CoChat
Sign Up
Cited by 369

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Advances in the physiology of gastric emptying

Goyal, Raj K., Guo, Yanmei, Mashimo, Hiroshi·2019·Neurogastroenterology & Motility
DOI 10.1111/nmo.13546PMC PMC6850045
Open this paper in CoChat — free account

Abstract

There have been many recent advances in the understanding of various aspects of the physiology of gastric motility and gastric emptying. Earlier studies had discovered the remarkable ability of the stomach to regulate the timing and rate of emptying of ingested food constituents and the underlying motor activity. Recent studies have shown that two parallel neural circuits, the gastric inhibitory vagal motor circuit (GIVMC) and the gastric excitatory vagal motor circuit (GEVMC), mediate gastric inhibition and excitation and therefore the rate of gastric emptying. The GIVMC includes preganglionic cholinergic neurons in the DMV and the postganglionic inhibitory neurons in the myenteric plexus that act by releasing nitric oxide, ATP, and peptide VIP. The GEVMC includes distinct gastric excitatory preganglionic cholinergic neurons in the DMV and postganglionic excitatory cholinergic neurons in the myenteric plexus. Smooth muscle is the final target of these circuits. The role of the intramuscular interstitial cells of Cajal in neuromuscular transmission remains debatable. The two motor circuits are differentially regulated by different sets of neurons in the NTS and vagal afferents. In the digestive period, many hormones including cholecystokinin and GLP‐1 inhibit gastric emptying via the GIVMC, and in the inter‐digestive period, hormones ghrelin and motilin hasten gastric emptying by stimulating the GEVMC. The GIVMC and GEVMC are also connected to anorexigenic and orexigenic neural pathways, respectively. Identification of the control circuits of gastric emptying may provide better delineation of the pathophysiology of abnormal gastric emptying and its relationship to satiety signals and food intake.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1111/nmo.13546

