Intravenous lipid emulsions to deliver omega 3 fatty acids

Carpentier, Yvon; Hacquebard, Mirjam

doi:10.1016/j.plefa.2006.05.004

Cited by 33 publications

(22 citation statements)

References 27 publications

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“…NEFAs are produced de novo by adipocytes or lipolysis of plasma triacylglycerol in chylomicrons or very-low density lipoproteins, transported by serum albumin, and incorporated in adipocytes or muscle cells [36]. NEFAs are also abundant in both cerebral vasculature as well as in the CSF [37], [38], and in the brain, long-chain NEFAs (C12–C26) are abundant.…”

Section: Introductionmentioning

confidence: 99%

Non-Esterified Fatty Acids Generate Distinct Low-Molecular Weight Amyloid-β (Aβ42) Oligomers along Pathway Different from Fibril Formation

et al. 2011

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Amyloid-β (Aβ) peptide aggregation is known to play a central role in the etiology of Alzheimer’s disease (AD). Among various aggregates, low-molecular weight soluble oligomers of Aβ are increasingly believed to be the primary neurotoxic agents responsible for memory impairment. Anionic interfaces are known to influence the Aβ aggregation process significantly. Here, we report the effects of interfaces formed by medium-chain (C9–C12), saturated non-esterified fatty acids (NEFAs) on Aβ42 aggregation. NEFAs uniquely affected Aβ42 aggregation rates that depended on both the ratio of Aβ:NEFA as well the critical micelle concentration (CMC) of the NEFAs. More importantly, irrespective of the kind of NEFA used, we observed that two distinct oligomers, 12–18 mers and 4–5 mers were formed via different pathway of aggregation under specific experimental conditions: (i) 12–18 mers were generated near the CMC in which NEFAs augment the rate of Aβ42 aggregation towards fibril formation, and, (ii) 4–5 mers were formed above the CMC, where NEFAs inhibit fibril formation. The data indicated that both 12–18 mers and 4–5 mers are formed along an alternate pathway called ‘off-pathway’ that did not result in fibril formation and yet have subtle structural and morphological differences that distinguish their bulk molecular behavior. These observations, (i) reflect the possible mechanism of Aβ aggregation in physiological lipid-rich environments, and (ii) reiterate the fact that all oligomeric forms of Aβ need not be obligatory intermediates of the fibril formation pathway.

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Section: Introductionmentioning

confidence: 99%

Non-Esterified Fatty Acids Generate Distinct Low-Molecular Weight Amyloid-β (Aβ42) Oligomers along Pathway Different from Fibril Formation

et al. 2011

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“…cardiac arrhythmia following anesthesia and surgery (1). A first study conducted in normal volunteers indeed documented that the bolus intravenous injection of 50 ml of a novel 20% (w/v) medium-chain triglyceride:fish oil emulsion caused within 60 min a marked increase of the phospholipid weight percentage of ω3 fatty acids in both circulating leucocytes and platelets (2).…”

Section: Introductionmentioning

confidence: 99%

Rapid lipid enrichment in ω3 fatty acids: Plasma data

Carpentier¹,

Peltier²,

Portois³

et al. 2008

Int J Mol Med

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Abstract. The bolus intravenous injection of a novel mediumchain triglyceride:fish oil emulsion to normal subjects was recently reported to enrich within 60 min the phospholipid content of leucocytes and platelets in long-chain polyunsaturated ω3 fatty acids. The present study, conducted in second generation ω3-depleted rats, aimed at investigating whether such a procedure may also increase within 60 min the phospholipid content of ω3 fatty acids in cells located outwards the bloodstream, in this case liver cells, and whether this coincides with correction of the perturbation in the liver triglyceride fatty acid content and profile otherwise prevailing in these rats. This first report deals mainly with the fatty acid pattern of plasma lipids in male ω3-depleted rats that were non-injected or injected with either the ω3-rich emulsion or a control medium-chain triglyceride:olive oil emulsion. The results provide information on the fate of the exogenous lipids present in the lipid emulsions and injected intravenously 60 min before sacrifice. Moreover, in the uninjected ω3-depleted rats the comparison between individual plasma and liver measurements indicated positive correlations in the fatty acid profile of phospholipids and triglycerides.

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“…One potential mechanism for cardiac protection other than the ones already discussed is the bradycardic effect of DHA, which could lower myocardial oxygen consumption during ischemia. In addition, previous cellular studies suggest that n-3 PUFAs could suppress inflammation (7,33), reduce platelet aggregations (38), decrease resultant ischemic oxidative injury (13), and/or inhibit apoptotic signals (12). A recent study reported that, in rabbits, dietary-fed EPA reduced subsequent induced myocardial infarct sizes via the activation of Ca 2ϩ -activated K ϩ channels and nitric oxidemediated mechanisms (24).…”

Section: Discussionmentioning

confidence: 99%

Pericardial delivery of omega-3 fatty acid: a novel approach to reducing myocardial infarct sizes and arrhythmias

Xiao¹,

Sigg²,

Ujhelyi³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Basic and clinical evidence suggests that omega-3 (n-3) polyunsaturated fatty acids (PUFAs) decrease fatal arrhythmias and infarct sizes. This study investigated if pericardial delivery of n-3 PUFAs would protect the myocardium from ischemic damages and arrhythmias. Acute myocardial infarctions were induced in 23 pigs with either 45 min balloon inflations or clamp occlusions of the left anterior descending coronary arteries and 180 min reperfusion. Docosahexaenoic acid (C22:6n-3, DHA, 45 mg), one of the main n-3 PUFAs in fish oil, was infused within the pericardial space only during the 40-min stabilizing phase, 45 min ischemia and initial 5 min reperfusion. Hemodynamics and cardiac functions were very similar between the DHA-treated and control groups. However, DHA therapy significantly reduced infarct sizes from 56.8 +/- 4.9% for controls (n = 12) to 28.8 +/- 7.9% (P < 0.01) for DHA-treated animals (n = 11). Compared with controls, DHA-treated animals significantly decreased heart rates and reduced ventricular arrhythmia scores during ischemia. Furthermore, three (25%) control animals experienced eight episodes of ventricular fibrillation (VF), and two died subsequent to unsuccessful defibrillation. In contrast, only 1 (9%) of 11 DHA-treated pigs elicited one episode of VF that was successfully converted via defibrillation to normal rhythm; thus, mortality was reduced from 17% in the controls to 0% in the DHA-treated animals. These data demonstrate that pericardial infusion of n-3 PUFA DHA can significantly reduce both malignant arrhythmias and infarct sizes in a porcine infarct model. Pericardial administration of n-3 PUFAs could represent a novel approach to treating or preventing myocardial infarctions.

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Intravenous lipid emulsions to deliver omega 3 fatty acids

Cited by 33 publications

References 27 publications

Non-Esterified Fatty Acids Generate Distinct Low-Molecular Weight Amyloid-β (Aβ42) Oligomers along Pathway Different from Fibril Formation

Non-Esterified Fatty Acids Generate Distinct Low-Molecular Weight Amyloid-β (Aβ42) Oligomers along Pathway Different from Fibril Formation

Rapid lipid enrichment in ω3 fatty acids: Plasma data

Pericardial delivery of omega-3 fatty acid: a novel approach to reducing myocardial infarct sizes and arrhythmias

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