Explore chapters and articles related to this topic
Modulation of Lipid Biosynthesis by Stress in Diatoms
Published in Gokare A. Ravishankar, Ranga Rao Ambati, Handbook of Algal Technologies and Phytochemicals, 2019
Bing Huang, Virginie Mimouni, Annick Morant-Manceau, Justine Marchand, Lionel Ulmann, Benoit Schoefs
As in most eukaryotes, diatoms produce TAGs mainly via the acyl-CoA dependent Kennedy pathway (Mühlroth et al., 2013). This pathway begins with the acylation of G3P by acyl-CoA:glycerol-3-phosphate acyl transferase (GPAT), resulting in the formation of lysophosphatidic acid (LPA), which may be further acylated to produce phosphatidic acid (PA) by the acyl-CoA dependent acyl-CoA:LPA acyltransferase (LPAAT) enzyme (also called acyl-glycerol-3-phosphate acyltransferase [AGPAT]) (Balamurugan et al., 2017). PA may be dephosphorylated by phosphatidic acid phosphatase (PAP) to produce DAG, which in turn, by incorporating the third acyl-CoA thanks to DGAT, will form TAG (Zulu et al., 2018). Different bioengineering studies were performed on diatoms to understand the regulation power of these enzymes on the synthesis of lipids. The strategy to overproduce enzymes involved in TAG assembly is called the “pull strategy.”
Emerging ergogenic aids for strength/power development
Published in Jay R Hoffman, Dietary Supplementation in Sport and Exercise, 2019
PA is a biosynthetic precursor to membrane glycerophospholipids and triacylglycerol. It can be synthesized via three major ways: 1) most commonly via de novo synthesis originating from glycerol-3-phosphate (a molecule formed during glycolysis). Two acylation reactions take place via the enzymes glycerol-3-phosphate acyltransferase and lysophosphatidic acid acyltransferase to form PA; 2) hydrolysis of phosphatidylcholine – the enzyme phospholipase D catalyzes the cleavage of the phosphodiester bond forming PA and choline; and 3) phosphorylation of diacylglycerol (DAG) by DAG kinase – DAG may be generated from triacylglycerol (from stored fat) or from the phospholipid phosphatidylinositol (6).
Phosphonic Acids And Phosphonates As Antimetabolites
Published in Richard L. Hilderbrand, The Role of Phosphonates in Living Systems, 2018
In vitro enzymatic studies with (21) indicate a number of interesting points. While (21) serves as a substrate for CDP-diglyceride:sn-glycerol-3-phosphate phosphatidyltransferase and is an inhibitor of the anaerobic sn-glycerol-3-phosphate:NAD(P) oxidoreductase of E. coli,6,123 it does not appear to interact with the catabolic membrane-bound sn-glycerol-3-phosphate dehydrogenase, CDP-diglyceride:L-serine phosphatidyltransferase, or acyl coenzyme A:sn-glycerol-3-phosphate acyltransferase.123 The lack of interaction in these latter systems is attributed to the loss of binding capability resulting from the substitution of a methylene group for the esteratic oxygen of the natural substrate (vide supra).
Women with Subclinical Hypothyroidism are at Higher Prevalence of Metabolic Syndrome and Its Components Compared to Men in an Older Chinese Population
Published in Endocrine Research, 2021
Ling Deng, Lin Wang, Xiaoxia Zheng, Ping Shuai, Yuping Liu
Glycerol-3-phosphate-acyltransferase 3 (GPAT3) is a rate-limiting enzyme for the synthesis of TG. TSH can directly induce the activity of GPAT3 and thereby promote the synthesis of TG in differentiated 3T3-L1 adipocytes. Mice with SCH had a 35% increase in white fat mass compared to wild-type mice.34 Adipose triglyceride lipase (ATGL) is a rate-limiting enzyme that controls TG lipolysis. TSH has an inhibitory effect on ATGL expression in mature fat cells. The expression of ATGL in epididymal adipose tissue of Tshr-/- mice was significantly higher than that of Tshr+/+ mice.35 TSH can contribute to obesity by increasing the accumulation of TG through the above two pathways. Studies have indicated that MetS is a metabolic abnormality on the basis of obesity. Therefore, it is reasonable to assume that obesity may be an intermediate factor linking thyroid dysfunction and MetS.
Aberrant lipid metabolism as a therapeutic target in liver cancer
Published in Expert Opinion on Therapeutic Targets, 2019
Evans D. Pope, Erinmarie O. Kimbrough, Lalitha Padmanabha Vemireddy, Phani Keerthi Surapaneni, John A. Copland, Kabir Mody
AMPK is a multifaceted player in cellular metabolic functions, in part via its central role in lipid metabolism in its actions controlling the concentration of circulating FFAs by activating FAO, and by inhibiting lipolysis and lipogenesis. Within FA metabolism, AMPK inhibits de novo synthesis of FAs, cholesterol, and triglycerides (TG), encourages FA uptake, and activates FAO [104] (Figure 2). AMPK exerts an inhibitory effect upon FA synthesis via induction of the inhibitory phosphorylation of two critical players in this process: ACC and sterol regulatory element-binding protein 1 (SREBP1c) [105,106]. Additionally, AMPK inhibits cholesterol synthesis by inducing inhibitory phosphorylation of HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis [107]. Its impact upon TG synthesis is accomplished by AMPK’s inhibitory action upon glycerol-3-phosphate acyltransferase, the enzyme catalyzing the first committed step of TG synthesis [108]. AMPK increases FA uptake by controlling, via unclear mechanisms, the translocation of transporter CD36 to the plasma membrane. Once inside, FAs are transported to the mitochondria for beta-oxidation by carnityl palmitoyltransferase-1 (CPT-1). AMPK increases FAO by increasing CPT-1 activity by inducing the inhibitory phosphorylation of ACC2. ACC2 is an enzyme which lies adjacent to CPT-1 in the outer membrane of the mitochondria where it inhibits production of malonyl-CoA, a very potent allosteric inhibitor of CPT-1 [104,106].
Design of artificial cells: artificial biochemical systems, their thermodynamics and kinetics properties
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Adamu Yunusa Ugya, Lin Pohan, Qifeng Wang, Kamel Meguellati
A bottom-up approach is to build a stack of non-biotic components which are assembled to create de novo an artificial cell with a phospholipid bilayer and self-replicating DNA via a genetic program [18]. Typically, the approach involves three basic elements, which include information-carrying molecules (DNA or RNA), metabolic systems, and cell membranes. Two membrane proteins, sn-glycerol-3-phosphate acyltransferase (GPAT) and lyo-phosphatidic acid transferase (LPAAT), are produced by protein synthesis using recombinant element systems (PURE) enclosed in liposomes [23].