Effect of endothelial cell denudation on fatty acid metabolism by rabbit aorta

1990 ◽  
Vol 259 (2) ◽  
pp. H442-H447
Author(s):  
I. Takasaki ◽  
R. A. Cohen ◽  
A. V. Chobanian ◽  
P. Brecher
Keyword(s):  
Arachidonic Acid ◽  
Fatty Acid ◽  
Endothelial Cell ◽  
Vascular Endothelial Cells ◽  
Rabbit Aorta ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Cotton Swab ◽  
Acid Esterification

The potential regulatory role of vascular endothelial cells in fatty acid uptake and metabolism by arterial tissue was studied in vitro using aortic segments from New Zealand White rabbits. Endothelium was left intact or was removed either by scraping with forceps or by rubbing with a cotton swab. Aortic segments were incubated with [14C]oleate or [14C]arachidonate, and oxidation and esterification were measured. Endothelial cell denudation by forceps or cotton swab caused a decrease in oxidation of both oleic and arachidonic acid. Esterification of oleic and arachidonic acid into phospholipid was also significantly reduced by removing the endothelium; the percent reduction was less when endothelium was removed by cotton swab than it was by forceps. Incorporation into phospholipid was reduced by cotton swab treatment, but incorporation into triglyceride was unaffected. Forceps treatment reduced oleic acid esterification into both triglyceride and phospholipid. The studies suggest that arterial endothelium has a role in fatty acid oxidation and esterification and that fatty acid utilization may be a useful metabolic index of vascular injury.

Theobromine ameliorates nonalcoholic fatty liver disease by regulating hepatic lipid metabolism via mTOR signaling pathway in vivo and in vitro

2020 ◽  
Author(s):  
Dan Wei ◽  
Shaofei Wu ◽  
Jie Liu ◽  
Xiaoqian Zhang ◽  
Xiaoling Guan ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Signaling Pathway ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Uptake ◽  
Mtor Signaling ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Mtor Signaling Pathway

Theobromine, a methylxanthine present in cocoa, has been shown to possess many beneficial pharmacological properties such as anti-oxidative stress, anti-inflammatory property, and anti-microbial activity. In this study, we investigated the effects of theobromine on NAFLD and the possible underlying mechanisms in vivo and in vitro. The results showed that theobromine reduced body weight, fat mass and improved dyslipidemia. Theobromine decreased liver weight, mitigated liver injury, and significantly reduced hepatic TG level in mice with obesity. Histological examinations also showed hepatic steatosis was alleviated after theobromine treatment. Furthermore, theobromine reversed the elevated mRNA and protein expression of SREBP-1c, FASN, CD36, FABP4 and the suppressed expression of PPARα, CPT1a in the liver of mice with obesity, which were responsible for lipogenesis, fatty acid uptake and fatty acid oxidation respectively. In vitro, theobromine also downregulated SREBP-1c, FASN, CD36, FABP4 and upregulated PPARα, CPT1a mRNA and protein levels in hepatocytes in a dose-dependent manner, while these changes were reversed by L-Leucine, an mTOR agonist. The present study demonstrated that theobromine improved NAFLD by inhibiting lipogenesis, fatty acid uptake and promoting fatty acid oxidation in the liver and hepatocytes, which might be associated with its suppression of mTOR signaling pathway.

Utilization of endogenous lipid, glycogen, and protein by rabbit aorta

1982 ◽  
Vol 243 (1) ◽  
pp. H128-H132 ◽  
Author(s):  
R. Odessey ◽  
K. V. Chace
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Specific Activity ◽  
Rabbit Aorta ◽  
Acid Oxidation ◽  
O2 Consumption ◽  
Endogenous Fatty Acid ◽  
Endogenous Lipid

The utilization of endogenous stores by rabbit aorta in vitro was measured. In substrate-free medium glycogen disappearance may account for less than 20% of the tissue O2 consumption during incubations of less than 2-3 h. At longer times (or in the presence of glucose) glycogen catabolism is negligible. Calculations from the rate of proteolysis suggest that oxidation of endogenously generated amino acids accounts for less than 7-10% of the oxygen consumption. Furthermore, the presence of amino-oxyacetate, a transaminase inhibitor, did not alter the ATP-ADP ratio. By contrast, measurements of the disappearance of tissue triglyceride indicate that endogenous lipid could meet the fuel requirements of the aorta. Direct measurement of intracellular fatty acid oxidation was obtained by measuring acyl carnitine specific activity and 14CO2 production from [1-14C]palmitate. Fatty acid oxidation could account for at least 90% of the total O2 consumption, and 83% of the fatty acids consumed were derived from endogenous tissue stores. Octanoate was found to inhibit both exogenous and endogenous fatty acid oxidation. These findings may indicate that shorter-chain fatty acids may be preferentially utilized by the aorta.

