RGD Reference Report - Acyl-coenzyme A:cholesterol acyltransferase-2 (ACAT-2) is responsible for elevated intestinal ACAT activity in diabetic rats. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

Acyl-coenzyme A:cholesterol acyltransferase-2 (ACAT-2) is responsible for elevated intestinal ACAT activity in diabetic rats.

Authors: Hori, M  Satoh, M  Furukawa, K  Sakamoto, Y  Hakamata, H  Komohara, Y  Takeya, M  Sasaki, Y  Miyazaki, A  Horiuchi, S 
Citation: Hori M, etal., Arterioscler Thromb Vasc Biol. 2004 Sep;24(9):1689-95. Epub 2004 Jul 8.
RGD ID: 1581191
Pubmed: PMID:15242859   (View Abstract at PubMed)
DOI: DOI:10.1161/01.ATV.0000137976.88533.13   (Journal Full-text)

OBJECTIVE: Diabetes-induced dyslipidemia is seen in streptozotocin-induced diabetic rats. This is caused, in part, by elevated intestinal acyl-coenzyme A:cholesterol acyltransferase (ACAT) activity. Because two ACAT isozymes (ACAT-1 and ACAT-2) were identified, in the present study we determined which ACAT isozyme was involved in the elevated intestinal ACAT activity in diabetic rats. METHODS AND RESULTS: We cloned a full-length cDNA of rat ACAT-2. Its overexpression in ACAT-deficient AC29 cells demonstrated that the ACAT activity is derived from the cloned cDNA, and a 45-kDa protein of rat ACAT-2 cross-reacts with an anti-human ACAT-2 antibody. The tissue distribution of rat ACAT-2 mRNA revealed its restricted expression to liver and small intestine. Immunohistochemical analyses using an anti-human ACAT-2 antibody demonstrated that ACAT-2 is localized in villus-crypt axis of rat small intestine. The intestinal ACAT activity in diabetic rats was significantly immunodepleted by an anti-ACAT-2 antibody but not by an anti-ACAT-1 antibody. Finally, intestinal ACAT-2 in diabetic rats significantly increased at both protein and mRNA levels as compared with that in control rats. CONCLUSIONS: Our data demonstrate that ACAT-2 isozyme is responsible for the increased intestinal ACAT activity of diabetic rats, suggesting an important role of ACAT-2 for dyslipidemia in diabetic patients. Diabetic rats exhibit dyslipidemia caused, in part, by elevated intestinal acyl-coenzyme A:cholesterol acyltransferase (ACAT) activity. We determined which ACAT isozyme (ACAT-1 or ACAT-2) was involved in the elevated intestinal ACAT activity in diabetic rats. We demonstrated an important role of ACAT-2, implicating its involvement in dyslipidemia in diabetic patients.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Experimental Diabetes Mellitus  ISOSoat2 (Rattus norvegicus)1581191; 1581191 RGD 
Experimental Diabetes Mellitus  IDA 1581191 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Soat2  (sterol O-acyltransferase 2)

Genes (Mus musculus)
Soat2  (sterol O-acyltransferase 2)

Genes (Homo sapiens)
SOAT2  (sterol O-acyltransferase 2)


Additional Information