Development of a novel polygenic model of NIDDM in mice heterozygous for IR and IRS-1 null alleles

Article Abstract:

Mice which are double heterozygous for null alleles in the insulin receptor and insulin receptor substrate-1 genes which rendered them highly insulin resistant, were used as experimental disease model for non-insulin-dependent diabetes mellitus (NIDDM). The mice were observed to develop NIDDM in an age-dependent manner. The results of immunoprecipitation assay and Western blot analysis revealed that the genetic and molecular mechanisms behind NIDDM involve the combination of two mild effects in the insulin signaling cascade, leading to insulin resistance and subsequent progression to a diabetic phenotype.

Analysis, Usage, Development and progression, Genotype, Genotypes, Blood sugar, Blood glucose, Laboratory animals, Immunoassay, Insulin receptors, Western immunoblotting, Western blot

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Tissue-specific knockout of the insulin receptor in pancreatic beta cells creates an insulin secretory defect similar to that in type 2 diabetes

Article Abstract:

The role of insulin signaling in mice pancreatic beta cells was investigated using the Cre-loxP system to inactivate the insulin receptor gene in the beta cells. Mice lacking in the insulin receptor gene were found to display a selective loss of insulin secretion in response to glucose and an impairment in glucose tolerance, indicating that the insulin receptor plays an important role in glucose sensing by the beta cells. Results also suggested that impairments in insulin signaling at the beta cell level influence the changes in insulin secretion in type 2 diabetes.

Mice, Mice (Rodents), Glucose, Pancreatic beta cells

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Loss of ARNT/HIF1 beta mediates altered gene expression and pancreatic-islet dysfunction in human type 2 diabetes

Article Abstract:

Multiple changes in expression of genes that are important in beta cell function were identified by using oligonucleotide microarrays and real-time polymerase chain reaction (PCR) of pancreatic islets isolated from humans with type 2 diabetes versus normal glucose-tolerant controls. The expression of the transcription factor aryl hydrocarbon receptor nuclear translocator (ARNT) declined by 90 percent.

Science & research, Gene expression, Genetic research, DNA microarrays

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