Gastric Motor and Sensory Functions in Obesity

Park, Moo In; Camilleri, Michael

doi:10.1038/oby.2005.51

Cited by 87 publications

(62 citation statements)

References 75 publications

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“…Another possible mechanism for an effect of CM3 could be through an increase in the feeling of satiation, because of a sheer volume effect. It has been reported that gastric distention induces feelings of fullness and satiation (26). In specific, chemoreceptors and mechanoreceptors in the stomach wall signal satiation through vagal and splanchnic nerves (43).…”

Section: Control Cm3mentioning

confidence: 99%

Effect of a Cellulose‐containing Weight‐loss Supplement on Gastric Emptying and Sensory Functions

Berthold¹,

Unverdorben²,

Degenhardt³

et al. 2008

Obesity

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2CM3, a highly cross-linked cellulose in capsule form, expands in the stomach to a size several fold of its original volume. It is purported to induce a prolonged feeling of satiation and a delay in gastric emptying, thus promoting weight loss. We examined whether CM3 delays gastric emptying (using the stable isotope 13 C-octanoic breath test) and whether it influences subjective feelings of appetite sensations (using visual analog scales, VASs). We performed a double-blind randomized placebo-controlled crossover trial in 19 moderately obese but otherwise healthy subjects (mean age 55 ± 9 years, BMI 31.1 ± 4.6 kg/m 2 ). The subjects were treated with six capsules of CM3 or matching placebo 30 min before a standardized solid meal. Breath collection and VASs were performed over 4 h every 15 min and 30 min, respectively. Half-excretion time of 13 CO 2 in breath, indicating gastric emptying half time, was the primary outcome parameter. The study was powered to detect a change in gastric emptying of 20-30 min. Mean 13 CO 2 half-excretion time changed from 2.3 ± 0.4 to 2.4 ± 0.33 h (mean difference +6 min, 95% confidence interval (CI) -3 to +15 min; P = 0.17). Appetite sensations (hunger, satiation, fullness, prospective food consumption, desire to eat something sweet, salty, savory, or fatty) changed over time during the course of the postprandial phase but were not influenced by CM3 (repeated measures ANOVA). In obese subjects, acute administration of the weight-loss supplement CM3 does not delay gastric emptying and does not influence subjective appetite sensations.

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Section: Control Cm3mentioning

confidence: 99%

Effect of a Cellulose‐containing Weight‐loss Supplement on Gastric Emptying and Sensory Functions

Berthold¹,

Unverdorben²,

Degenhardt³

et al. 2008

Obesity

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“…Gastric parameters such as stomach distention are another important source of negative feedback (37). Feelings of hunger and satiety have long been associated with gastric motor and sensory functions, and more importantly, gastric and intestinal signals have been reported to interact (14,18,42).…”

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confidence: 99%

The role of the stomach in the control of appetite and the secretion of satiation peptides

Steinert

Meyer‐Gerspach

Beglinger

2012

American Journal of Physiology-Endocrinology and Metabolism

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It is widely accepted that gastric parameters such as gastric distention provide a direct negative feedback signal to inhibit eating; moreover, gastric and intestinal signals have been reported to synergize to promote satiation. However, there are few human data exploring the potential interaction effects of gastric and intestinal signals in the short-term control of appetite and the secretion of satiation peptides. We performed experiments in healthy subjects receiving either a rapid intragastric load or a continuous intraduodenal infusion of glucose or a mixed liquid meal. Intraduodenal infusions (3 kcal/min) were at rates comparable with the duodenal delivery of these nutrients under physiological conditions. Intraduodenal infusions of glucose elicited only weak effects on appetite and the secretion of glucagon-like peptide-1 (GLP-1) and peptide YY (PYY). In contrast, identical amounts of glucose delivered intragastrically markedly suppressed appetite (P Ͻ 0.05) paralleled by greatly increased plasma levels of GLP-1 and PYY (Յ3-fold, P Ͻ 0.05). Administration of the mixed liquid meal showed a comparable phenomenon. In contrast to GLP-1 and PYY, plasma ghrelin was suppressed to a similar degree with both intragastric and intraduodenal nutrients. Our data confirm that the stomach is an important element in the short-term control of appetite and suggest that gastric and intestinal signals interact to mediate early fullness and satiation potentially by increased GLP-1 and PYY secretions. small intestine; humans; glucagon-like peptide-1; gut; interactions EATING IS ORGANIZED INTO DISCRETE MEALS and determined by meal size and meal frequency. Multiple regulatory pathways seem to promote or inhibit eating and thus regulate energy balance. Gastrointestinal (GI) satiation signals such as cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), or peptide YY (PYY) as examples are secreted from the small and large intestine in response to food ingestion and signal to the brain via neural or endocrine pathways to inhibit eating (8). Their plasma levels are low in the fasting state and rise during a meal, which is consistent with the satiating effect observed when peripherally infused in rats and humans (1,19,26). In contrast, the peptide ghrelin is secreted from the stomach during fasting and plasma level fall shortly after meals consistent with a hunger-inducing action observed in rats and humans (47,53).Gastric parameters such as stomach distention are another important source of negative feedback (37). Feelings of hunger and satiety have long been associated with gastric motor and sensory functions, and more importantly, gastric and intestinal signals have been reported to interact (14,18,42). We and other groups could show that in humans oral preloads combined with (exogenously administered or endogenously stimulated) CCK or GLP-1 synergistically increase satiation and reduce food intake (9, 29, 33). Furthermore, Feinle et al. (12) demonstrated that sensory responses to gastric distension are altered by duodenal inf...

