ID 111630
Author
Ogino, Tomoe The University of Tokushima
Zhu, Min The University of Tokushima
Murakami, Takashi The University of Tokushima
Kuwajima, Masamichi The University of Tokushima
Keywords
pancreatectomy
β-cell mass
Wistar fatty rat
Content Type
Journal Article
Description
Wistar fatty rat, which has been established by transferring the fa gene of Zucker fatty rat to the Wistar Kyoto rat, has many features in common with human NIDDM. It exhibits hyperglycemic obesity with hyperinsulinemia and insulin resistance. It is unclear, however, whether a defect in the β-cell proliferation is related to the onset of diabetes mellitus together with insulin resistance in this model rat. To determine this, we compared non-fasting plasma glucose levels, insulin content and β-cell mass in the remnant pancreas of Wistar fatty rats with those in their diabetic-resistant lean counterparts after a 70% partial pancreatectomy. We also examined whether such a defect, if present, could be improved by either phlorizin or nicotinamide. We further investigated if there were any differences in these parameters between the phenotypically identical but genotypically different Wistar lean rats with a gene type of homogeneous Fa/Fa and that of heterogeneous Fa/fa. Male rats, 6 weeks of age, were allocated at random into two groups : 70% pancreatectomy (Px) and sham-pancreatectomy (sham). A sustained hyperglycemia was evident in the Px Wistar fatty rats after surgery, which was accompanied by a reduction of insulin content and β-cell mass in the remnant pancreas. The changes in insulin content and β-cell mass were unaffected by restoration of normoglycemia, induced by phlorizin injection. The administration of nicotinamide partially ameliorated the sustained hyperglycemia by a slight but not significant increase in β-cell mass. No discernible difference in the above parameters was observed between the Wistar lean rats with Fa/Fa and those with Fa/fa. These findings suggest that Wistar fatty rats have a poor capacity for proliferation of pancreatic β-cells, which causes the onset of overt diabetes along with insulin resistance due to extreme obesity.
Journal Title
The Journal of Medical Investigation
ISSN
13431420
NCID
AA11166929
Publisher
The University of Tokushima School of Medicine
Volume
45
Issue
1-4
Start Page
103
End Page
110
Sort Key
103
Published Date
1998-08
EDB ID
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher