Gastric emptying rate before and after orthodontic treatment examined with the [ 13 C] breath test: A pilot study

2018 ◽  
Vol 153 (3) ◽  
pp. 347-354 ◽  
Author(s):  
Jumpei Suzuki ◽  
Kazuo Shimazaki ◽  
Sarina Koike ◽  
Takashi Ono
2002 ◽  
Vol 282 (2) ◽  
pp. R366-R371 ◽  
Author(s):  
K. E. Castiglione ◽  
N. W. Read ◽  
S. J. French

Previous work has shown that the gastric emptying rate in animals and humans can adapt due to previous dietary intake. The present study investigated whether adaptation in gastric emptying rate due to consumption of a high-fat diet (HFD) is nutrient specific in humans. Gastric emptying of high-fat and high-carbohydrate test meals was measured (using gamma scintigraphy) before and after consumption of an HFD for 14 days in eight free-living male volunteers. Visual analog ratings of appetite were recorded throughout each test. There was no effect of HFD on any parameters of gastric emptying rate (lag phase, half-emptying time, and linear emptying rate) measured for carbohydrate test meals. HFD led to an acceleration of the linear emptying rate of the high-fat test meal (0.36 vs. 0.47%/min; P < 0.05). All meals reduced appetite ratings, but there were no differences between tests. These results support our previous findings of accelerated gastric emptying of high-fat test meals following an HFD and show that these changes appear to be nutrient specific, confirming recent studies in rats.


2017 ◽  
Vol 16 ◽  
pp. 1-8
Author(s):  
Noraini Abu Bakar ◽  
Wisam Kamil ◽  
Lina Al Bayati ◽  
Basma Ezzat Mustafa

Introduction: During orthodontic tooth movement, the early response of periodontal tissues to mechanical stress is an acute inflammatory reaction. Mechanical stress from orthodontic appliances is believed to induce cells in the periodontal ligament (PDL) to form biologically active substances, such as enzymes and cytokines, responsible for connective tissue remodeling (Nishijima Y et al 2006). Leptin, a polypeptide hormone has been classified as a cytokine (Zhang et al 1994). Earlier findings concluded that leptin at high local concentrations protects the host from inflammation and infection as well as maintaining bone levels. It has been also suggested that leptin plays a significant role in bone formation by its direct effect on osteoblasts (Alparslan et al 2010). This pilot study aimed to study leptin in saliva and its association with tooth movement during initial orthodontic alignment. Objectives: To determine if there are any differences in saliva leptin level before and after orthodontic alignment. Material and methods: Ten orthodontic patients (7 girls and 3 boys; mean age, 16.76 ± 1.1 years) with crowding (up to 5mm) that required orthodontic fixed appliances, on a non-extraction basis as part of the treatment plan, were recruited in this longitudinal study. Orthodontic study models were constructed at baseline and at 6- weeks after orthodontic treatment commenced. Full fixed orthodontic appliances with initial 0.014” Nickel Titanium archwire placed. The amount of crowding was measured, before and after initial alignment with an electronic digital caliper (Max-Cal, Japan Micrometer Ltd, Tokyo, Japan) with an accuracy of up to 0.01mm. Unstimulated morning saliva sample were collected at all visits, after at least an 8-hour period of fasting and no-toothbrushing. After centrifugation (4000x g;10min), the samples were stored at -25C and tested using Leptin Abnova LEP Human ELISA kit (KA3080) which was subsequently analyzed. Subjects’ periodontal health status was also monitored throughout the study. Ethical approval (ID IREC 262) was received on 7th April 2014 from International Islamic University Malaysia Research Ethics Committee (IREC). Results: Leptin concentration in saliva was significantly decreased in a time-dependant manner (t(9)=8.60, p<0.001), from before orthodontic treatment (7016.45± 425.15 pg/mL) and 6 weeks after bond-up (4901.92±  238.64 pg/mL). Conclusion: Leptin concentration in saliva is decreased during orthodontic tooth movement in initial alignment stage.


