Maternal hypothyroxinemia disrupts neurotransmitter metabolic enzymes in developing brain.

Maternal thyroid status influences early brain development and, consequently, cognitive and motor function in humans and rats. The biochemical targets of maternal thyroid hormone (TH) action in fetal brain remain poorly defined. A partially thyroidectomized rat dam model was therefore used to investigate the influence of maternal hypothyroxinemia on the specific activities of cholinergic and monoaminergic neurotransmitter metabolic enzymes in the developing brain. Maternal hypothyroxinemia was associated with reduced monoamine oxidase (MAO) activity in fetal whole brain at 16 and 19 days gestation (dg). A similar trend was observed for choline acetyltransferase (ChAT) activity. In contrast, DOPA decarboxylase (DDC) activity was markedly elevated at 21 dg. Further study of these enzymes at 14 dg showed no differences between normal and experimental progeny - suggesting they become TH sensitive after this age. Tyrosine hydroxylase (TyrH) and acetylcholinesterase (AChE) activities were unaffected prenatally. During postnatal development, the activities of TyrH, MAO, DDC and, to a lesser extent, AChE were increased in a brain region- and age-specific manner in experimental progeny. The prenatal disturbances noted in this study may have wide-ranging consequences since they occur when neurotransmitters have putative neurotropic roles in brain development. Furthermore, the chronic disturbances in enzyme activity observed during postnatal life may affect neurotransmission, thereby contributing to the behavioural dysfunction seen in adult progeny of hypothyroxinemic dams.     

Inhibition of vascular adhesion protein-1 modifies hepatic steatosis in vitro and in vivo

BACKGROUNDNon-alcoholic fatty liver disease (NAFLD) is associated with obesity, insulin resistance and dyslipidaemia and currently is estimated to affect up to a third of all individuals in developed countries. Current standard of care for patients varies according to disease stage, but includes lifestyle interventions common insulin sensitizers, antioxidants and lipid modifiers. However, to date specific therapies have shown little histological or fibrosis stage improvement in large clinical trials, and there is still no licensed therapy for NAFLD. Given the high prevalence, limited treatment options and significant screening costs for the general population, new treatments are urgently required.AIMTo assess the potential for inhibition of the amine oxidase enzyme vascular adhesion protein-1 (VAP-1) to modify hepatic lipid accumulation in NAFLD.METHODSWe have used immunochemical and qPCR analysis to document expression of VAP-1 and key functional proteins and transporters across the NAFLD spectrum. We then utilised hepatocytes in culture and human precision cut liver slices in concert with selective enzyme activity inhibitors to test the effects of activating the semicarbazide-sensitive amine oxidase activity of VAP-1 on hepatic lipid uptake and triglyceride export. A murine model of NAFLD was also used to determine the consequences of VAP-1 knockout and gene expression arrays were used to quantify the effects of VAP-1 activity on key lipid modifying and proinflammatory gene expression.RESULTSWe confirmed that increasing severity of NAFLD and progression to cirrhosis was associated with a significant increase in hepatocellular VAP-1 expression. Hepatocytes in vitro exposed to recombinant VAP-1 and its substrate methylamine showed increased lipid accumulation as determined by quantification of Oil Red O uptake. This was recapitulated using hydrogen peroxide, and lipid accumulation was accompanied by changes in expression of the lipid transporter molecules FABP3, FATP6, insulin receptor subunits and PPARα. Human liver tissue exposed to recombinant VAP-1 or substrates for endo/exogenous VAP-1 produced less triglyceride than untreated tissue and demonstrated an increase in steatosis. This response could be inhibited by using bromoethylamine to inhibit the SSAO activity of VAP-1, and mice deficient in VAP-1/AOC3 also demonstrated reduced steatosis on high fat diet. Exposure of human liver tissue to methylamine to activate VAP-1 resulted in increased expression of FABP2 and 4, FATP3-5, caveolin-1, VLDLR, PPARGC1 and genes associated with the inflammatory response.CONCLUSIONOur data confirm that the elevations in hepatic VAP-1 expression reported in nonalcoholic steatohepatitis can contribute to steatosis, metabolic disturbance and inflammation. This suggests that targeting the semicarbazide sensitive amine oxidase capacity of VAP-1 may represent a useful adjunct to other therapeutic strategies in NAFLD.     