Abstract 107: Acetyl-coa Carboxylase 2 Prevents Cardiomyocyte Hypertrophy by Reducing Glucose Reliance

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Julia Ritterhoff ◽  
Dan Shao ◽  
Rong Tian
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Cardiac Hypertrophy ◽  
Cardiomyocyte Hypertrophy ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Acetyl Coa Carboxylase ◽  
Acetyl Coa ◽  
The Impact

In cardiac hypertrophy, the adult heart switches from mainly using fatty acids to increased reliance on glucose to maintain its energetic demands. Reducing fatty acid overload and further increasing glucose reliance has been suggested to be beneficial in the diseased state. Recently, however, it has been shown that increasing fatty acid oxidation (FAO) by cardiac-specific deletion of Acetyl-CoA Carboxylase 2 (ACC2) maintains cardiac energetics and prevents cardiac dysfunction as well as cardiomyocyte hypertrophy during chronic pressure overload. However, it remained unclear, how increased FAO specifically prevented cardiomyocyte hypertrophy. Thus, the goal of this study was to determine the impact of ACC2 deletion on cardiomyocyte hypertrophy in vitro . Adenoviral-mediated knock-down (KD) of ACC2 in adult rat ventricular cardiomyocytes (CMs) resulted in a 70% downregulation of ACC2 mRNA. In standard CM medium (medium M199, 5.5mM glucose) ACC2 KD resulted in a similar increase in CM growth after phenylephrine (PE) treatment as control CMs (+39±10% in control vs. 41±16% in ACC2 KD CMs). Supplementation of 0.4 mM mixed long-chain fatty acids (FA) and 0.1 mU/ml insulin had no effect on cardiomyocyte morphology or hypertrophic response after PE treatment (+42±6%). However, ACC2 KD effectively prevented CM hypertrophy after PE stimulation in the presence of FA/insulin (+9±6%). Whereas PE stimulation in control CMs increased glucose uptake (+28±8%) and reduced fatty acid uptake (-25±6%), both were normalized after ACC2 KD. Inhibiting FAO by etomoxir or increasing glucose utilization by dichloroacetate abolished the beneficial effects of ACC2 KD after PE stimulation. When cultured in glucose-free medium supplemented with FA, ACC2 KD was incapable of preventing cardiomyocyte hypertrophy. Together, these data indicate that increased FAO after ACC2 deletion prevents cardiomyocyte hypertrophy by reducing glucose reliance, suggesting that rather increasing than reducing FAO is beneficial in cardiac hypertrophy.

Altered endothelial cell-mediated arterial dilation in dogs with D. immitis infection

1987 ◽  
Vol 253 (5) ◽  
pp. H1325-H1329 ◽  
Author(s):  
L. Kaiser ◽  
J. F. Williams ◽  
E. A. Meade ◽  
H. V. Sparks
Keyword(s):  
Arachidonic Acid ◽  
Endothelial Cell ◽  
Vascular Reactivity ◽  
Vascular Endothelial Cells ◽  
Seasonal Pattern ◽  
Muscle Relaxation ◽  
Arachidonic Acid Metabolism ◽  
Smooth Muscle Relaxation

Vascular endothelial cells regulate arterial diameter in vivo and in vitro. Stimulation of endothelial cell muscarinic receptors by acetylcholine results in the production and release of a nonprostaglandin metabolite of arachidonic acid that causes vascular smooth muscle relaxation. We examined femoral artery endothelium-dependent vasodilator responses in normal dogs and dogs with heartworm (Dirofilaria immitis) infection. Endothelium-dependent vascular reactivity was attenuated in dogs with D. immitis infection studied in the spring but not in the fall. The dilator response was inversely related to the number of female worms but not related to the presence of circulating microfilariae. Indomethacin markedly depressed responses to acetylcholine in dogs with D. immitis but did not alter acetylcholine-induced dilation in normal dogs. These data suggest that D. immitis releases substances that alter distal arterial endothelial cell arachidonic acid metabolism. The seasonal pattern may reflect the onset of maximal reproductive activity in the spring and its decline as the vector season ends in the fall.

