RGD Reference Report - Obesity resistance and multiple mechanisms of triglyceride synthesis in mice lacking Dgat. - Rat Genome Database

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Obesity resistance and multiple mechanisms of triglyceride synthesis in mice lacking Dgat.

Authors: Smith, SJ  Cases, S  Jensen, DR  Chen, HC  Sande, E  Tow, B  Sanan, DA  Raber, J  Eckel, RH  Farese RV, JR 
Citation: Smith SJ, etal., Nat Genet 2000 May;25(1):87-90.
RGD ID: 734536
Pubmed: PMID:10802663   (View Abstract at PubMed)
DOI: DOI:10.1038/75651   (Journal Full-text)

Triglycerides (or triacylglycerols) represent the major form of stored energy in eukaryotes. Triglyceride synthesis has been assumed to occur primarily through acyl CoA:diacylglycerol transferase (Dgat), a microsomal enzyme that catalyses the final and only committed step in the glycerol phosphate pathway. Therefore, Dgat has been considered necessary for adipose tissue formation and essential for survival. Here we show that Dgat-deficient (Dgat-/-) mice are viable and can still synthesize triglycerides. Moreover, these mice are lean and resistant to diet-induced obesity. The obesity resistance involves increased energy expenditure and increased activity. Dgat deficiency also alters triglyceride metabolism in other tissues, including the mammary gland, where lactation is defective in Dgat-/- females. Our findings indicate that multiple mechanisms exist for triglyceride synthesis and suggest that the selective inhibition of Dgat-mediated triglyceride synthesis may be useful for treating obesity.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
obesity  ISODgat1 (Mus musculus)734536; 734536 RGD 
obesity  IMP 734536 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Dgat1  (diacylglycerol O-acyltransferase 1)

Genes (Mus musculus)
Dgat1  (diacylglycerol O-acyltransferase 1)

Genes (Homo sapiens)
DGAT1  (diacylglycerol O-acyltransferase 1)


Additional Information