Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin resistance is associated with hyperglycemia and dyslipidemia and promotes atherosclerosis. Although insulin resistance is associated with adipocytokines, little is known about the association in patients with stroke without diabetes mellitus. The aim of the current study was to examine the relationship among insulin resistance, visceral fat area, and adipocytokines in patients with stroke. This study design was cross-sectional in a university hospital. We studied 60 patients with stroke and no history of diabetes mellitus who had hyperglycemia or hypertriglyceridemia or reduced fasting plasma high-density lipoprotein cholesterol. We measured insulin resistance, the plasma level of tumor necrosis factor (TNF)-alpha, adiponectin, and the visceral fat area. Insulin resistance was defined by the homeostasis model assessment and the level of insulin at 120 minutes after consuming oral glucose. We classified two groups (insulin sensitive or insulin resistant). In all, 21 of 60 patients (35.0%) had insulin resistance and 35 (58.3%) had hyperinsulinemia. Compared with insulin-sensitive patients with stroke (n = 18), insulin-resistant patients with stroke (n = 21) had significantly wider visceral fat areas and a high level of plasma TNF-alpha. The plasma level of adiponectin in insulin-resistant patients with stroke was similar to that in insulin-sensitive patients. Insulin-resistant patients with stroke in this study had a large amount of visceral fat and increased levels of TNF-alpha. We recommend that obese patients with stroke should be examined for insulin resistance to reduce the risk of the development of atherosclerosis.
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PMID:Insulin resistance in patients with stroke is related to visceral fat obesity and adipocytokines. 1858 36

Plasma VLDL accumulation in Gram-negative sepsis is partly ascribed to an increased hepatic VLDL production driven by pro-inflammatory cytokines. We previously showed that hepatocytes of the Kupffer cell (KC)-rich periportal area are major contributors to enhanced VLDL production in lipopolysaccharide (LPS)-injected rats. However, it remains to be established whether KC generated products directly affect the number (apoB) and composition of secreted VLDL. Using rat primary cells, we show here that hepatocytes respond to stimulation by soluble mediators released by LPS-stimulated Kupffer cells with enhanced secretion of apoB and triglycerides in phospholipid-rich VLDL particles. Unstimulated KC products also augmented the secretion of normal VLDL, doubling apoB mRNA abundance. IL-1beta treatment resulted in concentration-dependent increases of hepatocyte apoB mRNA and protein secretion, increases that were greater, but not additive, when combined with IL-6 and TNF-alpha. Lipid secretion and MTP mRNA levels were unaffected by cytokines. In summary: (i) enhanced secretion of phospholipid-rich VLDL particles is a net hepatocyte response to LPS-stimulated KC products, which gives a clue about the local role of Kupffer cells in septic dyslipidemia induction; and (ii) pro-inflammatory cytokines act redundantly to enhance apoB secretion involving translational apoB up-regulation, but other humoral components or KC mediators are necessary to accomplish increased lipid association.
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PMID:Kupffer cell products and interleukin 1beta directly promote VLDL secretion and apoB mRNA up-regulation in rodent hepatocytes. 1866 11

This study was designed to assess the diagnostic value of dynamic patterns of anti-inflammatory cytokines (IL-1b, IL-6, TNF-alpha) in patients with ischemic heart disease (IHD) and restenosis of coronary stents 14 months after their implantation for long-term prophylaxis of dyslipoproteinemia. A total of 40 patients with IHD of advanced functional classes (FC) were examined. Blood cytokine levels were measured before, 1 day, and 12-18 months after coronary stenting. Two groups of 23 and 17 patients included cases with recurrent angina and without it respectively. The main parameters measured in the study were in-stent restenosis rate, incidence of' acute myocardial infarction (AMI), mortality rate, frequency of hospitalization for unstable angina, and the levels of proinflammatory cytokines. Considerable activation of cytokines in patients with post-infarction cardiac dysfunction who rarely resorted to therapy with statins (16.7%) was associated with the high rate of recurrent coronary insufficiency related to in-stent occlusion (8.7%), progressive atherosclerosis (65.2%), impaired myocardial perfusion, and restenosis of coronary stents (26.1%). Patients lacking apparent expression of serum cytokines after revascularization while receiving efficacious secondary prophylaxis of dyslipidemia (13.8 and 17% decrease of triglycerides (TG) and low density lipoproteins (LDL) cholesterol respectively, p = 0.04) had left ventricular ejection fraction (LVEF) improved by 12.5% (p = 0.03%), left ventricular end diastolic pressure (LVEDP) decreased by 15.8% (p = 0.03), and frequency of ischemic perfusion defect (PD) reduced by 45.3% (p = 0.01). Moreover, they showed low incidence of progressive coronary atherosclerosis (17.6%) in the absence of in-stent restenosis. It is concluded that the frequency of restenosis of coronary stents after endovascular myocardial revascularization depends on the preprocedural rise in IL-1b content (R = 0.62, p = 0.0023). It is concluded that long-term secondary prophylaxis of dyslipoproteinemia in patients with ischemic dysfunction at risk of coronary restenosis effectively (more than thrice) decreases the occurrence of coronary stent restenosis after endovascular revasularization.
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PMID:[The role of cytokines in restenosing coronary stents and the efficiency of its secondary prophylaxis with statins]. 1881 44