Role of nonalcoholic fatty liver disease in the development of insulin resistance and diabetes

Nonalcoholic fatty liver disease (NAFLD) is a common disease that is usually accompanied by insulin resistance (IR). Whether or how NAFLD and IR are temporally and mechanistically related is controversial. Recent studies focus on their epidemiology, the importance of dietary fat, the role of adipocytokines and the sterol regulatory element-binding protein-1c. NAFLD and IR may progress to severe diseases, such as cirrhosis, diabetes or both, and understanding the pathogenesis of the precursor conditions has preventive and therapeutic implications. This review focuses on the possible relationships between NAFLD and IR and the treatment options available.     

Serum levels of hepatoprotective peptide adiponectin in non-alcoholic fatty liver disease

OBJECTIVE: Adiponectin is an adipose tissue-specific protein that has anti-inflammatory, antidiabetic and antiobesity effects. It has been suggested that adiponectin has a hepatoprotective role. Non-alcoholic fatty liver disease (NAFLD) is becoming more prevalent with increasingly adverse clinical outcomes. In this study, serum adiponectin levels were investigated in patients with NAFLD to determine its possible role on hepatic inflammation and injury. METHODS: Twenty-nine biopsy-proven NAFLD patients (14 women, 15 men) with elevated liver enzymes, 20 clinically diagnosed NAFLD patients (13 women, seven men) with normal liver enzymes, and 20 healthy adults (10 women, 10 men) were enrolled. From fasting blood samples, serum adiponectin levels were measured by enzyme-linked immunosorbent assay. The body mass index, serum glucose, insulin, cholesterol and triglyceride levels were determined. RESULTS: Serum adiponectin levels were 4.99+/-2.1, 9.49+/-3.91 and 7.74+/-4.41 micro/ml in the NAFLD with elevated liver enzymes, NAFLD with normal liver enzymes and healthy adult control groups, respectively. The mean serum adiponectin level in the NAFLD with elevated liver enzymes group was significantly lower than those of other groups tested (P<0.001). Insulin, cholesterol and triglyceride levels of NAFLD patients with elevated liver enzymes were significantly higher than control groups (P<0.05) but were not significantly different from the NAFLD group with normal liver enzymes (P>0.05). On histopathologic examination, the mean serum adiponectin levels of non-alcoholic steatohepatitis patients with grade 2 or more inflammatory activity was significantly lower than patients with grade 1 inflammatory activity (P=0.013). CONCLUSION: Serum adiponectin levels are significantly lower in NAFLD patients with elevated liver enzymes. Non-alcoholic steatohepatitis patients show lower levels of adiponectin with higher grades of inflammation.     

Abnormal glucose tolerance in young male patients with nonalcoholic fatty liver disease

Objective: The association of nonalcoholic fatty liver disease (NAFLD) with insulin resistance and metabolic syndrome has been documented for obese men and middle‐aged men. This study was designed to determine the relationship between NAFLD and the oral glucose tolerance test (OGTT) to predict preclinical diabetes in nondiabetic young male patients (<30 years old). Methods: A total of 75 male patients who had elevated liver enzymes and who were diagnosed with NAFLD were enrolled in this study. A standard 75 g OGTT was carried out on all patients. Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) were defined as a fasting plasma glucose (FPG) level ≥100 mg/dl but <126 mg/dl, and a 2‐h post‐load glucose on the OGTT of ≥140 mg/dl, but <200 mg/dl respectively. Results: According to the OGTT results, 24 (32%) patients were diagnosed as having IGT and 12 (16%) patients were diagnosed as having diabetes. Among the 48 patients with normal fasting glucose, 18 (37.6%) patients showed abnormal glucose tolerance (15 had IGT and three had diabetes). The NAFLD patients with abnormal glucose tolerance showed significant differences in age, weight, body mass index, waist–hip ratio, alanine aminotransferase, total bilirubin, total cholesterol, low‐density lipoprotein cholesterol, triglyceride, insulin, FPG and homeostasis model for insulin resistance (HOMA‐IR). Multiple regression analysis showed that age, FPG and HOMA‐IR were independent predictors of abnormal glucose tolerance. Conclusions: Although the patients were young men, an OGTT should be recommended for NAFLD patients with elevated liver enzymes and IFG to predict the risk of type 2 diabetes.     

