Effects of ethanol on lipids and atherosclerosis

Hannuksela, Minna L.; Rämet, Maria E.; Nissinen, A; Liisanantti, Marja K.; Savolainen, Markku J.

doi:10.1016/j.pathophys.2003.10.009

Cited by 62 publications

(32 citation statements)

References 92 publications

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“…However, others have demonstrated that activation of PKA by cAMP-elevating agents results in CGRP release (32), suggesting the adenylyl cyclase/cAMP/PKA-dependent signaling may occur upstream from CGRP release. It has also been reported that CGRP increases the activity of protein kinase C (PKC) (2,31) and induces the expression of heme oxygenase-1 (HO-1) (29,33), signaling events that we and others have implicated as obligatory downstream effectors in early-and late-phase ethanol and ischemic preconditioning (1,6,8,14,18,24,26,29,31,41,42). Additionally, interventions that raise intracellular cAMP levels induce HO-1 via a PKA-dependent pathway (16,30).…”

Section: Discussionmentioning

confidence: 95%

“…While the protective effects induced by ethanol consumption have been attributed to its effects on plasma lipids, platelet function, and fibrinolytic activity (14), more recent work indicates that antecedent ethanol ingestion induces the development of an anti-inflammatory phenotype in postcapillary venules such that these vessels fail to support leukocyte adhesion and emigration in tissues exposed to ischemia-reperfusion (I/R) (18,41,42). The molecular basis for the powerful antiadhesive effects induced by ethanol ingestion appears to involve prevention of adhesion molecule expression by the endothelium (7,8,33).…”

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confidence: 99%

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Role of calcitonin gene-related peptide in the postischemic anti-inflammatory effects of antecedent ethanol ingestion

Kamada¹,

Gaskin²,

Yamaguchi³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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The aim of this study was to determine the role of calcitonin gene-related peptide (CGRP) in the postischemic anti-inflammatory effects of antecedent ethanol ingestion. Ethanol was administered to wild-type C57BL/6 mice on day 1 as a bolus by gavage at a dose that produces a peak plasma ethanol of 45 mg/dl 30 min after administration. Twenty-four hours later (day 2), the superior mesenteric artery was occluded for 45 min followed by 70 min of reperfusion (I/R). Intravital fluorescence microscopy was used to quantify the numbers of rolling (LR) and adherent (LA) leukocytes labeled with carboxyfluorescein diacetate succinimidyl ester in postcapillary venules of the small intestine. I/R increased LR and LA, effects that were prevented by antecedent ethanol. The postischemic anti-inflammatory effects of ethanol consumption were abolished by administration of a specific CGRP receptor antagonist [CGRP-(8-37)] or after sensory nerve neurotransmitter depletion using capsaicin administered 4 days before ethanol ingestion, which initially induces rapid release of CGRP from sensory nerves, thereby depleting stored neuropeptide. Administration of exogenous CGRP or induction of endogenous CGRP release by treatment with capsaicin 24 h before I/R mimicked the postischemic anti-inflammatory effects of antecedent ethanol ingestion. Preconditioning with capsaicin 24 h before I/R was prevented by coincident treatment with CGRP-(8-37), while exogenous CGRP induced an anti-inflammatory phenotype in mice depleted of CGRP by capsaicin administration 4 days earlier. Our results indicate that the effect of antecedent ethanol ingestion to prevent postischemic LR and LA is initiated by a CGRP-dependent mechanism.

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Section: Discussionmentioning

confidence: 95%

mentioning

confidence: 99%

Role of calcitonin gene-related peptide in the postischemic anti-inflammatory effects of antecedent ethanol ingestion

Kamada¹,

Gaskin²,

Yamaguchi³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…HDL concentration decreases and LDL concentration increases with the degree of impairment of liver function in ethanol fed rats 38 . The increased levels of VLDL and LDL in ethanol treated rats observed in our study are known to be cytotoxic to cells and tissues.…”

Section: Discussionmentioning

confidence: 93%

Untitled

2011

IJPSR

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Our aim was to determine the effect of rutin, a flavonol glycoside on ethanol induced hepatic lipid accumulation in experimental rats. Male albino Wistar rats were randomized into four groups. Groups 1 and 2 received isocaloric glucose. Hepatic injury was induced in groups 3 and 4 by administering 20% ethanol via intragastric intubation for 60days. In addition, groups 2 and 4 were given rutin (100 mg/kg) daily for the last 30 days of the experiment. Ethanol alone administered rats showed a significant increase in the levels of total cholesterol (TC), triglycerides (TG), free fatty acids (FFA), phospholipids (PL), low density lipoproteins (LDL) and very low density lipoproteins (VLDL) with a concomitant decrease in the levels of high density lipoproteins (HDL). Haematoxylin and eosin staining of the liver of ethanol alone fed rats showed inflammatory cell infiltrates and fatty changes Supplementation with rutin reversed the ethanol induced alterations in lipid profile and also restored the liver histology which appeared similar to the control rats. Together the results obtained clearly reveal the protective effects of rutin against lipid accumulation in the circulation and liver.

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“…8 Alcohol ingestion is known to increase plasma triglyceride concentrations by increasing triglyceride synthesis and production of very low density lipoprotein (VLDL) particles in the liver. 9 …”

Section: Discussionmentioning

confidence: 99%