Cites

4 of 4 references verified0 citation errors · 0 not checkable

Statistics

Figures

Figure 1 Gastric emptying rates vary with the physical characteristic and caloric density of food. (A) Effect of physical characteristics of food on the rate of gastric emptying. Note that water or 5% glucose leaves the stomach at a fast rate, and digestible solids begin to leave after a lag period and leave the stomach slowly. Large pieces of indigestible solids are retained in the stomach during the digestive period and are then rapidly emptied. (B) Effect of caloric density of the liquid meal. Note that water leaves the stomach very fast and only 50% remains in the stomach at 10 min. High‐calorie liquids empty at a slower rate with 50% remaining in the stomach at 2 h. Low‐calorie liquids empty at an intermediate rate so the 50% leave the stomach by 1 h
Figure 1 Gastric emptying rates vary with the physical characteristic and caloric density of food. (A) Effect of physical characteristics of food on the rate of gastric emptying. Note that water or 5% glucose leaves the stomach at a fast rate, and digestible solids begin to leave after a lag period and leave the stomach slowly. Large pieces of indigestible solids are retained in the stomach during the digestive period and are then rapidly emptied. (B) Effect of caloric density of the liquid meal. Note that water leaves the stomach very fast and only 50% remains in the stomach at 10 min. High‐calorie liquids empty at a slower rate with 50% remaining in the stomach at 2 h. Low‐calorie liquids empty at an intermediate rate so the 50% leave the stomach by 1 hCC BY-NC · PubMed Central
Figure 2 Anatomic and functional parts of the human stomach, the gastric tunnel (Magenstrasse), and the pylorus. (A) Anatomic and functional parts of the stomach. The stomach includes three multifunctional, interconnected structures: pressure pump, peristaltic pump, and a grinder. The pressure pump includes anatomic fundus and proximal corpus. The peristaltic pump includes anatomic distal corpus and pyloric antrum. The pressure and peristaltic pumps form the propulsive unit. The anatomic correlate of the grinder is the pylorus that includes the anatomic pyloric canal and pyloric sphincter. Modified from Adler.15 (B) A functional tunnel along the lesser curvature of the stomach, called Magenstrasse, that may allow liquids to bypass the slower movement of the solid food through the stomach to accomplish a very fast gastric emptying. The figure identifies the initial location of particles emptied during 10 min, gray shaded with the time period of emptying, t emptying. From Pal et al10 (C) Details of the pyloric complex which includes the proximal muscle loop and the distal muscle loop formed by the pyloric sphincter. The proximal and distal muscle loops are ~2 cm away from each other on the greater curvature but merge together on the lesser curvature of the stomach. The loops enclose a triangular cavity with the merged muscle loops forming a torus at the lesser curve. The pyloric torus fits into the groove left between the proximal and distal muscle loops along the greater curvature, like a pastel and mortar, to form a perfect grinder. Pylorus provides mechanical grinding and food that has been tenderized by acid‐pepsin, to form chyme. The proximal muscle loop and the pyloric sphincter are separately regulated and can work independently
Figure 2 Anatomic and functional parts of the human stomach, the gastric tunnel (Magenstrasse), and the pylorus. (A) Anatomic and functional parts of the stomach. The stomach includes three multifunctional, interconnected structures: pressure pump, peristaltic pump, and a grinder. The pressure pump includes anatomic fundus and proximal corpus. The peristaltic pump includes anatomic distal corpus and pyloric antrum. The pressure and peristaltic pumps form the propulsive unit. The anatomic correlate of the grinder is the pylorus that includes the anatomic pyloric canal and pyloric sphincter. Modified from Adler.15 (B) A functional tunnel along the lesser curvature of the stomach, called Magenstrasse, that may allow liquids to bypass the slower movement of the solid food through the stomach to accomplish a very fast gastric emptying. The figure identifies the initial location of particles emptied during 10 min, gray shaded with the time period of emptying, t emptying. From Pal et al10 (C) Details of the pyloric complex which includes the proximal muscle loop and the distal muscle loop formed by the pyloric sphincter. The proximal and distal muscle loops are ~2 cm away from each other on the greater curvature but merge together on the lesser curvature of the stomach. The loops enclose a triangular cavity with the merged muscle loops forming a torus at the lesser curve. The pyloric torus fits into the groove left between the proximal and distal muscle loops along the greater curvature, like a pastel and mortar, to form a perfect grinder. Pylorus provides mechanical grinding and food that has been tenderized by acid‐pepsin, to form chyme. The proximal muscle loop and the pyloric sphincter are separately regulated and can work independentlyCC BY-NC · PubMed Central