Author(s):  
Cong Xie ◽  
Weikun Huang ◽  
Linda E Watson ◽  
Stijn Soenen ◽  
Richard L Young ◽  
...  

Abstract Context Both gastric emptying and the secretion of glucagon-like peptide-1 (GLP-1) are major determinants of postprandial glycemia in health and type 2 diabetes (T2D). GLP-1 secretion after a meal is dependent on the entry of nutrients into the small intestine, which, in turn, slows gastric emptying. Objective To define the relationship between gastric emptying and the GLP-1 response to both oral and small intestinal nutrients in subjects with and without T2D. Design We evaluated: (i) the relationship between gastric emptying (breath test) and postprandial GLP-1 levels after a mashed potato meal in 73 T2D subjects; (ii) inter-individual variations in GLP-1 response to (a) intraduodenal glucose (4kcal/min) during euglycemia and hyperglycemia in 11 healthy, and 12 T2D, subjects, (b) intraduodenal fat (2kcal/min) in 15 T2D subjects, and (c) intraduodenal protein (3kcal/min) in 10 healthy subjects; and (iii) the relationship between gastric emptying (breath test) of 75g oral glucose and the GLP-1 response to intraduodenal glucose (4kcal/min) in 21 subjects (9 healthy, 12 T2D). Results The GLP-1 response to the mashed potato meal was unrelated to the gastric half-emptying time (T50). The GLP-1 responses to intraduodenal glucose, fat and protein varied substantially between individuals, but intra-individual variation to glucose was modest. The T50 of oral glucose was related directly to the GLP-1 response to intraduodenal glucose (r=0.65, P=0.002). Conclusions In a given individual, gastric emptying is not a determinant of the postprandial GLP-1 response. However, the intrinsic gastric emptying rate is determined in part by the responsiveness of GLP-1 to intestinal nutrients.


1994 ◽  
Vol 267 (5) ◽  
pp. R1257-R1265 ◽  
Author(s):  
Joel M. Kaplan ◽  
William Siemers ◽  
Harvey J. Grill

The notion that satiation signals are derived from the stomach with no additional contribution of postgastric sources (J. A. Deutsch. In: Handbook of Behavioral Neuroscience. Food and Water Intake. 1990, vol. 10, p. 151–182) was evaluated in two experiments. In experiment 1, the gastric contents were withdrawn after the rat met the satiety criterion for an initial intraoral intake test (12.5% glucose delivered at 1.0 ml/min). Ten minutes later, the intraoral infusion was continued until the rat again met the satiety criterion. We found that rats reingested an amount closely corresponding to the amount withdrawn, in agreement with previous studies using spout-licking tests. Despite a lower gastric emptying rate during reingestion than during the initial test, the amount recovered from the stomach (both volume and solute content) after reingestion was significantly less (gastric volume 16% less; gastric glucose 18% less) than that withdrawn initially. In experiment 2, a portion (8 ml) of the gastric contents was removed after the end of an initial intraoral intake test and, after 10 min, rats were again given an opportunity to ingest to satiety. The procedure was repeated for a total of three withdrawals (24 ml) and three reingestion opportunities. Rats accurately replaced the amounts withdrawn such that net intake at the end of the experiment did not differ from that ingested during the initial test. In addition, the amount recovered from the stomach after the terminal test was considerably less (gastric volume 25% less; gastric glucose 29% less) than that recovered at the end of single-test control sessions. Both experiments show that gastric feedback cannot alone account for the termination of intraoral intake. The results suggest that rats defend total intake and do so via the integration of signals derived from postgastric as well as gastric sources. stomach; satiation Submitted on November 15, 1993 Accepted on May 12, 1994


2010 ◽  
Vol 35 (1) ◽  
pp. 27-33 ◽  
Author(s):  
D. G. M. SUTTON ◽  
A. BAHR ◽  
T. PRESTON ◽  
R. M. CHRISTLEY ◽  
S. LOVE ◽  
...  

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