Effect of insulin on in vitro intestinal fatty acid esterification in the rat

1980 ◽  
Vol 238 (4) ◽  
pp. E364-E370
Author(s):  
Y. F. Shiau ◽  
P. G. Holtzapple
Keyword(s):  
Fatty Acid ◽  
Blood Glucose ◽  
Glucose Metabolism ◽  
Marked Decrease ◽  
Blood Glucose Concentration ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Acid Esterification ◽  
Fatty Acid Esterification

We have previously shown that glucose metabolism plays an important role in modifying intestinal fatty acid esterification. Because it is well known that glucose metabolism is under insulin regulation, we examined the effect of insulin on intestinal fatty acid esterification. Insulin pretreatment led to a marked decrease in in vitro intestinal fatty acid esterification, but this decrease was abolished by maintaining blood glucose above 80 mg/dl. Addition of insulin to the incubation medium failed to produce any effect on intestinal fatty acid esterification. The decreased fatty acid esterification on hypoglycemic rats was not associated with changes in fatty acid uptake or lipid esterifying enzyme activities. However, there was a significant increase in the production of volatile metabolites of fatty acid. We conclude that 1) insulin itself has no effect on intestinal fatty acid esterification, 2) the effects observed in this study are due to insulin-induced hypoglycemia, 3) hypoglycemia does not alter intestinal fatty acid uptake or intrinsic esterification activity, but leads to preferential oxidation rather than esterification of fatty acid by the small intestine, and 4) the critical blood glucose concentration needed to maintain normal esterification in the rat was approximately at 80 mg/dl.

In Vitro Incorporation and Metabolism of Icosapentaenoic and Docosahexaenoic Acids in Human Platelets - Effect on Aggregation

1986 ◽  
Vol 56 (01) ◽  
pp. 057-062 ◽  
Author(s):  
Martine Croset ◽  
M Lagarde
Keyword(s):  
Arachidonic Acid ◽  
Fatty Acid ◽  
Platelet Aggregation ◽  
Fatty Acid Distribution ◽  
Thromboxane A2 ◽  
Human Platelets ◽  
Aggregation Response ◽  
Docosahexaenoic Acids ◽  
Membrane Level

SummaryWashed human platelets were pre-loaded with icosapentaenoic acid (EPA), docosahexaenoic acid (DHA) or EPA + DHA and tested for their aggregation response in comparison with control platelets. In fatty acid-rich platelets, an inhibition of the aggregation could be observed when induced by thrombin, collagen or U-46619. The strongest inhibition was observed with DHA-rich platelets and it was reduced when DHA was incorporated in the presence of EPA.Study of fatty acid distribution in cell lipids after loading showed that around 90% of EPA or DHA taken up was acylated into phospholipids and a very small amount (less than 2%) remained in their free and hydroxylated forms. DHA was more efficiently acylated into phosphatidylethanolamine (PE) than into phosphatidylinositol (PI) in contrast to what observed with EPA, and both acids were preferentially incorporated into phosphatidylcholine (PC). EPA inhibited total incorporation of DHA and increased its relative acylation into PE at the expense of PC. In contrast, DHA did not affect the acylation of EPA. Upon stimulation with, thrombin, EPA was liberated from phospholipids and oxygenated (as judged by the formation of its monohydroxy derivative) whereas DHA was much less metabolized, although consistently transferred into PE.It is concluded that EPA and DHA might affect platelet aggregation via different mechanisms when pre-loaded in phospholipids. Whereas EPA is known to alter thromboxane A2 metabolism from endogenous arachidonic acid, by competing with it, DHA might act directly at the membrane level for inhibiting aggregation.

