Targeted inactivation of kinesin-1 in pancreatic β-cells in vivo leads to insulin secretory deficiency.

ABSTRACT:

Objective

Suppression of Kinesin-1 by antisense oligonucleotides, or overexpression of dominant-negative acting kinesin heavy chain, has been reported to affect the sustained phase of glucose-stimulated insulin secretion in β-cells in vitro. In this study, we examined the in vivo physiological role of Kinesin-1 in β-cell development and function.

Research design and methods

A Cre-LoxP strategy was used to generate conditional knockout mice in which the Kif5b gene is specifically inactivated in pancreatic β-cells. Physiological and histological analyses were carried out in Kif5b knockout mice as well as littermate controls.

Results

Mice with β-cell specific deletion of Kif5b (Kif5b(fl/)⁻:RIP2-Cre) displayed significantly retarded growth as well as slight hyperglycemia

SUBMITTER: Cui J 

PROVIDER: S-EPMC3012189 | biostudies-literature | 2011 Jan

REPOSITORIES: biostudies-literature