Assessment of diabetic nephropathy in the Akita mouse

Jae Hyung Chang, Susan Gurley

Research output: Chapter in Book/Report/Conference proceedingChapter

8 Citations (Scopus)

Abstract

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.
Pages17-29
Number of pages13
ISBN (Print)9781627030670
DOIs
StatePublished - Jan 1 2012
Externally publishedYes

Publication series

NameMethods in Molecular Biology
Volume933
ISSN (Print)1064-3745

Fingerprint

Diabetic Nephropathies
Type 1 Diabetes Mellitus
Bradykinin Receptors
Ketogenic Diet
Kidney
Urine Specimen Collection
Albuminuria
Nitric Oxide Synthase Type III
Wounds and Injuries
Point Mutation
Hyperglycemia
Albumins
Insulin
Genes

Keywords

  • 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

Cite this

Chang, J. H., & Gurley, S. (2012). Assessment of diabetic nephropathy in the Akita mouse. In Animal Models in Diabetes Research (pp. 17-29). (Methods in Molecular Biology; Vol. 933). Humana Press Inc.. https://doi.org/10.1007/978-1-62703-68-7_2

Assessment of diabetic nephropathy in the Akita mouse. / Chang, Jae Hyung; Gurley, Susan.

Animal Models in Diabetes Research. Humana Press Inc., 2012. p. 17-29 (Methods in Molecular Biology; Vol. 933).

Research output: Chapter in Book/Report/Conference proceedingChapter

Chang, JH & Gurley, S 2012, Assessment of diabetic nephropathy in the Akita mouse. in Animal Models in Diabetes Research. Methods in Molecular Biology, vol. 933, Humana Press Inc., pp. 17-29. https://doi.org/10.1007/978-1-62703-68-7_2
Chang JH, Gurley S. Assessment of diabetic nephropathy in the Akita mouse. In Animal Models in Diabetes Research. Humana Press Inc. 2012. p. 17-29. (Methods in Molecular Biology). https://doi.org/10.1007/978-1-62703-68-7_2
Chang, Jae Hyung ; Gurley, Susan. / Assessment of diabetic nephropathy in the Akita mouse. Animal Models in Diabetes Research. Humana Press Inc., 2012. pp. 17-29 (Methods in Molecular Biology).
@inbook{fa9b237d373b401aa0b82d348b4523ed,
title = "Assessment of diabetic nephropathy in the Akita mouse",
abstract = "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.",
keywords = "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",
author = "Chang, {Jae Hyung} and Susan Gurley",
year = "2012",
month = "1",
day = "1",
doi = "10.1007/978-1-62703-68-7_2",
language = "English (US)",
isbn = "9781627030670",
series = "Methods in Molecular Biology",
publisher = "Humana Press Inc.",
pages = "17--29",
booktitle = "Animal Models in Diabetes Research",

}

TY - CHAP

T1 - Assessment of diabetic nephropathy in the Akita mouse

AU - Chang, Jae Hyung

AU - Gurley, Susan

PY - 2012/1/1

Y1 - 2012/1/1

N2 - 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.

AB - 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.

KW - 24-h urine collection

KW - Albuminuria

KW - Angiotensin-converting enzyme 2

KW - Bradykinin receptor

KW - Diabetic nephropathy

KW - Endothelial nitric oxide synthase

KW - Genetic susceptibility

KW - Glomerular filtration rate

KW - Ketogenic diet

KW - Mouse metabolic cage

KW - Mouse model of type I diabetes

UR - http://www.scopus.com/inward/record.url?scp=84934440597&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84934440597&partnerID=8YFLogxK

U2 - 10.1007/978-1-62703-68-7_2

DO - 10.1007/978-1-62703-68-7_2

M3 - Chapter

C2 - 22893398

AN - SCOPUS:84934440597

SN - 9781627030670

T3 - Methods in Molecular Biology

SP - 17

EP - 29

BT - Animal Models in Diabetes Research

PB - Humana Press Inc.

ER -