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Phosphatidate Phosphohydrolase Activity in the Liver
Published in David N. Brindley, John R. Sabine, Phosphatidate Phosphohydrolase, 2017
The administration of l-thyroxine to rats for 5 days increased the ability of liver homogenates to synthesize diacylglycerols and triacylglycerols from glycerol phosphate but without significantly increasing the activity of glycerol phosphate acyltransferase.73 These results indicate an increased activity of phosphatidate phosphohydrolase. This conclusion was later confirmed in rats that had been injected for 5 or 7 days with l-thyroxine when the phosphohydrolase activity was expressed per milligram of soluble protein8 or per gram wet weight,31 respectively. However, there was no significant increase in the phosphohydrolase activity when the results were expressed per total liver. The long-term treatment of rats of l-thyroxine also stimulated the synthesis of triacylglycerols as measured in vivo from intraportally injected [3H]-glycerol and [14C]-palmitate.8 This may be part of a general stimulation of metabolism. The increase in triacylglycerol synthesis was also accompanied by a decrease in the accumulation of 3H and 14C in diacylglycerol.8 This possibly indicates a stimulation in diacylglycerol acyltransferase activity as suggested from earlier work.74
Increasing the Sensitivity of Adipocytes and Skeletal Muscle Cells to Insulin
Published in Christophe Wiart, Medicinal Plants in Asia for Metabolic Syndrome, 2017
In adipocytes, absorbed fatty acids from very low density lipoproteins or chylomicrons are re-esterified to glycerol via a reaction involving glycerol-3-phosphate acyltransferase, 1-acylglycerol-3-phosphate acyl transferase, phosphatidate phosphohydrolase, and diacylglycerol acyltransferase-1.173 Diacylglycerol acyltransferase-1 in adipocytes catalyzes the acylation of 1,2-diacylglycerol into triglyceride which is a rate limiting step in triglyceride synthesis in adipose tissues.173 Aphadilactone A and aphadilactone C (Figure 4.8) isolated from the leaves of Aphanamixis grandifolia Bl. inhibited diacylglycerol acyltransferase-1 activity by 2 5.5% and 85.9% at 10 μM in vitro.174
Mesenteric physiology
Published in John Calvin Coffey, Rishabh Sehgal, Dara Walsh, Mesenteric Principles of Gastrointestinal Surgery, 2017
J. CALVIN COFFEY, RISHABH SEHGAL, AWAD M. JARRAR, MATTIAS SOOP
Abbreviations: DGAT, diacylglycerol acyltransferase; FAT/CD36, fatty acid transporter/cluster of differentiation 36; GHR, growth hormone receptor; HSL, hormone-sensitive lipase; NA, noradrenaline; OM, omental; SAT, subcutaneous adipose tissue; TR, thyroid receptor ; VS, visceral.
JianPi-QingHua formula attenuates nonalcoholic fatty liver disease by regulating the AMPK/SIRT1/NF-κB pathway in high-fat-diet-fed C57BL/6 mice
Published in Pharmaceutical Biology, 2023
Jing Tian, Mengjie Cai, Shenyi Jin, Qingguang Chen, Jiahui Xu, Qiuyue Guo, Zihui Yan, Xu Han, Hao Lu
The AMPK/SIRT1 pathway affected lipid metabolism through the following genes including lipogenesis, lipolysis and triglyceride synthesis. As presented in Figure 5(G), the expression of lipogenesis-related genes including Sterol Regulatory Element-Binding Protein (SREBP1) and fatty acid synthase (FASN) were remarkably elevated in HFD-fed mice (p < 0.05), and JPQH reduced the expression of SREBP1 and FASN (p < 0.05). In addition, JPQH lowered the mRNA level of adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) in the liver, which are lipolysis-related genes (Figure 5(H)). In the wake of JPQH administration, diacylglycerol acyltransferase (DGAT), the triglyceride synthesis, was downregulated (Figure 5(I)). The above experiments indicated that JPQH inhibited hepatic lipid accumulation by activating the AMPK/SIRT1 pathway.
Recent developments in pharmacotherapy for hypertriglyceridemia: what’s the current state of the art?
Published in Expert Opinion on Pharmacotherapy, 2020
Matilda Florentin, Michael S Kostapanos, Panagiotis Anagnostis, George Liamis
Acyl-coA: diacylglycerol acyltransferase (DGAT)-1 is an enzyme required for TG synthesis from absorbed dietary fat. In particular, it catalyzes the final step of TG biosynthesis and is abundant in enterocytes of the small intestine and adipose tissue [125]. Its inhibition has been suggested as an attractive target to reduce postprandial TG levels, especially in patients with FCS. Two molecules have been developed for this purpose, pradigastat (Novartis, Switzerland) and AZD7687 (AstraZeneca, UK). The latter compound has been associated with severe gastrointestinal adverse effects, which have suspended its use [126]. Early data emerged from DGAT-1 knockout mice, showing a reduction in postprandial hypertriglyceridemia, obesity and insulin resistance compared with the conventional type [127].
Obesity medications in development
Published in Expert Opinion on Investigational Drugs, 2020
Candida J. Rebello, Frank L. Greenway
Dietary triacylglycerol (TAG) is cleaved by lipases in the lumen of the gut to monoacylglycerol and free fatty acids which are taken up by the intestinal epithelial cells and re-esterified into TAG inside the epithelial cells. The TAG assembled in enterocytes is then incorporated into chylomicrons and enter the lymphatic system. Diacylglycerol acyltransferase 1 (DGAT1) plays a key role in the absorption of dietary fat as it catalyzes the final step in the biosynthesis of TAG [59] DGAT1 is most highly expressed in the small intestine and adipose tissue and the deletion of DGAT1 or inhibition of DGAT1 in rodents reduces body weight and adiposity, increases the secretion of GLP-1 and PYY, and slows gastric emptying [60–64]. Animal studies suggest that DGAT1 inhibition has therapeutic potential in the treatment of obesity.