Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
Atherosclerosis 2009 May
PMID:LDL-cholesterol lowering increases plasma apelin in isolated hypercholesterolemia. 1884 2

Obesity is associated with accelerated atherosclerosis. Adipokines may directly influence vessel wall homeostasis by influencing the function of endothelial cells, arterial smooth muscle cells, and modulating inflammation. Recently, visceral adipose tissue-derived serpin (vaspin) was identified as a novel adipokine related to obesity and its metabolic consequences. However, the regulation of vaspin serum concentrations in human atherosclerosis is unknown. We therefore assessed vaspin serum concentrations in 107 consecutive patients with carotid stenosis undergoing carotid endarterectomy (CEA) in relation to severity of atherosclerosis, measures of obesity and circulating markers of obesity and atherosclerosis. Vaspin serum concentrations were significantly lower in patients with carotid stenosis who experienced an ischemic event within 3 months before surgery compared to asymptomatic patients. However, circulating vaspin was not associated with measures of atherosclerosis severity as maximum percentage stenosis. Vaspin serum concentrations were indistinguishable before and after CEA. We found a significant correlation between vaspin and leptin serum concentrations supporting previous results that vaspin closely reflects body fat mass. In conclusion, our data show that low vaspin serum concentrations correlate with recently experienced ischemic events in patients with carotid stenosis despite the lack of an association between circulating vaspin and parameters of atherosclerosis severity.
Atherosclerosis 2009 May
PMID:Vaspin serum concentrations in patients with carotid stenosis. 1884 28

Adiponectin, an adipokine secreted by the white adipose tissue, plays an important role in regulating glucose and lipid metabolism and controlling energy homeostasis in insulin-sensitive tissues. A decrease in the circulating level of adiponectin has been linked to insulin resistance, type 2 diabetes, atherosclerosis, and metabolic syndrome. Adiponectin exerts its effects through two membrane receptors, AdipoR1 and AdipoR2. APPL1 is the first identified protein that interacts directly with adiponectin receptors. APPL1 is an adaptor protein with multiple functional domains, the Bin1/amphiphysin/rvs167, pleckstrin homology, and phosphotyrosine binding domains. The PTB domain of APPL1 interacts directly with the intracellular region of adiponectin receptors. Through this interaction, APPL1 mediates adiponectin signaling and its effects on metabolism. APPL1 also functions in insulin-signaling pathway and is an important mediator of adiponectin-dependent insulin sensitization in skeletal muscle. Adiponectin signaling through APPL1 is necessary to exert its anti-inflammatory and cytoprotective effects on endothelial cells. APPL1 also acts as a mediator of other signaling pathways by interacting directly with membrane receptors or signaling proteins, thereby playing critical roles in cell proliferation, apoptosis, cell survival, endosomal trafficking, and chromatin remodeling. This review focuses mainly on our current understanding of adiponectin signaling in various tissues, the role of APPL1 in mediating adiponectin signaling, and also its role in the cross-talk between adiponectin/insulin-signaling pathways.
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PMID:APPL1: role in adiponectin signaling and beyond. 1885 21

Monocyte chemotactic protein-1 and interleukin-6 are important inflammatory cytokines, which have close relationships with atherosclerosis. Visfatin is a novel adipokine involved in regulation of inflammatory cytokines, however, associations of visfatin with cytokines (MCP-1, IL-6) in human umbilical vein endothelial cells are unclear. The aim of this study was to determine whether visfatin has effects on the expression of MCP-1 and IL-6 in human umbilical vein endothelial cells. Enzyme-linked immunosorbent assay were used for measuring MCP-1 and IL-6 production in human umbilical vein endothelial cells. Real-time quantitative reverse-transcription polymerase chain reaction was used for determining MCP-1 and IL-6 mRNA expression. For the pathway determination following inhibitors were used: wortmannin [phosphatiylinositol 3-kinase (PI3K)], SB203580 [p38 mitogen-activated protein kinase (MAPK)], PD98059 [extracellular signal-regulated kinase (ERK) 1/2)], JNK inhibitor II [c-Jun NH 2-terminal kinase (JNK)]. We demonstrated that visfatin could obviously upregulate secretion of MCP-1and IL-6 in a dose- and time-dependent manner in human umbilical vein endothelial cells. Visfatin-induced effects were diminished by SB203580, wortmannin, and PD98059. In summary, these results suggest that visfatin-induced MCP-1 and IL-6 production involve p38 MAPK, PI3K, and ERK 1/2 pathways in human umbilical vein endothelial cells as determined by inhibition with specific inhibitors.
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PMID:Visfatin stimulates production of monocyte chemotactic protein-1 and interleukin-6 in human vein umbilical endothelial cells. 1900 99

