Hypothesis

Physiologic role of pancreatic somatostatin and the contribution of D-cell disorders to diabetes mellitus

Roger H Unger, E. Ipp, L. Schusdziarra, L. Orci

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

The demonstration of direct inhibitory actions of pharmacologic doses of somatostatin upon gastrointestinal function suggests the possibility that somatostatin may be a physiologic regulator of the rate of nutrient entry from the gut and thus provide the A-, B-, and D-cells with an influence over all avenues of nutrient flux. If so, the relative reduction in somatostatin-containing cells in the pancreatic islets of obese hyperglycemic mice might be responsible for some or all of the metabolic derangements of the obese hyperglycemic syndrome of mice, and conceivably its human counterpart as well. Hyposomatostatinemia would permit accelerated gastrointestinal function with more rapid entry of nutrients; higher postprandial nutrient levels would cause hyperinsulinemia and reduce the insulin sensitivity of glucoregulatory tissues. As hyperglycemia increased, the B-cell response to hyperglycemia would wane, further escalating the metabolic derangement. By contrast with the obese hyperglycemic syndrome, diabetes characterized by marked dimunution in B-cells is associated with an apparent augmentation of D-cells, perhaps reflecting a futile compensatory effort of D-cells to correct the hyperglycemia of insulin deficiency by inhibiting the entry rate of exogenous nutrients.

Original languageEnglish (US)
Pages (from-to)2081-2086
Number of pages6
JournalLife Sciences
Volume20
Issue number12
DOIs
StatePublished - Jun 15 1977

Fingerprint

Somatostatin-Secreting Cells
Medical problems
Obese Mice
Somatostatin
Nutrients
Diabetes Mellitus
Food
Hyperglycemia
B-Lymphocytes
Cells
Insulin
Pharmacologic Actions
Hyperinsulinism
Islets of Langerhans
Insulin Resistance
Demonstrations
Tissue
Fluxes

ASJC Scopus subject areas

  • Pharmacology

Cite this

Hypothesis : Physiologic role of pancreatic somatostatin and the contribution of D-cell disorders to diabetes mellitus. / Unger, Roger H; Ipp, E.; Schusdziarra, L.; Orci, L.

In: Life Sciences, Vol. 20, No. 12, 15.06.1977, p. 2081-2086.

Research output: Contribution to journalArticle

@article{f2a90409ad794ce885a0f7896dfb0906,
title = "Hypothesis: Physiologic role of pancreatic somatostatin and the contribution of D-cell disorders to diabetes mellitus",
abstract = "The demonstration of direct inhibitory actions of pharmacologic doses of somatostatin upon gastrointestinal function suggests the possibility that somatostatin may be a physiologic regulator of the rate of nutrient entry from the gut and thus provide the A-, B-, and D-cells with an influence over all avenues of nutrient flux. If so, the relative reduction in somatostatin-containing cells in the pancreatic islets of obese hyperglycemic mice might be responsible for some or all of the metabolic derangements of the obese hyperglycemic syndrome of mice, and conceivably its human counterpart as well. Hyposomatostatinemia would permit accelerated gastrointestinal function with more rapid entry of nutrients; higher postprandial nutrient levels would cause hyperinsulinemia and reduce the insulin sensitivity of glucoregulatory tissues. As hyperglycemia increased, the B-cell response to hyperglycemia would wane, further escalating the metabolic derangement. By contrast with the obese hyperglycemic syndrome, diabetes characterized by marked dimunution in B-cells is associated with an apparent augmentation of D-cells, perhaps reflecting a futile compensatory effort of D-cells to correct the hyperglycemia of insulin deficiency by inhibiting the entry rate of exogenous nutrients.",
author = "Unger, {Roger H} and E. Ipp and L. Schusdziarra and L. Orci",
year = "1977",
month = "6",
day = "15",
doi = "10.1016/0024-3205(77)90188-6",
language = "English (US)",
volume = "20",
pages = "2081--2086",
journal = "Life Sciences",
issn = "0024-3205",
publisher = "Elsevier Inc.",
number = "12",

}

TY - JOUR

T1 - Hypothesis

T2 - Physiologic role of pancreatic somatostatin and the contribution of D-cell disorders to diabetes mellitus

AU - Unger, Roger H

AU - Ipp, E.

AU - Schusdziarra, L.

AU - Orci, L.

PY - 1977/6/15

Y1 - 1977/6/15

N2 - The demonstration of direct inhibitory actions of pharmacologic doses of somatostatin upon gastrointestinal function suggests the possibility that somatostatin may be a physiologic regulator of the rate of nutrient entry from the gut and thus provide the A-, B-, and D-cells with an influence over all avenues of nutrient flux. If so, the relative reduction in somatostatin-containing cells in the pancreatic islets of obese hyperglycemic mice might be responsible for some or all of the metabolic derangements of the obese hyperglycemic syndrome of mice, and conceivably its human counterpart as well. Hyposomatostatinemia would permit accelerated gastrointestinal function with more rapid entry of nutrients; higher postprandial nutrient levels would cause hyperinsulinemia and reduce the insulin sensitivity of glucoregulatory tissues. As hyperglycemia increased, the B-cell response to hyperglycemia would wane, further escalating the metabolic derangement. By contrast with the obese hyperglycemic syndrome, diabetes characterized by marked dimunution in B-cells is associated with an apparent augmentation of D-cells, perhaps reflecting a futile compensatory effort of D-cells to correct the hyperglycemia of insulin deficiency by inhibiting the entry rate of exogenous nutrients.

AB - The demonstration of direct inhibitory actions of pharmacologic doses of somatostatin upon gastrointestinal function suggests the possibility that somatostatin may be a physiologic regulator of the rate of nutrient entry from the gut and thus provide the A-, B-, and D-cells with an influence over all avenues of nutrient flux. If so, the relative reduction in somatostatin-containing cells in the pancreatic islets of obese hyperglycemic mice might be responsible for some or all of the metabolic derangements of the obese hyperglycemic syndrome of mice, and conceivably its human counterpart as well. Hyposomatostatinemia would permit accelerated gastrointestinal function with more rapid entry of nutrients; higher postprandial nutrient levels would cause hyperinsulinemia and reduce the insulin sensitivity of glucoregulatory tissues. As hyperglycemia increased, the B-cell response to hyperglycemia would wane, further escalating the metabolic derangement. By contrast with the obese hyperglycemic syndrome, diabetes characterized by marked dimunution in B-cells is associated with an apparent augmentation of D-cells, perhaps reflecting a futile compensatory effort of D-cells to correct the hyperglycemia of insulin deficiency by inhibiting the entry rate of exogenous nutrients.

UR - http://www.scopus.com/inward/record.url?scp=0017701693&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0017701693&partnerID=8YFLogxK

U2 - 10.1016/0024-3205(77)90188-6

DO - 10.1016/0024-3205(77)90188-6

M3 - Article

VL - 20

SP - 2081

EP - 2086

JO - Life Sciences

JF - Life Sciences

SN - 0024-3205

IS - 12

ER -