Insulin resistance in development and progression of nonalcoholic fatty liver disease

Although insulin resistance(IR)is strongly associated with nonalcoholic fatty liver disease(NAFLD),the association of IR and NAFLD is not universal and correlation between IR and severity of NAFLD is still controversial.In this review,we summarize recent evidence that partially dissociates insulin resistance from NAFLD.It has also been reported that single-nucleotide polymorphisms in the diacylglycerol acyltransferase gene,rather than IR,account for the variability in liver fat content.Polymorphisms of the patatin-like phospholipase 3 gene have also been reported to be associated with NAFLD without metabolic syndrome,which suggests that genetic conditions that promote the development of fatty changes in the liver may occur independently of IR.Moreover,environmental factors such as nutrition and physical activity as well as small intestinal bacterial overgrowth have been linked to the pathogenesis of NAFLD,although some of the data are conflicting.Therefore,findings from both genetically engineered animal models and humans with genetic conditions,as well as recent studies that have explored the role of environmental factors,have confirmed the view that NAFLD is a polygenic disease process caused by both genetic and environmental factors.Therefore,IR is not the sole predictor of the pathogenesis of NAFLD.     

Effects of aging on monoamine oxidase activity of mouse and rabbit tissues

The effect of aging on the monoamine oxidase (MAO) activity in tissues of mice and rabbits was evaluated. There were no alterations in the MAO activity of liver, kidney, pancreas and brain (adult mice and rabbits) or testis and heart (adult mice) with aging. There were no alterations in the norepinephrine content of the brain, kidney and heart of older, mice. The present study indicates that increased MAO activity is not inevitably associated with aging in all species.     

Mean platelet volume in biopsy-proven non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD) is increasingly recognized as the most common cause of chronic liver disease worldwide. It has been shown that NAFLD has a strong association with metabolic syndrome and its component like insulin resistance (IR). Cardiovascular disease has a relation with NAFLD. Platelet volume is an indicator of platelet function and activation. Mean platelet volume (MPV) has been reported as a risk factor for atherothrombosis. In our study, we aimed to investigate the relation of MPV with NAFLD and IR in the NAFLD patients. A total of 54 patients with histologically proven NAFLD and 41 healthy age-matched control subject were enrolled in this study. The NAFLD subjects were divided into two subgroups: 42 patients in the insulin resistant group (median age 39.5, females 22 [52%]) and 12 patients in the insulin sensitive group (median age 38, females 5 [41.7%]). MPV were significantly higher in the NAFLD group in univariate analysis (p?<?0.05). In the NAFLD patients, we did not find any relation between steatosis grade, lobular inflammation, hepatocellular ballooning, NAFLD activity score and fibrosis with MPV value. Among the insulin resistant and sensitive groups in the NAFLD patients MPV values were similar. The results of this study showed that MPV, an indicator of platelet activation, increased in biopsy proven NAFLD patients but MPV is not correlated with the increase of IR in NAFLD patients. MPV is not related with inflammation and steatosis degree, hepatocellular ballooning and fibrosis in NAFLD patients.     

Non-alcoholic fatty liver disease in subjects with type 2 diabetes mellitus and non-diabetics with special reference to insulin resistance and hepatic histopathological changes

AimsNon alcoholic fatty liver disease (NAFLD) includes simple steatosis and non alcoholic steatohepatitis (NASH). The present study was intended to evaluate insulin resistance (IR) in patients with NAFLD and correlate Insulin resistance [IR] with histopathological grades of liver involvement.Material and MethodsIt constituted of forty two consecutive patients (ultrasonographically established) with fatty liver admitted to our hospital. Ninteen were patients with Type 2 diabetes mellitus, 23 were normoglycemic and 12 age-matched healthy persons served as controls. IR was assessed by using HOMA-IR. Histopathological grading and staging of NAFLD was done as per Brunt system.ResultsDiabetics had significantly higher IR than both the other groups while non diabetics with NAFLD also had higher IR (p  < 001) than controls. There was no difference in the HDLc values between the three groups, whereas all other lipid parameters were higher in the patients. The IR was significantly higher 6.83(±2.51) in patients with grade 3 NASH as compared to patients with grade I changes 3.04(±1.58) (p < 0.05) irrespective of glycemic status. Similarly, the level of total cholesterol was significantly higher in patients with grade-3 NASH as compared to grade-1. Serum billirubin and liver enzymes (AST, ALT, ALP) were significantly higher in subjects with Grade 3 NASH when compared with Grade-1.ConclusionInsulin resistance and dyslipidemia rather than the glycemic status.were the determinant factors that had positive correlation with higher histopathological grades of NAFLD.     

