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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We compared the levels of microparticles, platelet activation markers, soluble cell adhesion molecules, soluble selectins, and antioxidized low-density lipoprotein (anti-Ox LDL) antibody between patients with hyperlipidemia and control subjects. Binding of anti-glycoprotein (GP) IIb/IIIa and anti-GPIb monoclonal antibodies to platelets did not differ significantly between the hyperlipidemic patients and controls. However, expression of activation markers (CD62P, CD63, PAC-1, and annexin V) by platelets was higher in the hyperlipidemic patients with Type 2 diabetes. The levels of platelet-derived microparticles (PDMPs) and monocyte-derived microparticles (MDMPs) were significantly different in hyperlipidemic patients with Type 2 diabetes and controls. Soluble P-selectin (sP-selectin), soluble E-selectin (sE-selectin), and anti-Ox LDL antibody also showed higher levels in the hyperlipidemic patients with Type 2 diabetes. After treatment with eicosapentaenoic acid (EPA), the levels of CD62P, CD63, annexin V, PDMPs, and MDMPs, sE-selectin, and oxidized LDL antibody were reduced significantly. Triglyceride (TG) and total cholesterol levels were also decreased. Anti-Ox LDL antibodies and MDMPs were correlated positively with platelet CD62P (plt-CD62P) levels. These findings suggest that in hyperlipidemic patients with Type 2 diabetes, EPA may prevent complications caused by oxidized LDL, E-selectin, and activated platelets or monocytes.
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PMID:Effects of eicosapentaenoic acid on platelet activation markers and cell adhesion molecules in hyperlipidemic patients with Type 2 diabetes mellitus. 1273

Atherosclerosis is the leading cause of death in patients with diabetes mellitus, increasing mortality in all forms of the disease. Classical risk factors, including hyperlipidemia, hypertension and obesity, do not completely account for the increased incidence of atherosclerosis in diabetes. Some platelet activation markers such as CD62P, CD63, PAC-1, Annexin V and platelet-derived microparticles (PDMP) are elevated in patients with diabetes, since diabetic platelets often have increased sensitivity to secondary aggregation in response to agonist. PDMPs are thought to play a role in clinical disease because they express phospholipids that function as procoagulants. High shear stress can initiate both platelet aggregation and shedding of procoagulant-containing PDMP, suggesting that PDMP generation by high shear stress occurs in small diseased arteries and arterioles under various clinical conditions. Platelet activation markers were significantly higher in the hypertensive or hyperlipidemic patients than in the controls. Selectins and cell adhesion molecules were also higher in the hypertensive or hyperlipidemic patients, and they were significantly higher in these patients with diabetes. Activated microparticles and PDMP may contribute to the development of atherosclerosis in diabetes, and platelet activation markers seem to be useful for the assessment of vascular damage in these patients.
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PMID:[Platelet activation marker]. 1467 88

Diabetes and obesity are characterized by hyperlipidemia and represent risk factors for premature neurological disorders. Diabetic/obese animals have impaired adult neurogenesis. We hypothesize that lipotoxicity leading to neurogenesis impairment plays a role in the development of neurological complications. If so, normalizing neurogenesis in diabetes/obesity could be therapeutically useful in counteracting neurological dysfunction. The goal of this study was to determine the potential of pituitary adenylate cyclase-activating polypeptide (PACAP) to protect adult neural stem cells (NSCs) from lipotoxicity and to study the expression of PACAP receptors in NSCs under lipotoxic conditions in vitro and in the subventricular zone in vivo. The viability of NSCs isolated from the adult mouse brain subventricular zone was assessed in the presence of a high-fat milieu, as mimicked by palmitate, which characterizes diabetic lipotoxicity. Regulation studies of PACAP receptors were performed by quantitative PCR on NSCs in vitro or on subventricular tissues isolated from obese ob/ob mice and their lean littermates. We show that palmitate impairs NSC viability by promoting lipoapoptosis. We also show that PACAP counteracts lipotoxicity via PAC-1 receptor activation. Studies on PACAP receptor expression revealed that PAC-1 and VPAC-2 are expressed by NSC in vitro and are upregulated by palmitate treatment and that PAC-1, VPAC-1, and VPAC-2 are expressed in the subventricular zone/striatum in vivo and are upregulated in ob/ob mice. The present study reveals a previously uncharacterized role of PACAP to protect NSC from lipotoxicity and suggests a potential therapeutic role for PACAP receptor agonists in the treatment of neurological complications in obesity and diabetes.
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PMID:Pituitary adenylate cyclase-activating polypeptide counteracts the impaired adult neural stem cell viability induced by palmitate. 2218 70