Increased arachidonic acid uptake by platelets from insulin-dependent diabetics and diabetic rats

Pérez, C.; Ramiro, J. M.; Campillo, J. E.

doi:10.1016/0168-8227(89)90048-x

Cited by 8 publications

(5 citation statements)

References 9 publications

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“…Obese male SHHF rats resemble type 2 diabetics and have markedly increased circulating insulin and glucose levels (29), which might influence platelet AA and n-6 PUFA composition. The increased platelet AA level in the diabetic condition may be explained by stimulated AA incorporation into platelets (47)(48)(49). Takahashi et al (48) demonstrated that the AA incorporation into platelet phospholipids was significantly higher in type 2 diabetic patients than in age-matched control subjects.…”

Section: Discussionmentioning

confidence: 99%

Effect of Male Sex and Obesity on Platelet Arachidonic Acid in Spontaneous Hypertensive Heart Failure Rats

Park¹,

Liu-Stratton

Medeiros³

et al. 2004

Exp Biol Med (Maywood)

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Sexual dimorphism is observed in the progression to congestive heart failure and, ultimately, in longevity in spontaneously hypertensive heart failure (SHHF) rats. As platelet activation Illay impact development of cardiovascular diseases, we studied the effects of obesity and sex on platelet polyunsaturated fatty acid (PUFA) profile and its relationship to platelet aggregation in 6-month-old SHHF rats. After a 24-hr fast, blood Was Obtainedfor measurement of platelet phospholipid omega-6 (n-6) and omega-3 (n-3) PUFA. Collagen-induced platelet aggregation was measured by whole-blood Impedance aggreg-Ollletry. Obese male (OM) SHHF had significantly more platelet arachidonic acid (AA) and total n-6 PUFA than lean males (LMs), leanfemales (LFs), or obese females (OFs). Platelet aggregation Was enhanced in males compared to females, with OMs by 45% compared to OFs and with LMs by 28% compared to LFs. l'hou9h no difference was found between OFs and LFs, platelet aggregation was increased in OMs by 20% compared to LMs. l'hough not significantly different, lag time to initiate platelet aggregation tended to be shortest in OMs and then, in increasing duration, LMs, LFs, and OFs, suggesting that Platelets from male rats were quicker to aggregate than those from females. Platelet aggregation was correlated with platelet AA and total n-6 PUFA content. There was no relationship between n-3 PUFA and platelet aggregation. In SHHF rats, elevatedAA and n-s PUFA levels in platelets are associated with enhanced platelet aggregation. This relationship Is potentiated by obesity and male sex. Exp Bioi Med 229:657-664,2004

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Section: Discussionmentioning

confidence: 99%

Effect of Male Sex and Obesity on Platelet Arachidonic Acid in Spontaneous Hypertensive Heart Failure Rats

Park¹,

Liu-Stratton

Medeiros³

et al. 2004

Exp Biol Med (Maywood)

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“…Platelet phospholipase A 2 activity is increased in diabetic subjects (13). Increased incorporation of arachidonate into human and rat diabetic platelets has also been reported (14,15), which is thought to be due to increases in the thromboxane-synthesizing enzyme activity in the diabetic platelet (16). In this study, experiments were designed to study the effects of altered plasma fatty acid composition in diabetic platelet-poor plasma (PPP) on the incorporation of labeled long-chain fatty acids into healthy and diabetic RBCs to further elucidate the mechanisms for the altered fatty acid composition in the diabetic tissues.…”

mentioning

confidence: 90%

Decreased Incorporation of Long-Chain Fatty Acids into Erythrocyte Phospholipids of STZ-D Rats

Dang

Faas²,

Jethmalani³

et al. 1991

Diabetes

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We studied the mechanisms for the altered fatty acid composition in erythrocytes (RBCs) derived from streptozocin-induced diabetic (STZ-D) rats. After 3-wk duration of diabetes, blood glucose, plasma triglyceride, and plasma free-fatty acid levels were all significantly increased. In the diabetic platelet-poor plasma (PPP), the most significant increases in free fatty acids were stearate, linoleate, eicosatrienoate (n-6), and docosahexaenoate (n-3). Fatty acid composition of RBC phospholipids was also altered, with significant decreases in arachidonate, docosatetraenoate (n-6), and docosapentaenoate (n-6) and increases in linoleate and docosahexaenoate. Insulin treatment of the diabetic rats resulted in normalization of docosapentaenoate, arachidonate, and linoleate levels in RBC phospholipids but not of docosahexaenoate or docosatetraenoate levels. The incorporation of [5,6,8,9,11,12,14,15-3H]arachidonate into diabetic RBC phospholipids was significantly decreased compared with the corresponding control RBC, regardless of the incubation medium used, which was the PPP derived either from the control or diabetic rats. Therefore, the decreased incorporation of [5,6,8,9,11,12,14,15-3H]arachidonate into diabetic RBC phospholipids was independent of the altered lipid composition of the PPP incubation media. Furthermore, the decreased incorporation was not specific for arachidonate, because the incorporation of other long-chain fatty acids such as [9,10-3H]oleate, [1-14C]palmitate, [2-14C]eicosatrienoate (n-6), and [1-14C]linoleate into RBC phospholipids was also comparably decreased. More important, the decreased fatty acid incorporations were reversed by insulin treatment of the diabetic rat.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…CD36 has been recently suggested to be a more clinical marker of platelet activation than the activation-induced increase in the platelet surface expression of fibrinogen receptor (GPIIb-IIIa) and Pselectin [2]. Implication of our observation that CD36 is involved in AA-induced platelet aggregation may be highly significant since AA uptake by the platelets is increased in different diseases.However, further work is needed to understand the mechanism of increased expression of CD36 in diabetic platelets where the enhanced AA uptake was reported [9]. This work was supported by the Scottish Office Agriculture and Fisheries Deparhent.…”

