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Title: Analysis of the function of the agouti gene in obesity and diabetes

Abstract

This chapter discusses the agouti gene and dominant mutations in that gene that lead to agouti-induced obesity, and recent work with transgenic mice to elucidate the role of agouti in obesity. Agouti was cloned in 1992 by the lab of Rick Woychik at Oak Ridge National Laboratory, making it the first of many recently cloned mouse obesity genes. Sequence analysis predicted that mouse agouti is a secreted protein of 131 amino acids. The mature protein has a basic central region (lys57-arg85), a proline-rich domain (pro86-pro91) and a C-terminal region (cys 92-cys 13 1) containing 10 cysteine residues which form 5 disulfide bonds. The human homologue of agouti has also been cloned by the Woychik lab and maps to human chromosome 20q 11.2. Human agouti is 132 amino acids long and is 85% similar to the mouse agouti protein and is normally expressed in adipose tissue. The researchers have been able to recapitulate obesity, hyperinsulinemia, and hyperglycemia with the ubiquitous expression of agouti. Agouti expression in either liver and adipose tissue alone does not cause obesity, and there`s a dose-dependent effect of agouti on body weight, food efficiency, body temperature, and insulin and glucose levels.

Authors:
; ;  [1]
  1. and others
Publication Date:
Research Org.:
Oak Ridge National Lab. (ORNL), Oak Ridge, TN (United States)
Sponsoring Org.:
USDOE, Washington, DC (United States)
OSTI Identifier:
376394
Report Number(s):
CONF-9603200-1
ON: DE96015028; TRN: 96:005404
DOE Contract Number:  
AC05-96OR22464
Resource Type:
Conference
Resource Relation:
Conference: 2. annual international symposium on obesity, Washington, DC (United States), 4-6 Mar 1996; Other Information: PBD: 1996
Country of Publication:
United States
Language:
English
Subject:
55 BIOLOGY AND MEDICINE, BASIC STUDIES; ADIPOSE TISSUE; GENETIC CONTROL; DIABETES MELLITUS; TRANSGENIC MICE

Citation Formats

Mynatt, R L, Miltenberger, R J, and Klebig, M L. Analysis of the function of the agouti gene in obesity and diabetes. United States: N. p., 1996. Web.
Mynatt, R L, Miltenberger, R J, & Klebig, M L. Analysis of the function of the agouti gene in obesity and diabetes. United States.
Mynatt, R L, Miltenberger, R J, and Klebig, M L. 1996. "Analysis of the function of the agouti gene in obesity and diabetes". United States. https://www.osti.gov/servlets/purl/376394.
@article{osti_376394,
title = {Analysis of the function of the agouti gene in obesity and diabetes},
author = {Mynatt, R L and Miltenberger, R J and Klebig, M L},
abstractNote = {This chapter discusses the agouti gene and dominant mutations in that gene that lead to agouti-induced obesity, and recent work with transgenic mice to elucidate the role of agouti in obesity. Agouti was cloned in 1992 by the lab of Rick Woychik at Oak Ridge National Laboratory, making it the first of many recently cloned mouse obesity genes. Sequence analysis predicted that mouse agouti is a secreted protein of 131 amino acids. The mature protein has a basic central region (lys57-arg85), a proline-rich domain (pro86-pro91) and a C-terminal region (cys 92-cys 13 1) containing 10 cysteine residues which form 5 disulfide bonds. The human homologue of agouti has also been cloned by the Woychik lab and maps to human chromosome 20q 11.2. Human agouti is 132 amino acids long and is 85% similar to the mouse agouti protein and is normally expressed in adipose tissue. The researchers have been able to recapitulate obesity, hyperinsulinemia, and hyperglycemia with the ubiquitous expression of agouti. Agouti expression in either liver and adipose tissue alone does not cause obesity, and there`s a dose-dependent effect of agouti on body weight, food efficiency, body temperature, and insulin and glucose levels.},
doi = {},
url = {https://www.osti.gov/biblio/376394}, journal = {},
number = ,
volume = ,
place = {United States},
year = {Sun Sep 01 00:00:00 EDT 1996},
month = {Sun Sep 01 00:00:00 EDT 1996}
}

Conference:
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