Figure 3 A simplified gastric inhibitory vagal circuit (GIVC) and the gastric excitatory vagal circuit (GEVC). (A) The GIVC includes GIVMC and its inputs. GIVMC consists of preganglionic DMV‐C‐i neuron and postganglionic, NANC inhibitory neuron in the myenteric plexus (MP‐NANC‐i). See text for details of the neurotransmission. The DMV‐C‐i neurons receive excitatory input directly from the NTS‐CC‐i neurons via the α1‐receptors and through NTS‐PPG neurons via GHSR or GLP‐1 receptors. The NTS‐CC‐i neurons receive glutaminergic input from low‐threshold vagal afferents whose neurons are in the nodose ganglion (NG). (Arrow—stimulation; flat—inhibition). (B) The GEVC includes GEVMC and its inputs. GEVMC consists of preganglionic DMV‐C‐e neurons and postganglionic, cholinergic excitatory myenteric plexus (MP‐C‐e) neurons. DMV‐C‐e neurons receive strong inhibitory input from NTS‐GABA‐e neurons and NTS‐CC‐e neurons, and excitatory input from NTS‐GLUT‐e neurons. The NTS‐GABA‐e, NTS‐CC‐e, and NTS‐GLUT‐e neurons are interconnected and send integrated inhibitory input to the DMV‐C‐e neurons. NTS‐CC neurons also send inhibitory input to DMV‐C‐e neurons via the α2‐receptors. The inhibitory inputs from the NTS to DMV‐C‐e suppress spontaneously active DMV‐C‐e and cause gastric relaxation. On the other hand, suppression of the NTS‐GABA neurons NTS‐CC‐i disinhibits the spontaneously active DMV‐C‐e neurons leading to gastric excitation and fast gastric emptying as in acute hypoglycemia. See text for other details. (Arrow—stimulation; flat—inhibition)
Figure 3 A simplified gastric inhibitory vagal circuit (GIVC) and the gastric excitatory vagal circuit (GEVC). (A) The GIVC includes GIVMC and its inputs. GIVMC consists of preganglionic DMV‐C‐i neuron and postganglionic, NANC inhibitory neuron in the myenteric plexus (MP‐NANC‐i). See text for details of the neurotransmission. The DMV‐C‐i neurons receive excitatory input directly from the NTS‐CC‐i neurons via the α1‐receptors and through NTS‐PPG neurons via GHSR or GLP‐1 receptors. The NTS‐CC‐i neurons receive glutaminergic input from low‐threshold vagal afferents whose neurons are in the nodose ganglion (NG). (Arrow—stimulation; flat—inhibition). (B) The GEVC includes GEVMC and its inputs. GEVMC consists of preganglionic DMV‐C‐e neurons and postganglionic, cholinergic excitatory myenteric plexus (MP‐C‐e) neurons. DMV‐C‐e neurons receive strong inhibitory input from NTS‐GABA‐e neurons and NTS‐CC‐e neurons, and excitatory input from NTS‐GLUT‐e neurons. The NTS‐GABA‐e, NTS‐CC‐e, and NTS‐GLUT‐e neurons are interconnected and send integrated inhibitory input to the DMV‐C‐e neurons. NTS‐CC neurons also send inhibitory input to DMV‐C‐e neurons via the α2‐receptors. The inhibitory inputs from the NTS to DMV‐C‐e suppress spontaneously active DMV‐C‐e and cause gastric relaxation. On the other hand, suppression of the NTS‐GABA neurons NTS‐CC‐i disinhibits the spontaneously active DMV‐C‐e neurons leading to gastric excitation and fast gastric emptying as in acute hypoglycemia. See text for other details. (Arrow—stimulation; flat—inhibition)CC BY-NC · PubMed Central
Figure 4 Main sites of action of CCK and ghrelin. (A) Cholecystokinin (CCK) is a prototype breaking hormone. It acts to stimulate vagovagal circuit at multiple levels. CCK stimulates vagal afferents endings by paracrine effect and enhances glutamate release from the vagal afferent endings projecting onto NTS‐CC‐i neurons. CCK also directly or indirectly stimulates NTS‐CC‐i neurons, PPG‐i neurons, and NTS‐POMC‐S neurons. CCK stimulation of NTS‐CC‐i neurons activates DMV‐C‐i via the α1‐adrenergic receptor; stimulation of the NTS‐PPG‐i neurons via the GLP‐1 receptor on the DMV‐C‐i. CCK has also been shown to directly stimulate MP‐NANC‐i neurons, and may also stimulate DMV‐C‐i neurons. Thus, CCK acts at multiple sites to stimulate GIVC. Stimulation of NTS‐CC‐i neurons also inhibits DMV‐C‐e neurons via the α2‐adrenergic receptors. Thus, CCK also acts to inhibit GEVC. All these actions further augment the inhibitory effect of CCK on the gastric muscle. CCK also stimulates NTS‐POMC‐s neurons to generate satiety signals. (Arrow—stimulation; flat—inhibition). (B) Ghrelin is a gastric accelerating hormone. Ghrelin acts at multiple central and peripheral sites to stimulate gastric motility. Centrally, ghrelin inhibits NTS‐CC‐i neurons thereby inhibiting DMV‐C‐i. Ghrelin also inhibits NTS‐CC‐e to disinhibit DMV‐C‐e neurons. Ghrelin also disinhibits DMV‐C‐e neurons by inhibiting AP‐GABA‐e neurons that project onto DMV‐C‐e neurons. Ghrelin also acts on myenteric plexus and the smooth muscle. All these actions lead to strong gastric excitation. (Arrow—stimulation; flat—inhibition)
Figure 4 Main sites of action of CCK and ghrelin. (A) Cholecystokinin (CCK) is a prototype breaking hormone. It acts to stimulate vagovagal circuit at multiple levels. CCK stimulates vagal afferents endings by paracrine effect and enhances glutamate release from the vagal afferent endings projecting onto NTS‐CC‐i neurons. CCK also directly or indirectly stimulates NTS‐CC‐i neurons, PPG‐i neurons, and NTS‐POMC‐S neurons. CCK stimulation of NTS‐CC‐i neurons activates DMV‐C‐i via the α1‐adrenergic receptor; stimulation of the NTS‐PPG‐i neurons via the GLP‐1 receptor on the DMV‐C‐i. CCK has also been shown to directly stimulate MP‐NANC‐i neurons, and may also stimulate DMV‐C‐i neurons. Thus, CCK acts at multiple sites to stimulate GIVC. Stimulation of NTS‐CC‐i neurons also inhibits DMV‐C‐e neurons via the α2‐adrenergic receptors. Thus, CCK also acts to inhibit GEVC. All these actions further augment the inhibitory effect of CCK on the gastric muscle. CCK also stimulates NTS‐POMC‐s neurons to generate satiety signals. (Arrow—stimulation; flat—inhibition). (B) Ghrelin is a gastric accelerating hormone. Ghrelin acts at multiple central and peripheral sites to stimulate gastric motility. Centrally, ghrelin inhibits NTS‐CC‐i neurons thereby inhibiting DMV‐C‐i. Ghrelin also inhibits NTS‐CC‐e to disinhibit DMV‐C‐e neurons. Ghrelin also disinhibits DMV‐C‐e neurons by inhibiting AP‐GABA‐e neurons that project onto DMV‐C‐e neurons. Ghrelin also acts on myenteric plexus and the smooth muscle. All these actions lead to strong gastric excitation. (Arrow—stimulation; flat—inhibition)CC BY-NC · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Research works printed but not linked: 115

