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Gastric Inhibitory Polypeptide

John C Brown, Alison M. J. Buchan, Christopher H. S. McIntosh, Raymond A. Pederson

10.1002/cphy.cp060218

Source: Supplement 17: Handbook of Physiology, The Gastrointestinal System, Neural and Endocrine Biology

Originally published: 1989

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Gastric Inhibitory Effect of Gastric Inhibitory Polypeptide
2 Insulinotropic Action of GIP
3 Isolation and Purification of Porcine GIP
3.1 Amino Acid Sequence
3.2 Synthesis
4 GIP Receptors
5 Actions of GIP
5.1 Effect of GIP on Gastric Secretion
5.2 Effect of GIP on Insulin Secretion
5.3 Effect of GIP on Glucagon Secretion
5.4 Miscellaneous Actions of GIP
6 Radioimmunoassay
6.1 Development
6.2 Circulating Levels of Immunoreactive‐GIP
7 Immunocytochemical Localization of GIP
7.1 Light Microscopy
7.2 Ontogenic Development
7.3 Ultrastructure
Figure 1. Figure 1.

Pressure changes in gallbladder of dogs during intravenous infusion of 2 cholecystokinin‐pancreozymin (CCK‐PZ) preparations, containing 100 (open triangles) and 1,500 (open circles) IDU/mg, at dose of 0.2 IDU/min.

From Brown and Pederson 25
Figure 2. Figure 2.

Acid secretory changes from Bickel pouches of animals in Figure 1. Significantly different acid responses occurred with doses that were equipotent for gallbladder contraction. CCK‐PZ, cholecystokinin‐pancreozymin.

From Brown and Pederson 25
Figure 3. Figure 3.

Effect of intravenous infusion of gastric inhibitory peptide (GIP) (1.0 μg/min) on immunoreactive insulin (IRI) release and serum glucose in normal human volunteers receiving intravenous infusion of 0.5 g/min glucose for 60 min.

From Dupré et al. 51
Figure 4. Figure 4.

Amino acid sequences of porcine, human, and two synthesized analogues of GIP.
Figure 5. Figure 5.

125I‐labeled GIP binding to In 111 cells. A: 125I‐labeled GIP binding as function of time. B: competitive inhibition of 125I‐labeled GIP binding to cells by increasing concentrations of native GIP. Inset Scatchard plot of binding data.

From Amiranoff et al. 2
Figure 6. Figure 6.

Increase in cAMP levels in In 111 cells in response to GIP. A: time course of GIP effect on cAMP levels. B: concentration dependence of GIP in increasing cAMP levels.

From Amiranoff et al. 2
Figure 7. Figure 7.

Effect of time on GIP‐, pancreatic glucagon‐, and porcine (p) vasoactive intestinal peptide (VIP)‐induced cAMP production in HGT‐1 cells. Peptides were present in following concentrations: GIP, 0.1 μM; pancreatic glucagon, 0.3 μM; and VIP, 0.1 μM.

From Gespach et al. 69
Figure 8. Figure 8.

Effect of different concentrations of GIP, glucagon, and porcine (p) or chicken (c) vasoactive intestinal peptide (VIP) on cAMP production in HGT‐1 cells.

From Gespach et al. 69
Figure 9. Figure 9.

Release of GIP by intraduodenal acid. A: serum levels of glucose, immunoreactive (IR) insulin, and IR‐GIP after intraduodenal infusion of HCl in anesthetized rats. B: increase in IR‐GIP in healthy volunteers after intraduodenal infusion of HCl

From Ebert et al. 55). Reprinted with permission from The American Gastroenterological Association
Figure 10. Figure 10.

Effect of 1 h infusion of 0.25, 0.50, and 1.0 μg·kg−1·h−1 GIP on pentagastrin‐stimulated acid secretion from canine Heidenhain pouch.

From Pederson and Brown 140
Figure 11. Figure 11.

Gastric fistula (GF) and Heidenhain pouch (HP) responses to graded doses of pentagastrin (PG) with and without infusion of GIP (1 μg·kg−1·h−1).

From Soon‐Shiong et al. 183
Figure 12. Figure 12.