Adiponectin is a protein secreted into the circulation exclusively by adipocytes. It acts as an anti-diabetic and anti-atherogenic adipokine. Its plasma level is lowered in conditions of obesity, diabetes, and atherosclerosis. Within adipocytes, it is retained in the lumen of the endoplasmic reticulum by binding to the thiol protein ERp44 and released by another thiol protein, Ero1-Lalpha. Nuclear receptor PPARgamma ligand agonists appear to regulate its retention-release mechanism.
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PMID:New insights into thiol-mediated regulation of adiponectin secretion. 1901 26

Adipose tissue is critical in energy homeostasis. Adipose tissue 'buffers' the lipids and energy rich compounds which are pumped into the blood stream soon after meals. It senses, signals other organs like liver and brain about the energy reserves via adipokines. Adiponectin, the most abundant adipokine has insulin sensitizing, anti-inflammatory antiatherogenic and antisteatotic effects. Adipose tissue dysfunction is accompanied by abnormal lipid distribution and storage which contributes to diseases like diabetes, nonalcoholic fatty liver disease and atherosclerosis. Obesity and lipodystrophy are associated with dysfunctional adipocytes. Pre-adipocytes are easy to isolate and culture. A personalized depot specific liposuction to remove the inactive adipocytes followed by adipocyte repopulation could be useful in the treatment of these diseases.
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PMID:Adipose tissue transplantation may be a potential treatment for diabetes, atherosclerosis and nonalcoholic steatohepatitis. 1904 21

Insulin resistance often characterizes chronic uremia, and is associated with enhanced morbidity and mortality, because it may contribute to protein-energy wasting (in turn, an independent predictor of reduced survival), atherosclerosis, and cardiovascular death. Causes of insulin resistance in chronic uremia are complex and multifactorial. Obesity is emerging as an independent risk factor for chronic kidney disease, and an expected rise in number of obese uremic patients because of the ongoing worldwide obesity epidemic is likely to increase the prevalence of insulin resistance in chronic uremia in the near future. Similar to the general population, reported associations between obesity and insulin resistance in chronic uremia support a role of adipose tissue and altered adipokine profiles in insulin resistance in obese chronic kidney disease patients. Hormonal imbalances, chronic acidosis, and systemic inflammation and oxidative stress are uremia-associated relevant causes of insulin resistance in nonobese individuals. A further understanding of the causes of insulin resistance in chronic uremia represents a potential important tool in the design of more effective therapeutic strategies to reduce uremia-associated morbidity and mortality.
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PMID:Insulin resistance in chronic uremia. 1912 65