  1. 10.1016/j.clnu.2014.11.003 · DOI
  2. Ehrlein HJ, 2005, Gastrointestinal Motility
  3. 10.1016/0950-3528(91)90034-X · DOI
  4. 10.1016/0016-5085(85)90650-X · DOI
  5. 10.1016/0016-5085(88)90669-5 · DOI
  6. 10.1038/nrgastro.2016.76 · DOI · Paper page
  7. 10.1152/ajpendo.00199.2014 · DOI
  8. 10.2337/dc16-0351 · DOI
  9. 10.1152/ajpendo.00514.2007 · DOI
  10. 10.1016/j.jbiomech.2006.06.006 · DOI
  11. 10.1016/0016-5085(84)90085-4 · DOI
  12. 10.1016/S0016-5085(83)80232-7 · DOI
  13. 10.2967/jnmt.107.048116 · DOI
  14. 10.1016/j.jss.2009.01.035 · DOI
  15. 10.1111/j.1365-2982.2005.00664.x · DOI
  16. 10.1046/j.1365-2982.2001.00258.x · DOI
  17. 10.1113/jphysiol.1990.sp017999 · DOI
  18. Treacy PJ, 1992, Duodenal intramural nerves in control of pyloric motility and gastric emptying, Am J Physiol, 263, G1
  19. 10.1111/j.1365-2982.2011.01710.x · DOI
  20. 10.1136/gut.10.7.543 · DOI
  21. 10.1016/j.jchemneu.2008.05.002 · DOI
  22. 10.1038/nrgastro.2012.57 · DOI
  23. 10.1113/jphysiol.2003.049700 · DOI
  24. 10.1023/A:1012374408853 · DOI
  25. 10.1056/NEJM199208203270802 · DOI
  26. 10.1053/j.gastro.2008.06.039 · DOI
  27. 10.1016/j.neuroscience.2011.04.036 · DOI
  28. 10.1113/JP271600 · DOI
  29. 10.1113/JP271971 · DOI
  30. 10.1113/jphysiol.2013.254292 · DOI
  31. 10.1038/nrgastro.2016.161 · DOI
  32. 10.1152/ajpgi.00344.2007 · DOI
  33. 10.1056/NEJM199604253341707 · DOI
  34. 10.1152/ajpgi.00309.2006 · DOI
  35. 10.1152/ajpgi.00478.2002 · DOI
  36. 10.1146/annurev.physiol.68.040504.094635 · DOI · Paper page
  37. 10.1111/j.1469-7793.1999.369ae.x · DOI
  38. 10.1152/ajpgi.2001.280.3.G361 · DOI
  39. 10.1172/JCI107829 · DOI
  40. 10.1136/gut.14.4.300 · DOI
  41. 10.1097/00000658-197309000-00009 · DOI
  42. 10.1111/j.1469-7793.1997.197bo.x · DOI
  43. 10.1007/s00429-003-0357-y · DOI
  44. Malbert CH, 1995, Vagal control of pyloric resistance, Am J Physiol, 269, G558
  45. 10.1172/JCI108013 · DOI
  46. 10.1113/jphysiol.1992.sp018994 · DOI
  47. 10.1113/jphysiol.1993.sp019524 · DOI
  48. 10.1146/annurev.physiol.68.040504.094707 · DOI
  49. 10.1111/j.1469-7793.1997.479be.x · DOI
  50. 10.1152/ajpregu.00717.2005 · DOI
  51. 10.1371/journal.pone.0162146 · DOI
  52. 10.1152/ajpgi.00380.2014 · DOI
  53. 10.3389/fmed.2018.00001 · DOI
  54. 10.1152/ajpcell.00080.2014 · DOI
  55. 10.1113/JP271587 · DOI
  56. 10.1111/j.1365-2982.2010.01592.x · DOI
  57. 10.1523/JNEUROSCI.3502-07.2007 · DOI
  58. 10.1523/JNEUROSCI.3187-10.2011 · DOI
  59. 10.1152/ajpgi.00289.2003 · DOI
  60. 10.1152/ajpregu.00155.2003 · DOI
  61. 10.1152/ajpgi.90567.2008 · DOI
  62. 10.1523/JNEUROSCI.20-04-01393.2000 · DOI
  63. 10.1113/JP271972 · DOI
