Protein Variants | Comment | Organism |
---|---|---|
additional information | generation of cardiac-specific constitutive and inducible DGAT1 KO mouse models (cKO and iKO, respectively). Both models show reduced DGAT1 mRNA and protein with no effects on DGAT2 mRNA expression or cardiac triglyceride (TG) content, no differences between genotypes for cardiac lipid droplet number and morphology. Cardiac TG synthesis is modestly reduced with loss of DGAT1, increased oxidation of exogenous fatty acids occurs in DGAT1 iKO hearts, DGAT1 iKO hearts respond normally to high fat diet | Mus musculus |
Inhibitors | Comment | Organism | Structure |
---|---|---|---|
additional information | DGAT2 inhibitor alone has very modest effect but inhibition of both isoforms substantially reduced 13C fatty acid incorporation into triglyceride (TG) pool in the heart. Coinhibition of DGAT1/2 in the heart abrogates TG turnover and protects the heart against high fat diet-induced lipid accumulation with no adverse effects on basal or dobutamine-stimulated cardiac function. A DGAT2 inhibitor does not further change substrate oxidation in DGAT1 iKO mice | Mus musculus |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
acyl-CoA + 1,2-diacyl-sn-glycerol | Mus musculus | - |
CoA + 1,2,3-triacylglycerol | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | Q9DCV3 | - |
- |
Mus musculus | Q9Z2A7 | - |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
heart | greater abundance of isozyme DGAT2 mRNA in the heart compared to isozyme DGAT1 | Mus musculus | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
acyl-CoA + 1,2-diacyl-sn-glycerol | - |
Mus musculus | CoA + 1,2,3-triacylglycerol | - |
? |
Synonyms | Comment | Organism |
---|---|---|
DGAT 1 | - |
Mus musculus |
DGAT 2 | - |
Mus musculus |
diacylglycerol acyltransferase 1 | - |
Mus musculus |
diacylglycerol acyltransferase 2 | - |
Mus musculus |
General Information | Comment | Organism |
---|---|---|
malfunction | inactivation of DGAT1 or DGAT2 in adult mouse heart results in a moderate suppression of triglyceride (TG) synthesis and turnover. Partial inhibition of DGAT activity increases cardiac fatty acid oxidation without affecting PPARalpha signaling, myocardial energetics or contractile function. Coinhibition of DGAT1/2 in the heart abrogates TG turnover and protects the heart against high fat diet-induced lipid accumulation with no adverse effects on basal or dobutamine-stimulated cardiac function | Mus musculus |
malfunction | inactivation of DGAT1 or DGAT2 in adult mouse heart results in a moderate suppression of triglyceride (TG) synthesis and turnover. Partial inhibition of DGAT activity increases cardiac fatty acid oxidation without affecting PPARalpha signaling, myocardial energetics or contractile function. Coinhibition of DGAT1/2 in the heart abrogates TG turnover and protects the heart against high fat diet-induced lipid accumulation with no adverse effects on basal or dobutamine-stimulated cardiac function. Triglyceride storage is unaffected in DGAT1 inducible knockout (iKO) mice | Mus musculus |
metabolism | the last step in triglyceride (TG) synthesis is catalyzed by diacylglycerol:acyltransferase (DGAT) which esterifies the diacylglycerol with a fatty acid | Mus musculus |
physiological function | role of diacylglycerol acyltransferase (DGAT) 1 and 2 in cardiac metabolism and function | Mus musculus |
physiological function | role of diacylglycerol acyltransferase (DGAT) 1 and 2 in cardiac metabolism and function. The two DGAT isoforms in the heart have partially redundant function | Mus musculus |