Adrenomedullin (ADM) is a vasoactive peptide found to be related to obesity and its comorbidities: type 2 diabetes, hypertension, atherosclerosis, and coronary heart disease. ADM is increased both in plasma and in adipose tissue of obese individuals when compared to lean subjects and is considered as a member of the adipokine family. We determined plasma midregional proadrenomedullin (MR-proADM) concentrations in a cohort of 357 subjects with BMI ranging from 17.5 to 42.3 kg/m2 and no additional medical history. In parallel, 28 severely obese patients scheduled to undergo laparoscopic Roux-en-Y gastric bypass (RYGB) surgery were studied at two time points: before and 1 year after surgery. Outcome measurements were: MR-proADM, cortisol, leptin, C-reactive protein (CRP) thyroid-stimulating hormone (TSH), creatinine and metabolic parameters. BMI correlated significantly to plasma MR-proADM levels (r=0.714, P<0.001), also after adjustment for age and gender (r=0.767, P<0.001). In obese subjects, there was a positive relationship between MR-proADM and leptin (r=0.511, P=0.006). Following RYGB, plasma MR-proADM decreased from 0.76+/-0.03 to 0.62+/-0.02 pg/ml (P<0.0001). RYGB-induced changes in MR-proADM correlated significantly to changes in leptin (r=0.533, P=0.004) and in CRP (r=0.429, P=0.023). We conclude that BMI is an independent predictor of circulating MR-proADM levels. Weight loss after RYGB is associated with a significant decrease in plasma MR-proADM, which is related to surgery-induced changes in both circulating leptin and systemic inflammation.
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PMID:Plasma MR-proADM correlates to BMI and decreases in relation to leptin after gastric bypass surgery. 1924 78

Nuts are energy-dense foods, rich in total fat and unsaturated fatty acids. The favorable fatty acid profile probably contributes to the beneficial effects of nut consumption observed in epidemiologic studies (prevention of coronary heart disease and diabetes) and feeding trials (cholesterol lowering). Besides fat, the complex matrices of nuts contain many bioactive compounds: vegetable protein, fiber, minerals, tocopherols, and phenolic compounds. By virtue of their unique composition, nuts are likely to benefit newer cardiovascular risk biomarkers, such as LDL oxidizability, soluble inflammatory molecules, and endothelial dysfunction. Protection of LDL oxidation by nut intake has been documented in some, but not all, clinical studies. In one study, feeding one daily serving of mixed nuts was associated with lower oxidized LDL concentrations. Regarding inflammation, cross-sectional studies have shown that nut consumption is associated with lower concentrations of circulating inflammatory molecules and higher plasma adiponectin, a potent antiinflammatory adipokine. Clinical studies with nuts have documented reduced inflammatory cytokine concentrations but no consistent changes of C-reactive protein. Only walnuts have been formally tested for effects on endothelial function. After both walnut diets and single walnut meals, favorable vasoreactivity changes have been observed. Walnut consumption also reduced expression of endothelin 1, a potent endothelial activator, in an animal model of accelerated atherosclerosis. Beneficial effects on vascular reactivity may be ascribed to several constituents of walnuts: l-arginine, the precursor of nitric oxide, alpha-linolenic acid, and phenolic antioxidants. Although more studies are warranted, the emerging picture is that nut consumption beneficially influences cardiovascular risk beyond cholesterol lowering.
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PMID:Nuts and novel biomarkers of cardiovascular disease. 1932 61

The incidence of obesity has increased dramatically during recent decades. Obesity will cause a decline in life expectancy for the first time in recent history due to numerous co-morbid disorders. Adipocyte and adipose tissue dysfunction belong to the primary defects in obesity and may link obesity to several health problems including increased risk of insulin resistance, type 2 diabetes, fatty liver disease, hypertension, dyslipidemia, atherosclerosis, dementia, airway disease and some cancers. However, not all obese individuals develop obesity related metabolic or cardiovascular disorders potentially due to a preserved normal adipose tissue architecture and function. The majority of patients with obesity have an impaired adipose tissue function caused by the interaction of genetic and environmental factors which lead to adipocyte hypertrophy, hypoxia, a variety of stresses and inflammatory processes within adipose tissue. Ectopic fat accumulation including visceral obesity may be considered as a consequence of adipose tissue dysfunction, which is further characterized by changes in the cellular composition, increased lipid storage and impaired insulin sensitivity in adipocytes, and secretion of a proinflammatory, atherogenic, and diabetogenic adipokine pattern. This review focuses on the discussion of mechanisms causing or maintaining impaired adipose tissue function in obesity and potentially linking obesity to its associated disorders. A model is proposed how different pathogenic factors and mechanisms may cause dysfunction of adipose tissue.
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PMID:Adipose tissue dysfunction in obesity. 1935 89


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