Somatostatin secretion in cultured human islet cells from patients with nesidioblastosis: A compensatory mechanism?

James R. Upp; Jin Ishizuka; Thom E. Lobe; Sirnivasan Rajaraman; Courtney M. Townsend; James C. Thompson

doi:10.1016/S0022-3468(87)80734-0

Somatostatin secretion in cultured human islet cells from patients with nesidioblastosis: A compensatory mechanism?

James R. Upp, Jin Ishizuka, Thom E. Lobe, Sirnivasan Rajaraman, Courtney M. Townsend, James C. Thompson

Research output: Contribution to journal › Article › peer-review

2 Scopus citations

Abstract

Two patients with nesidioblastosis, one with persistent hypoglycemia and another who was asymptomatic, underwent pancreatic resection. Dispersed pancreatic islets were prepared from each patient. Insulin secretion from cultured islet cells was increased and somatostatin decreased in the symptomatic patient compared with the asymptomatic patient. Immunocytochemistry showed increased somatostatin-containing cells in the asymptomatic patient. We hypothesize that this may be the mechanism by which some patients with nesidioblastosis maintain normal serum glucose levels.

Original language	English (US)
Pages (from-to)	1185-1186
Number of pages	2
Journal	Journal of Pediatric Surgery
Volume	22
Issue number	12
DOIs	https://doi.org/10.1016/S0022-3468(87)80734-0
State	Published - Dec 1987
Externally published	Yes

Keywords

Beckwith-Wiedemann syndrome
Islets of Langerhans
hypoglycemia
insulin
nesiodioblastosis
somatostatin

ASJC Scopus subject areas

Surgery
Pediatrics, Perinatology, and Child Health

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10.1016/S0022-3468(87)80734-0

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title = "Somatostatin secretion in cultured human islet cells from patients with nesidioblastosis: A compensatory mechanism?",

abstract = "Two patients with nesidioblastosis, one with persistent hypoglycemia and another who was asymptomatic, underwent pancreatic resection. Dispersed pancreatic islets were prepared from each patient. Insulin secretion from cultured islet cells was increased and somatostatin decreased in the symptomatic patient compared with the asymptomatic patient. Immunocytochemistry showed increased somatostatin-containing cells in the asymptomatic patient. We hypothesize that this may be the mechanism by which some patients with nesidioblastosis maintain normal serum glucose levels.",

keywords = "Beckwith-Wiedemann syndrome, Islets of Langerhans, hypoglycemia, insulin, nesiodioblastosis, somatostatin",

author = "Upp, {James R.} and Jin Ishizuka and Lobe, {Thom E.} and Sirnivasan Rajaraman and Townsend, {Courtney M.} and Thompson, {James C.}",

note = "Funding Information: From the Departments of Surgery and Palhology, The University of Texas Medical Branch, Galveston. Supported by grantsf rom the National Institutes of Health (ROI DK 15241, POI DK 35608, and RCDA CA 00854) and from the American Cancer Society (PDT-220). Presented at the 18th Annual Meeting of the American Pediatric Surgical Association, Hilton tlead Island, South Carolina, May 6-9, 1987. Address reprint requests to James C. Thompson, MD, Department of Surgery, The University of Texas Medical Branch, Galveston, TX 77550. 9 1987 by Grune & Stratton, Inc. 0022-3468/87/2212-0024503.00/0",

year = "1987",

month = dec,

doi = "10.1016/S0022-3468(87)80734-0",

language = "English (US)",

volume = "22",

pages = "1185--1186",

journal = "Journal of Pediatric Surgery",

issn = "0022-3468",

publisher = "W.B. Saunders Ltd",

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TY - JOUR

T1 - Somatostatin secretion in cultured human islet cells from patients with nesidioblastosis

T2 - A compensatory mechanism?

AU - Upp, James R.

AU - Ishizuka, Jin

AU - Lobe, Thom E.

AU - Rajaraman, Sirnivasan

AU - Townsend, Courtney M.

AU - Thompson, James C.

N1 - Funding Information: From the Departments of Surgery and Palhology, The University of Texas Medical Branch, Galveston. Supported by grantsf rom the National Institutes of Health (ROI DK 15241, POI DK 35608, and RCDA CA 00854) and from the American Cancer Society (PDT-220). Presented at the 18th Annual Meeting of the American Pediatric Surgical Association, Hilton tlead Island, South Carolina, May 6-9, 1987. Address reprint requests to James C. Thompson, MD, Department of Surgery, The University of Texas Medical Branch, Galveston, TX 77550. 9 1987 by Grune & Stratton, Inc. 0022-3468/87/2212-0024503.00/0

PY - 1987/12

Y1 - 1987/12

N2 - Two patients with nesidioblastosis, one with persistent hypoglycemia and another who was asymptomatic, underwent pancreatic resection. Dispersed pancreatic islets were prepared from each patient. Insulin secretion from cultured islet cells was increased and somatostatin decreased in the symptomatic patient compared with the asymptomatic patient. Immunocytochemistry showed increased somatostatin-containing cells in the asymptomatic patient. We hypothesize that this may be the mechanism by which some patients with nesidioblastosis maintain normal serum glucose levels.

AB - Two patients with nesidioblastosis, one with persistent hypoglycemia and another who was asymptomatic, underwent pancreatic resection. Dispersed pancreatic islets were prepared from each patient. Insulin secretion from cultured islet cells was increased and somatostatin decreased in the symptomatic patient compared with the asymptomatic patient. Immunocytochemistry showed increased somatostatin-containing cells in the asymptomatic patient. We hypothesize that this may be the mechanism by which some patients with nesidioblastosis maintain normal serum glucose levels.

KW - Beckwith-Wiedemann syndrome

KW - Islets of Langerhans

KW - hypoglycemia

KW - insulin

KW - nesiodioblastosis

KW - somatostatin

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ER -

Somatostatin secretion in cultured human islet cells from patients with nesidioblastosis: A compensatory mechanism?

Abstract

Keywords

ASJC Scopus subject areas

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