Apelin, a relatively newer adipokine with various actions in cardiovascular system, was recently reported to decrease in dyslipidemia. The present study addresses whether plasma apelin increases after hypolipidemic intervention either through therapeutic life style change (TLC) or statin treatment. A total of 134 patients were subjected to treatment with a TLC intervention for 12 weeks. Of these, 116 successfully completed the period, and LDL-cholesterol level decreased to target level (<160 mg/dL) in 54 (46.5%) individuals. The remaining 62 patients were treated with rosuvastatin for 12 weeks, and 56 of them finished the study. Circulating apelin, adiponectin, leptin, TNF-alpha, hsCRP and insulin levels were determined both at baseline and after TLC intervention and statin treatment. There was no significant change in plasma apelin concentration in patients unresponsive to TLC (p=0.110). LDL-cholesterol lowering either through TLC or statin treatment was accompanied by an increase in plasma apelin (p=0.000, p=0.020) and adiponectin (p=0.001, p=0.011). Serum leptin decreased after successful TLC (p=0.042/male, p=0.023/female) but not after statin treatment (p=0.959/male, p=0.134/female). Serum TNF-alpha (p=0.902) and plasma hsCRP (p=0.135) levels remained unchanged after TLC intervention but decreased after statin treatment (p=0.000, p=0.023, respectively). Plasma insulin and homeostasis model assessment scores decreased after TLC (p=0.000 for both) but not rosuvastatin treatment (p=0.865, p=0.722, respectively). In conclusion, independent of the type of treatment, reduction in LDL-cholesterol levels in otherwise healthy people with isolated dyslipidemia results in an increase in plasma apelin concentration. More experiments may show a substantial role for this peptide in the mechanism of atherosclerosis.
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PMID:LDL-cholesterol lowering increases plasma apelin in isolated hypercholesterolemia. 1884 2

Berberine (BBR) has been shown to improve several metabolic disorders, such as obesity, type 2 diabetes, and dyslipidemia, by stimulating AMP-activated protein kinase (AMPK). However, the effects of BBR on proinflammatory responses in macrophages are poorly understood. Here we show that BBR represses proinflammatory responses through AMPK activation in macrophages. In adipose tissue of obese db/db mice, BBR treatment significantly downregulated the expression of proinflammatory genes such as TNF-alpha, IL-1beta, IL-6, monocyte chemoattractant protein-1 (MCP-1), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). Consistently, BBR inhibited LPS-induced expression of proinflammatory genes including IL-1beta, IL-6, iNOS, MCP-1, COX-2, and matrix metalloprotease-9 in peritoneal macrophages and RAW 264.7 cells. Upon various proinflammatory signals including LPS, free fatty acids, and hydrogen peroxide, BBR suppressed the phosphorylation of MAPKs, such as p38, ERK, and JNK, and the level of reactive oxygen species in macrophages. Moreover, these inhibitory effects of BBR on proinflammatory responses were abolished by AMPK inhibition via either compound C, an AMPK inhibitor, or dominant-negative AMPK, implying that BBR would downregulate proinflammatory responses in macrophages via AMPK stimulation.
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PMID:Berberine suppresses proinflammatory responses through AMPK activation in macrophages. 1920 54