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“…Although hyperglycaemia has been shown to induce proximal gastric relaxation [7] , the absolute increase in blood glucose level was small and therefore unlikely to have contributed significantly to the subsequent response. The diabetic patients had a higher BMI than the healthy volunteers, however no differences in either proximal gastric volume or compliance have been reported between obese and lean subjects [27,28] . Thus, a higher BMI in diabetic patients seems unlikely to have contributed to the differences in proximal gastric motility.…”

Section: Discussionmentioning

confidence: 83%

Proximal gastric motility in critically ill patients with type 2 diabetes mellitus

Nguyen¹

2007

WJG

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INTRODUCTIONIn the community, approximately 50% of patients with type 1 or 2 diabetes mellitus (DM) have gastroparesis [1] . Although gastric emptying of either a solid or semi-solid meal is consistently slow in these patients, gastric emptying of liquid meals is variable [1][2][3][4] . The aetiology of slow gastric emptying and the variable rate of liquid emptying are unclear, but may be related to hyperglycemia or autonomic neuropathy [1,[5][6][7] , factors that result in motor dysfunction of both the proximal and distal stomach [1,7,8] . Delayed gastric emptying is also common in critically ill patients [9][10][11] and is associated with disturbed motility of both the proximal and distal stomach [10,12,13] . In health, the proximal stomach is a major determinant of liquid gastric emptying and is regulated by feedback from the small intestine. In health, the fundus relaxes in response to the presence of nutrient in the duodenum [14] . Critically ill patients without DM have been reported to have impaired proximal gastric relaxation, reduced fundic wave activity and a failed recovery of proximal gastric volume to prestimulation level [12] . Currently, there are no data on the impact of DM on gastric motor function or emptying during critical illness, despite the fact that one-third of patients admitted to critical care units have DM [15] . Given that both DM and critical illness are risk factors for disturbed gastric motility, we hypothesized that critically ill patients with DM would have abnormal proximal gastric motor activity during fasting and in response to duodenal nutrient infusion, compared to non-diabetic critically ill patients and healthy humans. Abstract AIM: To investigate the proximal gastric motor response to duodenal nutrients in critically ill patients with longstanding type 2 diabetes mellitus. MATERIALS AND METHODS Subjects METHODS:Proximal gastric motility was assessed (using a barostat) in 10 critically ill patients with type 2 diabetes mellitus (59 ± 3 years) during two 60-min duodenal infusions of Ensure  (1 and 2 kcal/min), in random order, separated by 2 h fasting. Data were compared with 15 non-diabetic critically ill patients (48 ± 5 years) and 10 healthy volunteers (28 ± 3 years). RESULTS:Baseline proximal gastric volumes were similar between the three groups. In diabetic patients, proximal gastric relaxation during 1 kcal/min nutrient infusion was similar to non-diabetic patients and healthy controls. In contrast, relaxation during 2 kcal/ min infusion was initially reduced in diabetic patients (P < 0.05) but increased to a level similar to healthy humans, unlike non-diabetic patients where relaxation was impaired throughout the infusion. Duodenal nutrient stimulation reduced the fundic wave frequency in a dose-dependent fashion in both the critically ill diabetic patients and healthy subjects, but not in critically ill patients without diabetes. Fundic wave frequency in diabetic patients and healthy subjects was greater than in non-diabetic patients. CONCLUSION:In patients with d...

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Gastric Motor and Sensory Functions in Obesity

Cited by 87 publications

References 75 publications

Effect of a Cellulose‐containing Weight‐loss Supplement on Gastric Emptying and Sensory Functions

Effect of a Cellulose‐containing Weight‐loss Supplement on Gastric Emptying and Sensory Functions

The role of the stomach in the control of appetite and the secretion of satiation peptides

Proximal gastric motility in critically ill patients with type 2 diabetes mellitus

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