  64. 10.1111/j.1469-7793.2000.00105.x · DOI
  65. 10.1074/jbc.M115.654384 · DOI
  66. 10.1152/ajpregu.00179.2003 · DOI
  67. 10.1177/1535370216654228 · DOI
  68. 10.1152/ajpgi.00223.2017 · DOI
  69. 10.1113/JP272069 · DOI
  70. 10.1152/ajpgi.00395.2017 · DOI
  71. 10.1152/ajpgi.00363.2010 · DOI
  72. 10.1152/ajpgi.00382.2017 · DOI
  73. 10.1152/ajpgi.00043.2014 · DOI
  74. 10.1152/ajpgi.00180.2017 · DOI
  75. 10.3233/JPD-160817 · DOI
  76. 10.1053/j.gastro.2017.08.069 · DOI
  77. 10.1136/gut.2005.078121 · DOI
  78. 10.1113/jphysiol.2012.227959 · DOI
  79. 10.1152/ajpgi.00431.2003 · DOI
  80. 10.1152/ajpgi.00255.2016 · DOI
  81. 10.1113/jphysiol.2011.217497 · DOI
  82. 10.1016/0016-5085(95)90445-X · DOI
  83. 10.1124/jpet.104.072868 · DOI
  84. 10.1113/jphysiol.2010.191023 · DOI
  85. Willing AE, 1997, Gastric distension‐induced c‐fos expression in catecholaminergic neurons of rat dorsal vagal complex, Am J Physiol, 272, R59
  86. 10.1113/jphysiol.2009.175067 · DOI
  87. 10.1038/sj.ijo.0801910 · DOI
  88. 10.1152/ajpgi.00356.2010 · DOI
  89. 10.1152/ajpregu.00517.2006 · DOI
  90. 10.1038/nn1214 · DOI
  91. 10.1523/JNEUROSCI.4177-04.2005 · DOI
  92. 10.1016/0016-5085(86)90080-6 · DOI
  93. 10.1016/j.bbrc.2016.02.095 · DOI
  94. 10.1111/dom.13080 · DOI
  95. 10.1098/rstb.2006.1858 · DOI
  96. 10.1016/j.beem.2009.03.005 · DOI · Paper page
  97. 10.2337/db11-0489 · DOI
  98. 10.1023/A:1018863716749 · DOI
  99. 10.3109/00365527909179889 · DOI
  100. 10.5115/acb.2012.45.1.1 · DOI
  101. 10.1016/j.neuron.2017.09.043 · DOI
  102. 10.1007/164_2016_104 · DOI
  103. 10.1053/gast.2002.35954 · DOI
  104. 10.1152/ajpgi.00536.2006 · DOI
  105. 10.1210/en.2016-1815 · DOI
  106. 10.1177/1073858407311100 · DOI · Paper page
  107. 10.1111/nmo.12261 · DOI
  108. 10.1136/gut.2005.065896 · DOI
  109. 10.1016/j.regpep.2007.07.008 · DOI
  110. 10.1371/journal.pone.0064777 · DOI
  111. 10.1113/JP270788 · DOI
  112. 10.14814/phy2.13105 · DOI
  113. 10.1677/JME-09-0095 · DOI
  114. 10.1016/j.cmet.2006.09.004 · DOI
  115. 10.1523/JNEUROSCI.2742-12.2013 · DOI

Cited by

Sorted by citations

See all 369

Metadata

Authors
Goyal, R. K., Guo, Y., & Mashimo, H.
Affiliations
Department of Medicine, VA Boston Healthcare System Harvard Medical School Boston Massachusetts
ORCID
Venue
Neurogastroenterology & Motility
Publisher
Wiley
Published
2019-02-10
Volume
31
Issue
4
ISSN
  • 1350-1925
  • 1365-2982
DOI
10.1111/nmo.13546
PMC
PMC6850045
Cited by
369
References
4
Language
en
Licence
creativecommons.org/licenses/by-nc/4.0/ (vor)
Funders
U.S. Department of Veterans Affairs (5101 BX002806-04)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review