Increased islet beta cell replication adjacent to intrapancreatic gastrinomas in humans.

Increased islet beta cell replication adjacent to intrapancreatic gastrinomas in humans. Research Abstract Details 

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Increased islet beta cell replication adjacent to intrapancreatic gastrinomas in humans. Abstract Text:

J J Meier,A E Butler,R Galasso,R A Rizza,P C Butler,

AIMS/HYPOTHESIS: Type 1 and type 2 diabetes are characterised by a beta cell deficit. Islet hyperplasia has been described in patients with Zollinger-Ellison syndrome secondary to gastrin-producing tumours (gastrinomas), and gastrin therapy has increased beta cell mass in rodents and human islets in vitro. In the present studies we addressed the following questions: (1) In pancreas specimens from gastrinoma cases, is the fractional beta cell area increased? (2) If so, is this restricted to tumour-adjacent islets or also present in tumour-distant islets? (3) Is new beta cell formation (beta cell replication and islet neogenesis) increased and beta cell apoptosis decreased in pancreas specimens from gastrinoma cases? METHODS: Pancreas was obtained at surgery from four patients with Zollinger-Ellison syndrome caused by pancreatic gastrinomas and 15 control subjects at autopsy. RESULTS: Islet fractional beta cell area (p<0.001), islet size (p<0.001) and beta cell replication (Ki67 staining) (p<0.05) were increased in islets adjacent to the tumours, but not in tumour-distant pancreas, compared with control subjects. We did not observe any differences in beta cell apoptosis or in the number of insulin-positive cells in ducts either adjacent to or distant from the tumour. CONCLUSIONS/INTERPRETATION: One or more factors released by human gastrinomas increase beta cell replication in islets immediately adjacent to the tumour, but not in tumour-distant islets. While these findings demonstrate that adult human beta cells can be driven into the cell cycle, they caution against the therapeutic usefulness of gastrin, since islets located >1 cm away from the gastrinomas did not exhibit changes in beta cell turnover, despite markedly elevated systemic gastrin levels sufficient to cause severe gastrointestinal symptoms.

Increased islet beta cell replication adjacent to intrapancreatic gastrinomas in humans. Publishing Authors By Initials

JJ Meier,AE Butler,R Galasso,RA Rizza,PC Butler,

For similar zollinger-ellison syndrome research abstracts see: zollinger-ellison syndrome research

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Increased islet beta cell replication adjacent to intrapancreatic gastrinomas in humans. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Diabetologia

VOLUME: 49

Page Numbers: 2689-96

Journal Abbreviation: Diabetologia

ISSN: 0012-186X

DAY: 23

MONTH: 09

YEAR: 2006

Increased islet beta cell replication adjacent to intrapancreatic gastrinomas in humans. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 6777

Increased islet beta cell replication adjacent to intrapancreatic gastrinomas in humans. Keywords Mesh Terms:

KEYWORDS: Zollinger-Ellison Syndrome

MESH TERMS: surgery

Chemical & Substance for Abstract: Increased islet beta cell replication adjacent to intrapancreatic gastrinomas in humans. Information

Substance Name: Gastrins

Registry Number: 0

Grant and Affiliation Information for Increased islet beta cell replication adjacent to intrapancreatic gastrinomas in humans.

AFFILIATION: Larry Hillblom Islet Research Center, UCLA David Geffen School of Medicine, 24-130 Warren Hall, 900 Veteran Avenue, Los Angeles, CA 90095-7073, USA.

Country: Germany

AGENCY: United States NIDDK

GRANT: DK61539

ACRONYM: DK

MEDLINETA: Diabetologia

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