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Nuclear SREBP-1a causes loss of pancreatic beta-cells and impaired insulin secretion.

Abstract：

:Transgenic mice expressing nuclear sterol regulatory element-binding protein-1a under the control of the insulin promoter were generated to determine the role of SREBP-1a in pancreatic beta-cells. Only low expressors could be established, which exhibited mild hyperglycemia, impaired glucose tolerance, and reduced plasma insulin levels compared to C57BL/6 controls. The islets isolated from the transgenic mice were fewer and smaller, and had decreased insulin content and unaltered glucagon staining. Both glucose- and potassium-stimulated insulin secretions were decreased. The transgenic islets consistently expressed genes for fatty acids and cholesterol synthesis, resulting in accumulation of triglycerides but not cholesterol. PDX-1, BetaEpsilonTauAlpha2, MafA, and IRS-2 were suppressed, partially explaining the loss and dysfunction of beta-cell mass. The transgenic mice on a high fat/high sucrose diet still exhibited impaired insulin secretion and continuous beta-cell growth defect. Therefore, nuclear SREBP-1a, even at a low level, strongly disrupts beta-cell mass and function.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Iwasaki Y,Iwasaki H,Yatoh S,Ishikawa M,Kato T,Matsuzaka T,Nakagawa Y,Yahagi N,Kobayashi K,Takahashi A,Suzuki H,Yamada N,Shimano H

doi

10.1016/j.bbrc.2008.11.105

subject

Has Abstract

pub_date

2009-01-16 00:00:00

pages

545-50

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(08)02278-X

journal_volume

378

pub_type

杂志文章

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