From Soon‐Shiong et al. 183)

Acid output from gastric fistula (GF) and Heidenhain pouch (HP) in response to graded doses of pentagastrin (Pg) with bethanechol background, with or without infusion of GIP (1 μg·kg−1·h−1).
Figure 13. Figure 13.

Effect of GIP and vagal stimulation on release of somatostatin‐like immunoreactivity (SLI) from isolated perfused rat stomach. A: stomach perfused with Krebs‐Ringer bicarbonate buffer, and GIP (1 nM) introduced between time periods 10–30 min. Control perfusions with buffer alone. B: after buffer perfusion SLI release stimulated with GIP (1 nM) between periods 5–40 min. Vagal stimulation (7 V, 10 Hz, 5 ms duration) performed during periods 15–30 min.

From McIntosh et al. 121
Figure 14. Figure 14.

Effect of Met‐enkephalin on GIP‐stimulated somatostatin‐like immunoreactivity (SLI) secretion. After buffer perfusion, SLI release stimulated with GIP (1 nM) between periods 12–35 min. Met‐enkephalin introduced during periods 20–28 min at concentration of 1 μM (A) or 100 pM (B).

From McIntosh et al. 117
Figure 15. Figure 15.

Effect of naloxone on inhibition of somatostatin‐like immunoreactivity (SLI) secretion by vagal stimulation. After buffer perfusion, GIP (1 nM) introduced during periods 9–46 min. Vagal stimulation (7 V, 10 Hz, 5 ms duration) performed during periods 16–35 min and naloxone added during periods 20–30 min.

From McIntosh et al. 117
Figure 16. Figure 16.

Hypothetical pathway by which GIP may act as enterogastrone under physiological conditions.
Figure 17. Figure 17.

Effect of 1 h infusion of 0.25, 0.5, and 1.0 μg·kg−1·h−1 GIP on pepsin secretion from canine Heidenhain pouch.

From Pederson and Brown 140
Figure 18. Figure 18.

Effect of 5 ng/ml porcine GIP on integrated immunoreactive insulin (IRI) release from isolated, perfused rat pancreas in response to changes in glucose concentration.

From Brown 14
Figure 19. Figure 19.

Release of immunoreactive insulin (IRI) from isolated, perfused rat pancreas in response to 160 mg/dl glucose with and without 1.0 ng/ml porcine GIP.

From Brown et al. 21
Figure 20. Figure 20.

Effect of infusion of porcine GIP (6.67 ng·kg−1·min−1) on immunoreactive insulin (IRI), IR‐glucagon, and glucose infusion required to maintain stable glycemia at basal + 54 mg/dl. Results with GIP infusion are on right.

From Elahi et al. 57
Figure 21. Figure 21.

Effect of infusion of porcine GIP (6.67 ng·kg−1·min−1) on immunoreactive insulin (IRI), IR‐glucagon, and glucose infusion to maintain stable glycemia at basal + 143 mg/dl. Results with GIP infusion are on right.

From Elahi et al. 57
Figure 22. Figure 22.

Effect of varying glucose concentration on immuno‐reactive‐glucagon and immunoreactive insulin release from isolated, perfused rat pancreas in presence (filled circles) and absence (open circles) of GIP (5 ng/ml). Release of immunoreactive glucagon suppressed by increasing glucose concentration.
Figure 23. Figure 23.

Effect of intraduodenal (ID) saline or glucose on lower esophageal sphincter pressure (LESP) in dogs.

From Sinar et al. 174). Reprinted with permission from The American Gastroenterological Association
Figure 24. Figure 24.

Effect of injection into third ventricle in ovariectomized rats of 1.0 and 5.0 μg porcine GIP on plasma follicle stimulating hormone (FSH) concentrations (A) and plasma growth hormone (GH) concentrations (B).

From Ottlecz et al. 137
Figure 25. Figure 25.

Mean plasma immunoreactive GIP levels in 8 subjects after ingestion of meal. Seven different antisera were used in same assay system.

From Jorde et al. 85
Figure 26. Figure 26.

Effect on immunoreactive (IR) insulin release of introducing, as gradient, porcine GIP (0.1–1.0 ng/ml) into isolated, perfused rat pancreas preparation in control, total parenteral nutrition (TPN), and intestinal bypass‐treated animals.

From Pederson et al. 143
Figure 27. Figure 27.