Isotope tracer measures of meal fatty acid metabolism: reproducibility and effects of the menstrual cycle

2005 ◽  
Vol 288 (3) ◽  
pp. E547-E555 ◽  
Author(s):  
Ana Paola Uranga ◽  
James Levine ◽  
Michael Jensen
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Menstrual Cycle ◽  
Dietary Fat ◽  
Fatty Acid Uptake ◽  
Upper Body ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Lower Body

Oxidation and adipose tissue uptake of dietary fat can be measured by adding fatty acid tracers to meals. These studies were conducted to measure between-study variability of these types of experiments and assess whether dietary fatty acids are handled differently in the follicular vs. luteal phase of the menstrual cycle. Healthy normal-weight men ( n = 12) and women ( n = 12) participated in these studies, which were block randomized to control for study order, isotope ([3H]triolein vs. [14C]triolein), and menstrual cycle. Energy expenditure (indirect calorimetry), meal fatty acid oxidation, and meal fatty acid uptake into upper body and lower body subcutaneous fat (biopsies) 24 h after the experimental meal were measured. A greater portion of meal fatty acids was stored in upper body subcutaneous adipose tissue (24 ± 2 vs. 16 ± 2%, P < 0.005) and lower body fat (12 ± 1 vs. 7 ± 1%, P < 0.005) in women than in men. Meal fatty acid oxidation (3H2O generation) was greater in men than in women (52 ± 3 vs. 45 ± 2%, P = 0.04). Leg adipose tissue uptake of meal fatty acids was 15 ± 2% in the follicular phase of the menstrual cycle and 10 ± 1% in the luteal phase ( P = NS). Variance in meal fatty acid uptake was somewhat ( P = NS) greater in women than in men, although menstrual cycle factors did not contribute significantly. We conclude that leg uptake of dietary fat is slightly more variable in women than in men, but that there are no major effects of menstrual cycle on meal fatty acid disposal.

scholarly journals Interleukin-6 Increases Insulin-Stimulated Glucose Disposal in Humans and Glucose Uptake and Fatty Acid Oxidation In Vitro via AMP-Activated Protein Kinase

Diabetes ◽  
2006 ◽  
Vol 55 (10) ◽  
pp. 2688-2697 ◽  
Author(s):  
A. L. Carey ◽  
G. R. Steinberg ◽  
S. L. Macaulay ◽  
W. G. Thomas ◽  
A. G. Holmes ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Protein Kinase ◽  
Glucose Uptake ◽  
Fatty Acid Oxidation ◽  
Interleukin 6 ◽  
Glucose Disposal ◽  
Acid Oxidation ◽  
Amp Activated Protein Kinase

scholarly journals Critical Role for Hepatocyte-Specific eNOS in NAFLD and NASH

2021 ◽  
Author(s):  
Rory P. Cunningham ◽  
Mary P. Moore ◽  
Ryan J. Daskek ◽  
Grace M. Meers ◽  
Takamune Takahashi ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Critical Role ◽  
Acid Oxidation ◽  
Mitochondrial Fatty Acid Oxidation ◽  
Nonalcoholic Fatty Liver ◽  
Mitochondrial Fatty Acid ◽  
Endothelial Nitric Oxide

Regulation of endothelial nitric oxide synthase (eNOS) in hepatocytes may be an important target in nonalcoholic fatty liver disease (NAFLD) development and progression to steatohepatitis (NASH). In this study, we show genetic deletion and viral knockdown of hepatocyte-specific eNOS exacerbated hepatic steatosis and inflammation, decreased hepatic mitochondrial fatty acid oxidation and respiration, increased mitochondrial H<sub>2</sub>O<sub>2</sub> emission, and impaired the hepatic mitophagic (BNIP3 and LC3II) response. Conversely, overexpressing eNOS in hepatocytes in vitro and in vivo increased hepatocyte mitochondrial respiration and attenuated western diet induced NASH. Moreover, patients with elevated NAFLD activity score (histology score of worsening steatosis, hepatocyte ballooning, and inflammation) exhibited reduced hepatic eNOS expression which correlated with reduced hepatic mitochondrial fatty acid oxidation and lower hepatic protein expression of mitophagy protein BNIP3. The current study reveals an important molecular role for hepatocyte-specific eNOS as a key regulator of NAFLD/NASH susceptibility and mitochondrial quality control with direct clinical correlation to patients with NASH.

scholarly journals Pomegranate vinegar feeding enhances fatty acid oxidation: In vitro and in vivo

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
YEOJIN PARK ◽  
Elly Ok ◽  
Hyo Jung Lee ◽  
Ji Yeon Kim ◽  
Mi Kyung Kim ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation
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