Patients with rheumatoid arthritis (RA) are at risk of cardiovascular disorders. Pathogenesis of rapidly developing atherosclerosis in RA remains to be elucidated. The aim of this study was to compare cholesterol content in serum lipoprotein subfractions in patients with RA and healthy subjects and to establish relationship between lipid profile variations, severity of the disease, and plasma levels of anti-inflammatory cytokines. The study included 15 patients with active RA and 120 healthy subjects of comparable sex and age. RA was found to be associated with a significant decrease of cholesterol of high density (HDL2) and intermediate density (IDL) lipoproteins and its elevation in low density lipoproteins (LDL1-3). There was negative correlation between the latter parameter and disease activity index. No relationship between lipoprotein cholesterol and serum interleukins (IL-6, IL-8) TNF-alpha, and IFN-gamma) was documented. It is concluded that patients with RA exhibit proatherogenic changes of cholesterol content in different lipoprotein subfractions related to the severity of the disease. Further studies are needed to elucidate molecular mechanisms of dyslipidemia in RA and to ensure the choice of optimal targets for therapeutic modalities reducing the risk of cardiovascular disorders.
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PMID:[Relationship between blood lipid spectrum and activity of the disease in patients with rheumatoid arthritis]. 1922 8

Extrarenal calcifications, particularly affecting the cardiovascular system, are common observations which can be a source of serious complications in patients with chronic renal disease, especially those on dialysis. In these patients, cardiovascular disease - myocardial infarction, arrhythmia, calcified valvulopathy, stroke, peripheral ischemic arteriopathy, calciphylaxy, etc. - is the leading cause of death (more than 50%). These complications are closely related to the presence of vascular calcifications (VC) which are much more frequent, severe, and progressive than in the general population. Previously, these calcifications were considered to arise via a passive process within the context of comorbid conditions without specific signs of gravity: high blood pressure, atherosclerosis, aging, diabetes, smoking, dyslipidemia, chronic micro-inflammation, hyperhomocysteinemia, disorders of calcium-phosphorus metabolism. It is now established that VC arise via a complex, probably regulated, active process analogous to the processes leading to bone formation and/or remodeling. New insight provided by a large body of work designed to ascertain the mechanisms underlying the onset of VC has enabled the development of new diagnostic and therapeutic approaches. It is now possible to identify factors clearly favoring the formation of VC: TNF-alpha (which stimulates cell necrosis/apoptosis), CRP, oxidized lipids, AGEs, leptin, inorganic phosphate, high calcium-phosphorus product (CaxPO(4)), calcium, 1,25-OH(2)D(3) and Vitamin D(3), PTHrP (via an intracrine pathway), cyclic AMP, TGF-beta, bone morphogenic protein 2 (BMP2) and factors protective against the formation of VC: magnesium, HDL, inorganic pyrophosphate, albumin, ahsg/fetuin A, osteopontin (OPN), osteoprotegerin (OPG), osteonectin (ON), bone morphogenic protein 7 (BMP7), klotho, PTHrP (via a paracrine pathway), matrix gla protein (MGP), PTH (via Msx2) and vitamin K. In conclusion, until recently, neglected disorders of calcium-phosphorus metabolism are currently recognized as the main actors in the process leading to vascular mediacalcosis in patients with chronic kidney failure.
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PMID:[Origin of the mediacalcosis in kidney failure]. 1934 26