Neuroprotective Role of Neurokinin B (NKB) on β-amyloid (25–35) Induced Toxicity in Aging Rat Brain Synaptosomes: Involvement in Oxidative Stress and Excitotoxicity

The brain tissue has a large oxidative capacity, but its ability to combat oxidative stress is limited. In aging brain tissue the oxidative stress increases due to decreased activity of antioxidant enzymes and increased oxidative stress leading to neurodegeneration associated with excitotoxicity. The aim of the present study was to determine the effect of neuropeptides, neurokinin B (NKB) and amyloid beta protein fragment Aβ (25–35) and neurotransmitters N-methyl d-aspartate (NMDA) and Glutamate on rat brain synaptosomes of different age groups. Aging brain functions were assessed by measuring the activities of superoxide dismutase (Mn-SOD) and monoamine oxidase (MAO) and intrasynaptosomal [Ca²⁺]_i levels in presence of neuropeptides and neurotransmitters. Increase in age decreased the SOD and MAO enzyme activities; Aβ (25–35) addition further had damaging/toxic effects on the enzymes, whereas NKB alone and in combination with amyloid lowered the toxic effects caused by Aβ (25–35) addition, which was concentration (peptide) and age dependent. Oxidative stress and excitotoxicity are major consequences associated with the age, [Ca²⁺]_i was increased with the age and the neuropeptides and neurotransmitters elicited significant modulatory effects on it. Our study elucidates an increased activity of SOD, decreased activity of MAO and restoration of [Ca²⁺]_i levels in the presence of NKB and suggests an antioxidant, neuromodulatory and neuroprotective role of tachykinin peptide NKB against the beta amyloid induced toxicity.     

非酒精性脂肪肝患者血浆抵抗素水平测定及与胰岛素抵抗的相关性

目的 探讨血浆抵抗素水平变化在非酒精性脂肪肝（NAFLD）发病中的作用及与胰岛素抵抗（IR）的关系。方法选择32例单纯NAFLD患者（F组）、29例NAFLD并2型糖尿病患者（FD组）和30例体检正常者（对照组）,分别测定空腹血浆抵抗素、空腹血糖（FPG）及胰岛素（FINS）水平,计算胰岛素敏感指数（ISI）,并分析其相关性。结果F组和FD组血浆抵抗素水平、FINS及ISI均明显高于对照组,尤以FD组为著;且血浆抵抗素水平与FINS、FPG呈正相关,与ISI呈负相关。结论NAFLD患者血浆抵抗素水平升高（尤以并2型糖尿病者为著）,并与ISI呈负相关;此可能在NAFLD等IR相关性疾病的发生、发展中具有一定作用。     

非酒精性脂肪肝血尿酸水平与胰岛素抵抗的相关性

目的:研究非酒精性脂肪肝(non-alcoholic fatty liver,NAFL)患者血尿酸水平及其与胰岛素抵抗程度的相关性.方法:选取单纯NAFL患者40例,NAFL合并2型糖尿病患者(type2diabetes mellitus,T2DM)72例,健康体检者62名为研究对象.测定体重指数(body mass index,BMI),检测空腹血糖(fasting blood glucose,FBG)、尿酸(serum uric acid,SUA)、丙氨酸氨基转移酶(alanine aminotransferase,ALT)、门冬氨酸氨基转移酶(aspartate aminotransferase,AST)、胆固醇(cholesterol,TC)、甘油三酯(triglyceride,TG)、糖化血红蛋白(glycated hemoglobin,HbA1C)、尿微量白蛋白/尿肌酐(Ualb/UCr)等生化指标并行肝脏B超检查.放射免疫法测定空腹胰岛素(fasting insulin,FINS),计算胰岛素抵抗指数(HOMA IR).结果:NAFL合并T2DM组BMI、SUA、ALT、AST、TG、FBG、FINS、HOMA IR、HbA1C、Ualb/UCr、SF均高于对照组;与单纯NAFL比较,NAFL合并T2DM组胰岛素抵抗及SUA水平更重;相关性研究表明FBG、HOMA IR、HbA1C与SUA呈正相关.结论:NAFL患者存在明显的胰岛素抵抗及高血尿酸血症,且两者具有一定的相关性.降低胰岛素抵抗联合纠正尿酸代谢紊乱对防止NAFL的发生发展具有重要的临床意义.     

