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Literature summary for 2.3.1.20 extracted from

  • Roe, N.D.; Handzlik, M.K.; Li, T.; Tian, R.
    The role of diacylglycerol acyltransferase (DGAT) 1 and 2 in cardiac metabolism and function (2018), Sci. Rep., 8, 4983 .
    View publication on PubMedView publication on EuropePMC
Search for more literature for 2.3.1.20

Protein Variants

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

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/ Products (Substrates)

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

Organism UniProt Comment Textmining
Mus musculus Q9DCV3
-
-
Mus musculus Q9Z2A7
-
-

Source Tissue

Source Tissue Comment Organism Textmining
heart greater abundance of isozyme DGAT2 mRNA in the heart compared to isozyme DGAT1 Mus musculus
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
acyl-CoA + 1,2-diacyl-sn-glycerol
-
 Mus musculus CoA + 1,2,3-triacylglycerol
-
 ?

Synonyms

Synonyms Comment Organism
DGAT 1
-
 Mus musculus
DGAT 2
-
 Mus musculus
diacylglycerol acyltransferase 1
-
 Mus musculus
diacylglycerol acyltransferase 2
-
 Mus musculus

General Information

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