Cited by 104 publications

References 30 publications

Genetic variation inGlp1rexpression influences the rate of gastric emptying in mice

Genetic variation inGlp1rexpression influences the rate of gastric emptying in mice

Postgraduate Symposium The role of fat in gastric emptying and satiety: acute and chronic effects

Current literature in diabetes

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Delayed gastric emptying in the obese: an assessment using the non‐invasive 13C‐octanoic acid breath test

Cited by 104 publications

References 30 publications

Genetic variation inGlp1rexpression influences the rate of gastric emptying in mice

Genetic variation inGlp1rexpression influences the rate of gastric emptying in mice

Postgraduate Symposium The role of fat in gastric emptying and satiety: acute and chronic effects

Current literature in diabetes

Contact Info

Product

Resources

About

Delayed gastric emptying in the obese: an assessment using the non‐invasive ¹³C‐octanoic acid breath test