Monoamine oxidase and acetylcholinesterase in the neurohypophysis of the hagfish, Eptatretus burgeri

The peripheral region of both dorsal and ventral walls of the neurohypophyseal sac of the hagfish, Eptatretus burgeri, showed strong monoamine oxidase (MAO) activity. Acetylcholinesterase (AChE) activity was detected only in the dorsal wall anterior to the infundibular stalk and in the ventral wall, except for the ependymal cells. AChE was not detected in the dorsal wall posterior to the stalk, where aldehyde-fuchsin-positive material is deposited. From these distribution patterns of MAO and AChE the identity of the structural specializations of the neurohypophysis are discussed as compared with distributions of MAO and AChE in the median eminence and the pars nervosa of higher vertebrates.     

The Association of Metabolic Syndrome, Insulin Resistance and Non-alcoholic Fatty Liver Disease in Overweight/Obese Children

Background/Aim:

To study the prevalence of metabolic syndrome (MS), insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD) in overweight/obese children with clinical hepatomegaly and/or raised alanine aminotransferase (ALT).

Patients and Methods:

Thirty-three overweight and obese children, aged 2-13 years, presenting with hepatomegaly and/or raised ALT, were studied for the prevalence of MS, IR and NAFLD. Laboratory analysis included fasting blood glucose, serum insulin, serum triglycerides (TG), total cholesterol, high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c) and liver biochemical profile, in addition to liver ultrasound and liver biopsy.

Results:

Twenty patients (60.6%) were labeled with MS. IR was present in 16 (48.4%). Fifteen (44%) patients had biopsy-proven NAFLD. Patients with MS were more likely to have NAFLD by biopsy (P=0.001). Children with NAFLD had significantly higher body mass index, waist circumference, ALT, total cholesterol, LDL-c, TG, fasting insulin, and lower HDL-c compared to patients with normal liver histology (P< 0.05) and fitted more with the criteria of MS (80% vs. 44%). IR was significantly more common among NAFLD patients (73% vs. 28%).

Conclusion:

There is a close association between obesity, MS, IR and NAFLD. Obese children with clinical or biochemical hepatic abnormalities are prone to suffer from MS, IR and NAFLD.     

Diagnostic and therapeutic implications of the association between ferritin level and severity of nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD), defined by excessive liver fat deposition related to the metabolic syndrome, is a leading cause of progressive liver disease, for which accurate non-invasive staging systems and effective treatments are still lacking. Evidence has shown that increased ferritin levels are associated with the metabolic insulin resistance syndrome, and higher hepatic iron and fat content. Hyperferritinemia and iron stores have been associated with the severity of liver damage in NAFLD, and iron depletion reduced insulin resistance and liver enzymes. Recently, Kowdley et al demonstrated in a multicenter study in 628 adult patients with NAFLD from the NAFLD-clinical research network database with central re-evaluation of liver histology and iron staining that the increased serum ferritin level is an independent predictor of liver damage in patients with NAFLD, and is useful to identify NAFLD patients at risk of non-alcoholic steatohepatitis and advanced fibrosis. These data indicate that incorporation of serum ferritin level may improve the performance of noninvasive scoring of liver damage in patients with NAFLD, and that iron depletion still represents an attractive therapeutic target to prevent the progression of liver damage in these patients.     