Immunoreactive (IR) insulin response to 1.0 ng/ml GIP from isolated, perfused rat pancreas of lean and obese Zucker rats in presence of 80 mg/dl glucose.

From Chan et al. 35
Figure 28. Figure 28.

GIP‐containing cell in canine jejunum stained with monoclonal antibody (mouse, antibody 3.65H). Note close association with capillary, × 600.
Figure 29. Figure 29.

High‐magnification detail of GIP‐immunoreactive cell stained with monoclonal antibody (3.65 H) localized with 20 nm colloidal gold, × 1,000.


Figure 1.

Pressure changes in gallbladder of dogs during intravenous infusion of 2 cholecystokinin‐pancreozymin (CCK‐PZ) preparations, containing 100 (open triangles) and 1,500 (open circles) IDU/mg, at dose of 0.2 IDU/min.

From Brown and Pederson 25


Figure 2.

Acid secretory changes from Bickel pouches of animals in Figure 1. Significantly different acid responses occurred with doses that were equipotent for gallbladder contraction. CCK‐PZ, cholecystokinin‐pancreozymin.

From Brown and Pederson 25


Figure 3.

Effect of intravenous infusion of gastric inhibitory peptide (GIP) (1.0 μg/min) on immunoreactive insulin (IRI) release and serum glucose in normal human volunteers receiving intravenous infusion of 0.5 g/min glucose for 60 min.

From Dupré et al. 51


Figure 4.

Amino acid sequences of porcine, human, and two synthesized analogues of GIP.



Figure 5.

125I‐labeled GIP binding to In 111 cells. A: 125I‐labeled GIP binding as function of time. B: competitive inhibition of 125I‐labeled GIP binding to cells by increasing concentrations of native GIP. Inset Scatchard plot of binding data.

From Amiranoff et al. 2


Figure 6.

Increase in cAMP levels in In 111 cells in response to GIP. A: time course of GIP effect on cAMP levels. B: concentration dependence of GIP in increasing cAMP levels.

From Amiranoff et al. 2


Figure 7.

Effect of time on GIP‐, pancreatic glucagon‐, and porcine (p) vasoactive intestinal peptide (VIP)‐induced cAMP production in HGT‐1 cells. Peptides were present in following concentrations: GIP, 0.1 μM; pancreatic glucagon, 0.3 μM; and VIP, 0.1 μM.

From Gespach et al. 69


Figure 8.

Effect of different concentrations of GIP, glucagon, and porcine (p) or chicken (c) vasoactive intestinal peptide (VIP) on cAMP production in HGT‐1 cells.

From Gespach et al. 69


Figure 9.

Release of GIP by intraduodenal acid. A: serum levels of glucose, immunoreactive (IR) insulin, and IR‐GIP after intraduodenal infusion of HCl in anesthetized rats. B: increase in IR‐GIP in healthy volunteers after intraduodenal infusion of HCl

From Ebert et al. 55). Reprinted with permission from The American Gastroenterological Association


Figure 10.

Effect of 1 h infusion of 0.25, 0.50, and 1.0 μg·kg−1·h−1 GIP on pentagastrin‐stimulated acid secretion from canine Heidenhain pouch.

From Pederson and Brown 140


Figure 11.

Gastric fistula (GF) and Heidenhain pouch (HP) responses to graded doses of pentagastrin (PG) with and without infusion of GIP (1 μg·kg−1·h−1).

From Soon‐Shiong et al. 183


Figure 12.

From Soon‐Shiong et al. 183)

Acid output from gastric fistula (GF) and Heidenhain pouch (HP) in response to graded doses of pentagastrin (Pg) with bethanechol background, with or without infusion of GIP (1 μg·kg−1·h−1).


Figure 13.

Effect of GIP and vagal stimulation on release of somatostatin‐like immunoreactivity (SLI) from isolated perfused rat stomach. A: stomach perfused with Krebs‐Ringer bicarbonate buffer, and GIP (1 nM) introduced between time periods 10–30 min. Control perfusions with buffer alone. B: after buffer perfusion SLI release stimulated with GIP (1 nM) between periods 5–40 min. Vagal stimulation (7 V, 10 Hz, 5 ms duration) performed during periods 15–30 min.

From McIntosh et al. 121


Figure 14.

