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Endotoxic Shock and the Sphingomyelin Pathway
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
Cecil K. Joseph, Richard N. Kolesnick
A comparison of the structures of lipid A and cer-amide is shown in Figure 1. Carbons 1–3 of the reducing glucosamine of lipid A closely resemble Carbons 1–3 of ceramide (Fig. 1, boxed). This region is conserved in all biologically active LPS and ceramide analogs, and nearly all other portions of the molecules can be deleted or altered without destroying bioactivity. Experiments using molecular modeling and conformational dynamics to generate energy minimized structures of the reducing glucosamine of lipid A (GlcN-1, dephosphorylated form) and ceramide showed that positions C-l, C-2, and C-3 and their functional groups were nearly superimposible. A similar result was obtained when the 1-phosphylated forms of each lipid were compared. In contrast, molecular modeling of 1,2-diacylglycerol generated showed far less similarity.
Alpha Adrenergic Modulation of Impulse Initiation in Normal and Ischemic Cardiac Fibers
Published in Samuel Sideman, Rafael Beyar, Analysis and Simulation of the Cardiac System — Ischemia, 2020
We have done a series of experiments to tackle the phosphatidylinositol question, initially by using phospholipase C as a means to activate both IP3 and diacylglycerol. The major shortcoming of these experiments is that we applied phospholipase C extracellularly, so there are a lot of questions about what it is inducing; that is, is it doing precisely the same thing as would occur if it were acting within the membrane? At any rate, with phospholipase C, we saw the following: an increase in automaticity, blocked by ryanodine, but not by verapamil, suggesting that it is related to some event involving SR-calcium release rather than transsarcolemmal calcium flux. To consider diacylglycerol, we used an activated phorbol ester. This induced no change in automaticity, whatever.
Lifestyle Medicine and the Management of Prediabetes
Published in James M. Rippe, Lifestyle Medicine, 2019
Karla I. Galaviz, Lisa Staimez, Lawrence S. Phillips, Mary Beth Weber
Insulin resistance is increased via two mechanisms: (i) nonphysiological deposition of fat in visceral, hepatic, and intramyocellular sites, and (ii) intracellular sequestration of GLUT-4 glucose transporters in unexercised muscle, resulting in reduced glucose uptake.18 Free fatty acids, produced more readily in visceral abdominal fat, decrease insulin sensitivity, impair vascular reactivity, and also increase endothelial dysfunction. “Toxic messages” from the adipose organ, such as free fatty acids, altered cytokines (e.g., an increase in tumor necrosis factor-alpha and a decrease in adiponectin), and oxidative stress impair insulin action to restrain glucose production in the liver and promote glucose disposal in muscle.49 Increases in intracellular diacylglycerol (DAG) have been recently identified as an important mechanism of free fatty acid-induced insulin resistance in muscle and liver,50,51 disproving the “Randle hypothesis” of action via inhibition of pyruvate dehydrogenase.52,53 Polycystic ovary syndrome (PCOS) has also been linked to insulin resistance in women of reproductive age. Between 65%–70% of women with PCOS have insulin resistance,54 and they have been found to be more insulin resistant than age- and BMI-matched women without PCOS.55 Though the exact mechanism remains unclear, one theory suggests this is related to a post-insulin receptor defect that affects signal transduction, resulting in an increase in ovarian and adrenal androgens.54
Lipidomics biomarkers in women with polycystic ovary syndrome (PCOS) using ultra-high performance liquid chromatography–quadrupole time of flight electrospray in a positive ionization mode mass spectrometry
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2019
Camelia Larisa Vonica, Ioana Rada Ilie, Carmen Socaciu, Corina Moraru, Bogdan Georgescu, Anca Farcaş, Gabriela Roman, Andrada Alina Mureşan, Carmen Emanuela Georgescu
Using the sparse PLS-DA model, potential biomarkers (metabolites) were selected (Figure 1), ranked by the absolute values of their loadings. Significantly increased levels of triacylglycerol (TG) (18:2/18:2/0-18:0) (p = .012) in addition to cholestane-3beta, 5alpha, 6beta-triol (18:0/0:0) and cholestane-5alpha (18:1/0:0), which are members of sterol lipids class were encountered in PCOS and appeared as valuable variables to differentiate subjects with PCOS from controls in the model. Furthermore, univariate analysis derived from untargeted metabolomics showed an increasing trend (p < .1) for a series of diacylglycerol (DG) species (i.e. 18:1/20:0/0:0, 18:0/0:0/20:1, 22:4n6/0:0/18:4n3, 18:3/0:0/22:5, 20:0/0:0/20:0, 20:0/0:0/20:0, 18:1/24:0/0:0, 18:0/0:0/24:1), while DG (22:2/0:0/22:4) exhibited a decreasing trend in the PCOS group.
Biomarkers in diabetic neuropathy
Published in Archives of Physiology and Biochemistry, 2023
Kaveri M. Adki, Yogesh A. Kulkarni
Hyperglycaemia leads to the generation of diacylglycerol (DAG). DAG stimulates protein kinase C (PKC), which plays a vital role in the regulation of protein activation via serine and threonine that are important for cell homeostasis (Vincent et al. 2004). The excess PKC activates mitogen-activated protein kinase (MAPK). The MAPK generates transcription machinery of the nerve cells via phosphorylation of stress genes C-Jun kinases (JNK) and heat shock proteins (HSP). This leads to abnormal vascular signalling resulting in damage to nerve cells and nerve cells apoptosis (Tomlinson et al. 1992).
Advances in oxidative stress in pathogenesis of diabetic kidney disease and efficacy of TCM intervention
Published in Renal Failure, 2023
Xiaoju Ma, Jingru Ma, Tian Leng, Zhongzhu Yuan, Tingting Hu, Qiuyan Liu, Tao Shen
The protein kinase (PKC) pathway is critical in the oxidative stress-induced DKD occurrence and development. Under normal circumstances, the PKC in renal tissue is in an inactivated state. While upon hyperglycemia, it will be activated given the significant increase in intracellular diacylglycerol content [16]. Additionally, PKC can also be activated indirectly via AGE/RAGE and polyol pathways [17]. Activated PKC enhances NADPH oxidase activity and promotes the endothelial and mesangial cells to produce ROS, resulting in damage to renal tissue cells from oxidative stress [18].