非酒精性脂肪性肝病胰岛素抵抗程度与全血细胞计数的相关性

目的探讨伴或不伴2型糖尿病(T2DM)的非酒精性脂肪性肝病(NAFLD)胰岛素抵抗(IR)程度与全血细胞计数各参数的相关性。方法选取糖耐量正常并除外糖尿病史的单纯NAFLD患者102例,T2DM合并NAFLD患者104例,正常对照104例为研究对象,测定空腹血糖(FPG)、空腹胰岛素(FINS)和全血细胞计数,分析胰岛素抵抗指数(HOMA-IR)与全血细胞计数各参数的相关性。结果 T2DM合并NAFLD患者IR及全血细胞计数异常程度较单纯NAFLD患者更重;相关性研究表明男性HOMA-IR与WBC、NEU、LYM、RBC、HGB、HCT呈正相关,女性HOMA-IR与WBC、NEU、LYM、MID、RBC、HGB、HCT呈正相关。结论 NAFLD时白细胞参数和红细胞参数的变化与IR密切相关,T2DM的存在加重了IR对上述血细胞参数的影响。全血细胞计数可以作为反映NAFLD患者IR程度的一种简单实用的检验指标。     

Effect of L-dopa administration on islet monoamine oxidase activity and glucose-induced insulin release in the mouse

Previous studies have shown that the amine precursor L-3,4-dihydroxyphenylalanine (L-DOPA) is rapidly converted to its corresponding amine, dopamine, in islet beta-cells. In the present investigation, we studied the effect of acute L-DOPA administration on islet monoamine oxidase (MAO) activity and on glucose-induced insulin secretory response in mice. It was observed that at 2 min after intravenous L-DOPA administration, there was a marked increase (+35%) in islet MAO activity, with serotonin as substrate. At 7 min, MAO activity towards dopamine was enhanced by 32% and that towards serotonin and phenylethylamine (PEA) was decreased by 23 and 25%, respectively. The inhibitor of L-aromatic amino acid decarboxylase, benserazide, abolished L-DOPA-induced changes of MAO activity, suggesting that the formed dopamine, and not L-DOPA itself, was responsible for the observed effects. At 60 min, no effect by L-DOPA administration on islet MAO activity was noticed. L-DOPA (125 or 250 mumol/kg), given together with glucose, induced a decrease in glucose-induced insulin response. L-DOPA (125 mumol/kg), given 7 min before glucose, totally suppressed glucose-induced insulin response. This inhibition was eliminated through pretreatment with benserazide. Enhancement of glucose-stimulated insulin response, after deposition of horseradish peroxidase (HRP) in beta-cell vacuolar system, was suppressed by L-DOPA. We conclude that acute L-DOPA-induced dopamine accumulation in pancreatic islets is accompanied by rapid changes in MAO activity, concomitant with an inhibitory effect on glucose-stimulated insulin response. Increased hydrogen peroxide production, following increased MAO activity, may possibly augment the inhibitory effect of dopamine accumulation on insulin release.     

改善胰岛素抵抗治疗NAFLD/NASH的循证证据

非酒精性脂肪性肝病/非酒精性脂肪性肝炎(NAFLD/NASH)是指除外酒精和其他明确的肝损伤因素所致的以肝细胞脂肪沉积为特征的临床病理综合征。胰岛素抵抗(IR)与NAFLD/NASH的发病密切相关,因此改善IR或许可以减轻肝损伤。多项随机对照临床试验显示胰岛素增敏剂和逐渐减轻体质量(饮食疗法或体育锻炼等)对NAFLD的治疗有一定作用,但长期疗效尚不明确。本文对近年关于改善IR治疗NAFLD/NASH的临床试验作一综述。     

Antioxidant properties of statins

Statins block expression of protein subunits of Gi-proteins (p22phox and gp91phox) which determine oxidase activity of NADPH oxidases and expression of GTP-ase (NADPH activator). This leads to suppression of activity of prooxidant enzyme systems (NADPH oxidase, xanthine oxidase, oxidase activity of endothelial NO-synthase) and diminishment of production of most aggressive free radicals -- superoxide anion and peroxinitrite. Hyperproduction of these radicals is associated with lowering of nitric oxide (NO) level and augmented NO destruction, the state of oxidative stress and endothelial dysfunction. Statins increase expression of enzymes with antioxidant properties (catalases, paroxonases), augment resistance of low density lipoproteins to oxidation, decrease take up of oxidized low density lipoproteins by monocytes and differentiation of monocytes into macrophages at the account of suppression of cellular scavenger receptor CD36 gene expression. Thus statins are powerful antioxidants.