scholarly journals Altered Lipid Metabolism in Brain Injury and Disorders

2008 ◽  
pp. 241-268 ◽  
Author(s):  
Rao Muralikrishna Adibhatla ◽  
J. F. Hatcher
Keyword(s):  
Lipid Metabolism ◽  
Brain Injury ◽  
Altered Lipid Metabolism ◽  
Altered Lipid

scholarly journals Traumatic Brain Injury Impairs Systemic Vascular Function Through Altered Lipid Metabolism and Disruption of Inward-Rectifier Potassium (Kir2.1) Channels

2021 ◽  
Author(s):  
Adrian M. Sackheim ◽  
Nuria Villalba ◽  
Maria Sancho ◽  
Osama F. Harraz ◽  
Adrian D. Bonev ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Smooth Muscle ◽  
Lipid Metabolism ◽  
Brain Injury ◽  
Smooth Muscle Cells ◽  
Inward Rectifier ◽  
Channel Function ◽  
Altered Lipid Metabolism ◽  
Altered Lipid ◽  
Kir2.1 Channel

AbstractBACKGROUND AND PURPOSETrauma can lead to widespread vascular endothelial dysfunction, but the underlying mechanisms remain largely unknown. Strong inward-rectifier potassium channels (Kir2.1) play a critical role in the dynamic regulation of regional perfusion and blood flow. Kir2.1 channel activity is modulated by phosphatidylinositol 4,5-bisphosphate (PIP2), a minor membrane phospholipid that is degraded by phospholipase A2 (PLA2) in conditions of oxidative stress or severe inflammation. We hypothesized that PLA2–induced depletion of PIP2 impairs Kir2.1 channel function.METHODSA fluid percussion injury model of traumatic brain injury (TBI) in rats was used to study mesenteric resistance arteries 24 hours after injury. Patch-clamp electrophysiology in freshly isolated endothelial and smooth muscle cells was performed to monitor Kir2.1 conductance, and the functional responses of intact arteries were assessed using pressure myography. We analyzed circulating PLA2, hydrogen peroxide (H2O2), and metabolites to identify alterations in signaling pathways associated with PIP2 in TBI.RESULTSElectrophysiology analysis of endothelial and smooth muscle cells revealed a significant reduction of Ba2+-sensitive Kir2.1 currents after TBI. Additionally, dilations to elevated extracellular potassium and BaCl2- or ML 133-induced constrictions in pressurized arteries were significantly decreased following TBI, consistent with an impairment of Kir2.1 channel function. The addition of a PIP2 analog to the patch pipette successfully rescued endothelial Kir2.1 currents after TBI. Both H2O2 and PLA2 activity were increased after injury. Metabolomics analysis demonstrated altered lipid metabolism signaling pathways, including increased arachidonic acid, and fatty acid mobilization after TBI.CONCLUSIONSOur findings support a model in which increased H2O2-induced PLA2 activity after trauma hydrolyzes endothelial PIP2, resulting in impaired Kir2.1 channel function.

Integrated Metabolomics and Transcriptomics Analyses Reveal Altered Lipid Metabolism in Mouse Placentas Exposed to Alcohol

Placenta ◽  
2021 ◽  
Vol 112 ◽  
pp. e33
Author(s):  
Sze Ting (Cecilia) Kwan ◽  
Manjot Virdee ◽  
Nipun Saini ◽  
Kaylee Helfrich ◽  
Susan Smith
Keyword(s):  
Lipid Metabolism ◽  
Altered Lipid Metabolism ◽  
Altered Lipid ◽  
Integrated Metabolomics

The Decline of the Immune Response during Aging: the Role of an Altered Lipid Metabolism

1991 ◽  
Vol 621 (1 Physiological) ◽  
pp. 277-290 ◽  
Author(s):  
GEORG WICK ◽  
LUKAS A. HUBER ◽  
XU QING-BO ◽  
ELMAR JAROSCH ◽  
DIETHER SCHÖNITZER ◽  
...  
Keyword(s):  
Immune Response ◽  
Lipid Metabolism ◽  
Altered Lipid Metabolism ◽  
Altered Lipid

Low carnitine intake and altered lipid metabolism in infants

1989 ◽  
Vol 49 (4) ◽  
pp. 624-628 ◽  
Author(s):  
A L Olson ◽  
S E Nelson ◽  
C J Rebouche
Keyword(s):  
Lipid Metabolism ◽  
Altered Lipid Metabolism ◽  
Altered Lipid

scholarly journals Lysophosphatidylcholine acyltransferase 1 is downregulated by hepatitis C virus: impact on production of lipo-viro-particles

Gut ◽  
2016 ◽  
Vol 66 (12) ◽  
pp. 2160-2169 ◽  
Author(s):  
Frauke Beilstein ◽  
Matthieu Lemasson ◽  
Véronique Pène ◽  
Dominique Rainteau ◽  
Sylvie Demignot ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Hepatic Steatosis ◽  
Liver Lipid ◽  
Very Low Density Lipoproteins ◽  
Viral Particles ◽  
Triacylglycerol Content ◽  
Liver Lipid Metabolism ◽  
Infectious Cycle ◽  
Altered Lipid Metabolism ◽  
Altered Lipid

