Immunohistochemical examination with insulin and glucagon of pancreatic islet pathology in glut-4 deficient transgenic mice

Jacob J. Steinberg

Research output: Contribution to journalArticle

Abstract

Methods: Pancreases from wild type, heterozygous, and homozygous mice deficient in the GLUT-4 alleles were stained with polyclonal antibodies to insulin or glucagon (Biogenex) and a secondary antibody complexed with streptavidin-biotin (Dako). Results: Pancreases of males at 6 mos. and females at 5 wks.and 3-4 m., regardless of GLUT-4 genotype, revealed islets in proximity to ducts and vessels, individual islets attached to ducts, some clustering of bilobed islets to the same duct, and some incidence of dysmorphic ducts. The islets of the females at 5 wk showed a distinctive "crescent" shaped glucagon pattern and those at 3-4 m. a peripheral pattern with scattered central staining. The mates at 6 m. showed a peripheral pattern with scattered central staining. All homozygous GLUT-4 deficient mice showed smaller islets than wild types, with the females significantly hypocellular. The female hétérozygotes at 10-12 mos. showed smaller, fewer islets in focal locations. Glucagon staining revealed a variety of different patterns from discontinuous cortical with subcortical penetration (more characteristic of wild type) to crescents and scattered central staining. The number of cells staining for glucagon did not vary from wild type to hétérozygote. The male hétérozygotes revealed hypercellular, islets, with duct attachment and nisideoblastic changes and a range of glucagon patterns more subcortical than those of females. Conclusions: Features seen in pancreases of all genotypes early, persist in older heterozygous GLUT-4 mice and may not account for pathophysiologic differences.

Original languageEnglish (US)
JournalFASEB Journal
Volume10
Issue number6
StatePublished - 1996

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glucagon
islets of Langerhans
Pathology
Glucagon
Islets of Langerhans
Ducts
Transgenic Mice
insulin
genetically modified organisms
Insulin
Staining and Labeling
pancreas
mice
Pancreas
Genotype
Insulin Antibodies
streptavidin
Streptavidin
Antibodies
genotype

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

Immunohistochemical examination with insulin and glucagon of pancreatic islet pathology in glut-4 deficient transgenic mice. / Steinberg, Jacob J.

In: FASEB Journal, Vol. 10, No. 6, 1996.

Research output: Contribution to journalArticle

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abstract = "Methods: Pancreases from wild type, heterozygous, and homozygous mice deficient in the GLUT-4 alleles were stained with polyclonal antibodies to insulin or glucagon (Biogenex) and a secondary antibody complexed with streptavidin-biotin (Dako). Results: Pancreases of males at 6 mos. and females at 5 wks.and 3-4 m., regardless of GLUT-4 genotype, revealed islets in proximity to ducts and vessels, individual islets attached to ducts, some clustering of bilobed islets to the same duct, and some incidence of dysmorphic ducts. The islets of the females at 5 wk showed a distinctive {"}crescent{"} shaped glucagon pattern and those at 3-4 m. a peripheral pattern with scattered central staining. The mates at 6 m. showed a peripheral pattern with scattered central staining. All homozygous GLUT-4 deficient mice showed smaller islets than wild types, with the females significantly hypocellular. The female h{\'e}t{\'e}rozygotes at 10-12 mos. showed smaller, fewer islets in focal locations. Glucagon staining revealed a variety of different patterns from discontinuous cortical with subcortical penetration (more characteristic of wild type) to crescents and scattered central staining. The number of cells staining for glucagon did not vary from wild type to h{\'e}t{\'e}rozygote. The male h{\'e}t{\'e}rozygotes revealed hypercellular, islets, with duct attachment and nisideoblastic changes and a range of glucagon patterns more subcortical than those of females. Conclusions: Features seen in pancreases of all genotypes early, persist in older heterozygous GLUT-4 mice and may not account for pathophysiologic differences.",
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AB - Methods: Pancreases from wild type, heterozygous, and homozygous mice deficient in the GLUT-4 alleles were stained with polyclonal antibodies to insulin or glucagon (Biogenex) and a secondary antibody complexed with streptavidin-biotin (Dako). Results: Pancreases of males at 6 mos. and females at 5 wks.and 3-4 m., regardless of GLUT-4 genotype, revealed islets in proximity to ducts and vessels, individual islets attached to ducts, some clustering of bilobed islets to the same duct, and some incidence of dysmorphic ducts. The islets of the females at 5 wk showed a distinctive "crescent" shaped glucagon pattern and those at 3-4 m. a peripheral pattern with scattered central staining. The mates at 6 m. showed a peripheral pattern with scattered central staining. All homozygous GLUT-4 deficient mice showed smaller islets than wild types, with the females significantly hypocellular. The female hétérozygotes at 10-12 mos. showed smaller, fewer islets in focal locations. Glucagon staining revealed a variety of different patterns from discontinuous cortical with subcortical penetration (more characteristic of wild type) to crescents and scattered central staining. The number of cells staining for glucagon did not vary from wild type to hétérozygote. The male hétérozygotes revealed hypercellular, islets, with duct attachment and nisideoblastic changes and a range of glucagon patterns more subcortical than those of females. Conclusions: Features seen in pancreases of all genotypes early, persist in older heterozygous GLUT-4 mice and may not account for pathophysiologic differences.

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