Abstract
The objective of this study was to examine the release of insulin from cultured islet cells, taken from the pancreas of newborn and adult rats, in response to gastric inhibitory polypeptide (GIP), cholecystokinin-8 (CCK-8), calcitonin gene-related peptide (CGRP), and pancreastatin. GIP (10-9 - 10-7 M) potentiated glucose-stimulated release of insulin in a dose-dependent fashion from both newborn and adult islet cells. CCK-8 (>10-8 M) also increased glucose-stimulated release of insulin from newborn islet cells, however its effect was not significant and not as strong as that observed with adult islet cells. Culture of newborn islet cells for 3 weeks with media containing high concentrations of glucose (16.7 mM) enhanced insulin release in response to CCK-8. CGRP did not affect the release of insulin from newborn islet cells, whereas at 10-10 M, it reduced the release of insulin from adult islet cells by 66 ± 4%. Pancreastatin (10-9 - 10-8 M) did not affect the release of insulin from newborn islet cells when cells were incubated with 4.2 mM glucose, whereas it stimulated the release of insulin from adult islet cells in a dose-dependent fashion. When incubated with 16.7 mM glucose, pancreastatin inhibited the release of insulin from both newborn and adult islet cells. These results indicate that newborn islet cells experience developmental changes which render them responsive to enteric peptides.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 77-82 |
| Number of pages | 6 |
| Journal | Pancreas |
| Volume | 3 |
| Issue number | 1 |
| State | Published - 1988 |
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ASJC Scopus subject areas
- Endocrinology
- Gastroenterology
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A comparison of the insulinotropic and the insulin-inhibitory actions of gut peptides on newborn and adult rat islet cells. / Ishizuka, J.; Singh, Pomila; Greeley, G. H.; Townsend, Courtney; Cooper, C. W.; Tatemoto, K.; Thompson, J. C.
In: Pancreas, Vol. 3, No. 1, 1988, p. 77-82.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - A comparison of the insulinotropic and the insulin-inhibitory actions of gut peptides on newborn and adult rat islet cells
AU - Ishizuka, J.
AU - Singh, Pomila
AU - Greeley, G. H.
AU - Townsend, Courtney
AU - Cooper, C. W.
AU - Tatemoto, K.
AU - Thompson, J. C.
PY - 1988
Y1 - 1988
N2 - The objective of this study was to examine the release of insulin from cultured islet cells, taken from the pancreas of newborn and adult rats, in response to gastric inhibitory polypeptide (GIP), cholecystokinin-8 (CCK-8), calcitonin gene-related peptide (CGRP), and pancreastatin. GIP (10-9 - 10-7 M) potentiated glucose-stimulated release of insulin in a dose-dependent fashion from both newborn and adult islet cells. CCK-8 (>10-8 M) also increased glucose-stimulated release of insulin from newborn islet cells, however its effect was not significant and not as strong as that observed with adult islet cells. Culture of newborn islet cells for 3 weeks with media containing high concentrations of glucose (16.7 mM) enhanced insulin release in response to CCK-8. CGRP did not affect the release of insulin from newborn islet cells, whereas at 10-10 M, it reduced the release of insulin from adult islet cells by 66 ± 4%. Pancreastatin (10-9 - 10-8 M) did not affect the release of insulin from newborn islet cells when cells were incubated with 4.2 mM glucose, whereas it stimulated the release of insulin from adult islet cells in a dose-dependent fashion. When incubated with 16.7 mM glucose, pancreastatin inhibited the release of insulin from both newborn and adult islet cells. These results indicate that newborn islet cells experience developmental changes which render them responsive to enteric peptides.
AB - The objective of this study was to examine the release of insulin from cultured islet cells, taken from the pancreas of newborn and adult rats, in response to gastric inhibitory polypeptide (GIP), cholecystokinin-8 (CCK-8), calcitonin gene-related peptide (CGRP), and pancreastatin. GIP (10-9 - 10-7 M) potentiated glucose-stimulated release of insulin in a dose-dependent fashion from both newborn and adult islet cells. CCK-8 (>10-8 M) also increased glucose-stimulated release of insulin from newborn islet cells, however its effect was not significant and not as strong as that observed with adult islet cells. Culture of newborn islet cells for 3 weeks with media containing high concentrations of glucose (16.7 mM) enhanced insulin release in response to CCK-8. CGRP did not affect the release of insulin from newborn islet cells, whereas at 10-10 M, it reduced the release of insulin from adult islet cells by 66 ± 4%. Pancreastatin (10-9 - 10-8 M) did not affect the release of insulin from newborn islet cells when cells were incubated with 4.2 mM glucose, whereas it stimulated the release of insulin from adult islet cells in a dose-dependent fashion. When incubated with 16.7 mM glucose, pancreastatin inhibited the release of insulin from both newborn and adult islet cells. These results indicate that newborn islet cells experience developmental changes which render them responsive to enteric peptides.
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M3 - Article
VL - 3
SP - 77
EP - 82
JO - Pancreas
JF - Pancreas
SN - 0885-3177
IS - 1
ER -