ObjectiveHCV is intimately linked with the liver lipid metabolism, devoted to the efflux of triacylglycerols stored in lipid droplets (LDs) in the form of triacylglycerol-rich very-low-density lipoproteins (VLDLs): (i) the most infectious HCV particles are those of lowest density due to association with triacylglycerol-rich lipoproteins and (ii) HCV-infected patients frequently develop hepatic steatosis (increased triacylglycerol storage). The recent identification of lysophosphatidylcholine acyltransferase 1 (LPCAT1) as an LD phospholipid-remodelling enzyme prompted us to investigate its role in liver lipid metabolism and HCV infectious cycle.DesignHuh-7.5.1 cells and primary human hepatocytes (PHHs) were infected with JFH1-HCV. LPCAT1 depletion was achieved by RNA interference. Cells were monitored for LPCAT1 expression, lipid metabolism and HCV production and infectivity. The density of viral particles was assessed by isopycnic ultracentrifugation.ResultsUpon HCV infection, both Huh-7.5.1 cells and PHH had decreased levels of LPCAT1 transcript and protein, consistent with transcriptional downregulation. LPCAT1 depletion in either naive or infected Huh-7.5.1 cells resulted in altered lipid metabolism characterised by LD remodelling, increased triacylglycerol storage and increased secretion of VLDL. In infected Huh-7.5.1 cells or PHH, LPCAT1 depletion increased production of the viral particles of lowest density and highest infectivity.ConclusionsWe have identified LPCAT1 as a modulator of liver lipid metabolism downregulated by HCV, which appears as a viral strategy to increase the triacylglycerol content and hence infectivity of viral particles. Targeting this metabolic pathway may represent an attractive therapeutic approach to reduce both the viral titre and hepatic steatosis.

Metabolomics Reveals Altered Lipid Metabolism in a Mouse Model of Endometriosis

2016 ◽  
Vol 15 (8) ◽  
pp. 2626-2633 ◽  
Author(s):  
Mainak Dutta ◽  
Mallappa Anitha ◽  
Philip B. Smith ◽  
Christopher R. Chiaro ◽  
Meenu Maan ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Mouse Model ◽  
Altered Lipid Metabolism ◽  
Altered Lipid

scholarly journals Nootkatone, a Dietary Fragrant Bioactive Compound, Attenuates Dyslipidemia and Intramyocardial Lipid Accumulation and Favorably Alters Lipid Metabolism in a Rat Model of Myocardial Injury: An In Vivo and In Vitro Study

Molecules ◽  
2020 ◽  
Vol 25 (23) ◽  
pp. 5656
Author(s):  
M.F. Nagoor Meeran ◽  
Sheikh Azimullah ◽  
M Marzouq Al Ahbabi ◽  
Niraj Kumar Jha ◽  
Vinoth-Kumar Lakshmanan ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Rat Model ◽  
Lipid Accumulation ◽  
Heart Diseases ◽  
Radical Scavenging ◽  
Enzymatic Antioxidants ◽  
Protective Effects ◽  
Altered Lipid Metabolism ◽  
Altered Lipid

In the present study, we assessed whether nootkatone (NKT), a sesquiterpene in edible plants, can provide protection against dyslipidemia, intramyocardial lipid accumulation, and altered lipid metabolism in a rat model of myocardial infarction (MI) induced by subcutaneous injections of isoproterenol (ISO, 85 mg/kg) on days 9 and 10. The rats were pre- and co-treated with NKT (10 mg/kg, p.o.) administered daily for 11 days. A significant reduction in the activities of myocardial creatine kinase and lactate dehydrogenase, as well as non-enzymatic antioxidants, and alterations in lipids and lipoproteins, along with a rise in plasma lipid peroxidation and intramyocardial lipid accumulation, were observed in ISO-treated rats. ISO administration induced alterations in the activities of enzymes/expressions that played a significant role in altering lipid metabolism. However, NKT treatment favorably modulated all biochemical and molecular parameters altered by ISO and showed protective effects against oxidative stress, dyslipidemia, and altered lipid metabolism, attributed to its free-radical-scavenging and antihyperlipidemic activities in rats with ISO-induced MI. Additionally, NKT decreased the accumulation of lipids in the myocardium as evidenced from Oil red O staining. Furthermore, the in vitro observations demonstrate the potent antioxidant property of NKT. The present study findings are suggestive of the protective effects of NKT on dyslipidemia and the underlying mechanisms. Based on our findings, it can be suggested that NKT or plants rich in NKT can be promising for use as a phytopharmaceutical or nutraceutical in protecting the heart and correcting lipid abnormalities and dyslipidemia, which are risk factors for ischemic heart diseases.

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