We have previously reported that the obesity-associated proinflammatory cytokine, TNF-alpha, stimulates the overproduction of intestinal apolipoprotein (apo) B48 containing lipoproteins. In the current study, we have evaluated whether a water-soluble cinnamon extract [CE (Cinnulin PF)] attenuates the dyslipidemia induced by TNF-alpha in Triton WR-1339 treated hamsters, and whether CE inhibits the oversecrection of apoB48-induced by TNF-alpha in enterocytes in a 35S labeling study. In vivo, oral treatment of Cinnulin PF (50 mg per kg BW), inhibited the postprandial overproduction of apoB48-containing lipoproteins and serum triglyceride levels. In ex vivo 35S labeling studies, CE (10 and 20 microg/ml) inhibited the oversecretion of apoB48 induced by TNF-alpha treated enterocytes into the media. To determine the molecular mechanisms, TNF-alpha treated primary enterocytes isolated from chow-fed hamsters, were incubated with CE (10 microg/ml), and the expression of the inflammatory factor genes, IL1-beta, IL-6, and TNF-alpha, insulin signaling pathway genes, insulin receptor (IR), IRS1, IRS2, phosphatidylinositol 3-kinase (PI3-K), Akt1 and phosphatase and tensin homology (PTEN), as well as the key regulators of lipid metabolism, cluster of differentiation (CD)36, microsomal triglyceride transfer protein (MTTP), and sterol regulatory element binding protein (SREBP)-1c were evaluated. Quantitative real-time PCR assays showed that CE treatment decreased the mRNA expression of IL-1beta, IL-6 and TNF-alpha, improved the mRNA expression of IR, IRS1, IRS2, PI3K and Akt1, inhibited CD36, MTTP, and PTEN, and enhanced the impaired SREBP-1c expression in TNF-alpha treated enterocytes. These data suggest that a water extract of cinnamon reverses TNF-alpha-induced overproduction of intestinal apoB48 by regulating gene expression involving inflammatory, insulin, and lipoprotein signaling pathways. In conclusion, Cinulin PF improves inflammation related intestinal dyslipidemia.
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PMID:Cinnamon extract attenuates TNF-alpha-induced intestinal lipoprotein ApoB48 overproduction by regulating inflammatory, insulin, and lipoprotein pathways in enterocytes. 1959 46

Psoriasis is a chronic inflammatory, immune-mediated skin disease, which may cause significant deterioration in the quality of life. Recent evidence indicates that psoriasis and psoriatic arthritis are frequently associated with cardiometabolic diseases including myocardial infarction, stroke, diabetes, obesity, dyslipidemia and non-alcoholic fatty liver disease. Although the causal relationship between cardiometabolic comorbidities and psoriasis has not yet been completely proven, it appears that obesity is a relevant risk factor for the development of psoriasis and metabolic syndrome. In addition, moderate to severe psoriasis itself is a risk factor for cardiovascular disease and the metabolic syndrome. Some common genetic traits as well as inflammatory mechanisms may underlie the development of psoriasis and cardiometabolic comorbidities. The presence of comorbidities has important implications in the global approach to patients with psoriasis. Traditional systemic anti-psoriatic agents could negatively affect cardiometabolic comorbidities, and may have important interactions with drugs commonly used by psoriasis patients. In contrast, the recent findings that the risk of myocardial infarction is markedly reduced in rheumatoid arthritis patients who respond to anti-TNF-alpha therapy compared with non-responders supports the hypothesis that the anti-inflammatory effect of TNF-alpha blockers might potentially reduce the cardiovascular risk also in psoriasis patients. Finally, patients with moderate to severe psoriasis should be treated promptly and effectively, should also be encouraged to drastically correct their modifiable cardiovascular risk factors, in particular obesity and smoking habit.
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PMID:Cardiometabolic comorbidities and the approach to patients with psoriasis. 2009 57

The kidney is an important source of L-arginine, the endogenous precursor of nitric oxide (NO). Surgical problems requiring extensive renal mass reduction (RMR) decrease renal NO production, leading to multiple hemodynamic and homeostatic disorders manifested by hypertension, oxidative stress, and increased inflammatory cytokines. Using the RMR model of chronic renal failure (CRF), we assessed the effects of twelve weeks' administration of L-arginine and/or a mixture of antioxidants (L-carnitine, catechin, vitamins E and C) on plasma cytokines, soluble intercellular adhesion molecule-1 (sICAM-1), nitrate and nitrites (NO(2)/NO(3)), lipid profile, blood pressure, and renal function. CRF rats showed increased plasma IL-1 alpha, IL1-beta, IL-6, TNF-alpha, and sICAM-1 levels and decreased anti-inflammatory cytokines IL-4 and 10 levels, hypertension, and dyslipidemia. L-arginine treatment improved kidney functions, decreased systolic blood pressure, and decreased inflammatory cytokines levels. Antioxidants administration decreased inflammatory cytokines and sICAM-1 levels and increased IL-4 levels. Combined use of both L-arginine and the antioxidant mixture were very effective in their tendency to recover normal values of kidney functions, plasma cytokines, sICAM-1, blood pressure, NO(2)/NO(3), cholesterol, and triglycerides concentrations. Indeed, the effects of L-arginine and the antioxidants on the reduction of proinflammatory cytokines may open new perspectives in the treatment of uremia.
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PMID:Multiple antioxidants and L-arginine modulate inflammation and dyslipidemia in chronic renal failure rats. 2019 83


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