mentioning

confidence: 92%

“…However, further work is needed to understand the mechanism of increased expression of CD36 in diabetic platelets where the enhanced AA uptake was reported [9]. This work was supported by the Scottish Office Agriculture and Fisheries Deparhent.…”

mentioning

confidence: 92%

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Platelet membrane glycoprotein IV (CD36) is involved in arachidonic acid induced-platelet aggregation

Duttaroy¹,

Crosbie²,

Gordon³

et al. 1996

Biochemical Society Transactions

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Glycoprotcin (GP) IV (also known as GPIIIb and CD36) is present on the surface of human platelets and other cells, including endothelial cells, monocytes, erythrocytes and megakaryocytes [ 1,2].CD36 is coaposed of a highly gl ycosylated polypeptide chain with an apparent molecular mass of 88kDa [I]. CD36 has a number of putative ligands such as collagen, thrombospondin, oxidised LDL and unesterified free fatty acids (FFA) [ 1-51, This protein may play a number of roles in platelet function and pathophysiology as it is involved in the initial phase of platelet-collagen adhesion and thrombospondindependent platelet aggregation [2,6]. A series of studies have shown that CD36 is also involved in FFA uptake and this protein is strongly induced during the adipocyte differentiation and in diabetes [4,5]. However, the role of CD36 in FFA uptake by the platelets is not known. Aggregation of platelets is induced by aggregating agents like, ADP, collagen, epinephrine and this process is mediated by, in part, through the intracellular synthesis and release of thromboxane A2 (TxA2) [6-81. TxA2 is synthesised from arachidonic acid (AA) which is liberated from membrane phospholipids by phospholipases [8]. Similarly, when platelets are exposed to exogenous AA it is readily taken up by the platelets and in essence, the need for release of AA from membrane phospholipids is bypassed. The absorbed AA is then available to platelets and is rapidly converted to TxA2 which is a very potent platelet aggregator and vasoconstrictor [6,7].The extent to which this occurs depends largely on the concentration of AA used as well as the AA uptake activity of the platelets. AA uptake activity was found to be significantly higher in platelets from diabetic and other cardiovascular diseases [6,9], however the mechanism of AA uptake in human platelets is not known. The aims of this study were to investigate whether CD36 is involved in AA uptake and therefore in AA-induced platelet aggregation. Platelet rich plasma (PRP) was prepared from blood collected in sodium citrate (10% vlv of 3.8% citrate solution) from healthy volunteers who had not taken any medication for at least 14 days prior to phlebotomy. Gel filtered platelets (GFP) were prepared from platelet rich plasma using a Sepharose 4B column as described previously [7]. Aggregation of platelets was induced by either collagen or AA. Maximal amplitude of aggregation of WP was obtained with lOlg/ml collagen and 200 Fg/ml AA. Anti-CD36 monoclonal antibody (MAB) against a 19.7 kDa fragment corresponding to amino acids 70-242 of the human CD36 was used. Binding of [14C] fatty acids to GFP was carried out as described [lo-121. Typically, radiolabelled oleate or arachidonate (final concentration, 1lM) was mixed with serum albumin at 1: 1 molar ratio in phosphate buffered saline. To assess the effect of CD36 on plaielet fatty acid uptake, GFP (-los plateletdassay tube) were pre-incubated with the MAB (lOps/ml) for 20 min. at 22°C and subsequently binding studies were performed with the pretreated plate...

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Increased arachidonic acid uptake by platelets from insulin-dependent diabetics and diabetic rats

Cited by 8 publications

References 9 publications

Effect of Male Sex and Obesity on Platelet Arachidonic Acid in Spontaneous Hypertensive Heart Failure Rats

Effect of Male Sex and Obesity on Platelet Arachidonic Acid in Spontaneous Hypertensive Heart Failure Rats

Decreased Incorporation of Long-Chain Fatty Acids into Erythrocyte Phospholipids of STZ-D Rats

Platelet membrane glycoprotein IV (CD36) is involved in arachidonic acid induced-platelet aggregation

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