Effect of Met‐enkephalin on GIP‐stimulated somatostatin‐like immunoreactivity (SLI) secretion. After buffer perfusion, SLI release stimulated with GIP (1 nM) between periods 12–35 min. Met‐enkephalin introduced during periods 20–28 min at concentration of 1 μM (A) or 100 pM (B).

From McIntosh et al. 117


Figure 15.

Effect of naloxone on inhibition of somatostatin‐like immunoreactivity (SLI) secretion by vagal stimulation. After buffer perfusion, GIP (1 nM) introduced during periods 9–46 min. Vagal stimulation (7 V, 10 Hz, 5 ms duration) performed during periods 16–35 min and naloxone added during periods 20–30 min.

From McIntosh et al. 117


Figure 16.

Hypothetical pathway by which GIP may act as enterogastrone under physiological conditions.



Figure 17.

Effect of 1 h infusion of 0.25, 0.5, and 1.0 μg·kg−1·h−1 GIP on pepsin secretion from canine Heidenhain pouch.

From Pederson and Brown 140


Figure 18.

Effect of 5 ng/ml porcine GIP on integrated immunoreactive insulin (IRI) release from isolated, perfused rat pancreas in response to changes in glucose concentration.

From Brown 14


Figure 19.

Release of immunoreactive insulin (IRI) from isolated, perfused rat pancreas in response to 160 mg/dl glucose with and without 1.0 ng/ml porcine GIP.

From Brown et al. 21


Figure 20.

Effect of infusion of porcine GIP (6.67 ng·kg−1·min−1) on immunoreactive insulin (IRI), IR‐glucagon, and glucose infusion required to maintain stable glycemia at basal + 54 mg/dl. Results with GIP infusion are on right.

From Elahi et al. 57


Figure 21.

Effect of infusion of porcine GIP (6.67 ng·kg−1·min−1) on immunoreactive insulin (IRI), IR‐glucagon, and glucose infusion to maintain stable glycemia at basal + 143 mg/dl. Results with GIP infusion are on right.

From Elahi et al. 57


Figure 22.

Effect of varying glucose concentration on immuno‐reactive‐glucagon and immunoreactive insulin release from isolated, perfused rat pancreas in presence (filled circles) and absence (open circles) of GIP (5 ng/ml). Release of immunoreactive glucagon suppressed by increasing glucose concentration.



Figure 23.

Effect of intraduodenal (ID) saline or glucose on lower esophageal sphincter pressure (LESP) in dogs.

From Sinar et al. 174). Reprinted with permission from The American Gastroenterological Association


Figure 24.

Effect of injection into third ventricle in ovariectomized rats of 1.0 and 5.0 μg porcine GIP on plasma follicle stimulating hormone (FSH) concentrations (A) and plasma growth hormone (GH) concentrations (B).

From Ottlecz et al. 137


Figure 25.

Mean plasma immunoreactive GIP levels in 8 subjects after ingestion of meal. Seven different antisera were used in same assay system.

From Jorde et al. 85


Figure 26.

Effect on immunoreactive (IR) insulin release of introducing, as gradient, porcine GIP (0.1–1.0 ng/ml) into isolated, perfused rat pancreas preparation in control, total parenteral nutrition (TPN), and intestinal bypass‐treated animals.

From Pederson et al. 143


Figure 27.

Immunoreactive (IR) insulin response to 1.0 ng/ml GIP from isolated, perfused rat pancreas of lean and obese Zucker rats in presence of 80 mg/dl glucose.

From Chan et al. 35


Figure 28.

GIP‐containing cell in canine jejunum stained with monoclonal antibody (mouse, antibody 3.65H). Note close association with capillary, × 600.



Figure 29.

High‐magnification detail of GIP‐immunoreactive cell stained with monoclonal antibody (3.65 H) localized with 20 nm colloidal gold, × 1,000.

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Article Title: Gastric Inhibitory Polypeptide
 

How to Cite

John C Brown, Alison M. J. Buchan, Christopher H. S. McIntosh, Raymond A. Pederson. Gastric Inhibitory Polypeptide. Compr Physiol 2011, Supplement 17: Handbook of Physiology, The Gastrointestinal System, Neural and Endocrine Biology: 403-430. First published in print 1989. doi: 10.1002/cphy.cp060218