Assessment of diabetic nephropathy in the Akita mouse

Jae Hyung Chang, Susan B. Gurley

Research output: Chapter in Book/Report/Conference proceedingChapter

12 Scopus citations


Akita mice have type 1 diabetes mellitus caused by a spontaneous point mutation in the Ins2 gene which leads to misfolding of insulin, resulting in pancreatic β-cell failure. Akita mice develop pronounced and sustained hyperglycemia, high levels of albuminuria, and consistent histopathological changes, suggesting that these mice may be suitable as an experimental platform for modeling diabetic nephropathy. One key feature of diabetic kidney disease in Akita mice is that the severity of renal injury is significantly influenced by genetic background. In this chapter, we describe the Akita model and present some of the experimental studies utilizing Akita mice as a model of type 1 diabetes. For example, deficiency in bradykinin receptors, endothelial nitric oxide synthase, or angiotensin-converting enzyme 2 leads to development of functionally and structurally more advanced diabetic nephropathy in these mice, while ketogenic diet has been shown to reverse kidney injury associated with diabetes. This chapter also describes the application of 24-h urine collections from mice for careful measurement of urinary albumin excretion.

Original languageEnglish (US)
Title of host publicationAnimal Models in Diabetes Research
PublisherHumana Press Inc.
Number of pages13
ISBN (Print)9781627030670
StatePublished - Jan 1 2012
Externally publishedYes

Publication series

NameMethods in Molecular Biology
ISSN (Print)1064-3745


  • 24-h urine collection
  • Albuminuria
  • Angiotensin-converting enzyme 2
  • Bradykinin receptor
  • Diabetic nephropathy
  • Endothelial nitric oxide synthase
  • Genetic susceptibility
  • Glomerular filtration rate
  • Ketogenic diet
  • Mouse metabolic cage
  • Mouse model of type I diabetes

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics


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