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Naveed Sattar

Publications and source records attributed to Naveed Sattar.

At least 37 records · Page 2Linked to original sources
PubMed2006

Inflammatory suppression rapidly attenuates microvascular dysfunction in rheumatoid arthritis.

Rheumatoid arthritis (RA) is associated with greater risk of cardiovascular morbidity and mortality, the inflammatory component of RA being strongly linked to this excess risk. Endothelial dysfunction is linked to atherosclerosis and has been demonstrated in larger vessels in RA. In this pilot study, we determined for the first time whether skin microvascular function was impaired in patients with active RA and also determined its response to anti-inflammatory treatment. This was assessed non-invasively using laser Doppler imaging combined with iontophoresis of the vasodilators acetylcholine (ACh, endothelium dependent) and sodium nitroprusside (SNP, endothelium independent) to the forearm. Eight RA patients admitted for acute flare-ups were assessed before and following anti-inflammatory treatment. Standard laboratory indices were obtained along with pain perception (VAS). A control group of eight subjects was included for baseline comparison. Compared to this group, vascular function was substantially and significantly (P<0.00001) lower in RA patients. Following treatment, as CRP and VAS decreased, vascular function improved for both ACh (P<0.00001) and SNP (P=0.001), this improvement being significantly greater for ACh (P<0.001). Vascular dysfunction is evident in RA patients, even at the level of the cutaneous microcirculation, but improves as inflammation regresses. Assessment of cutaneous vascular function may be a useful, non-invasive surrogate indicator of vascular risk in RA, inclusive of myocardial microvascular abnormalities.

Acetylcholine↗
PubMed2006

Plasma leptin: associations with metabolic, inflammatory and haemostatic risk factors for cardiovascular disease.

BACKGROUND AND AIM: Leptin, an adipocyte-derived protein, regulating food intake and metabolism has been implicated in the development of coronary heart disease. We have examined the relationship between leptin and vascular risk factors including insulin resistance, metabolic, inflammatory and haemostatic risk factors. METHODS AND RESULTS: The study was carried out in 3640 non-diabetic men aged 60-79 years drawn from general practices in 24 British towns and who were not on warfarin. Leptin was strongly positively correlated with waist circumference (r=0.58; p<0.0001). Leptin concentrations decreased significantly with increasing physical activity and were lowered in cigarette smokers and elevated in men with pre-existing coronary heart disease and stroke; alcohol intake showed no association with leptin concentration. After adjustment for waist circumference and these lifestyle factors, increased leptin was independently associated with significant increases in insulin resistance, triglycerides, inflammatory markers (interleukin-6, C-reactive protein, fibrinogen, plasma viscosity), coagulation factor VIII, endothelial markers von Willebrand factor, tissue plasminogen activator, and fibrin D-dimer levels; and a decrease in HDL-cholesterol. No association was seen between leptin and blood pressure, total cholesterol, glucose or white cell count after adjusting for waist circumference. Further adjustment for insulin resistance abolished the relationships between leptin and triglycerides and HDL-cholesterol, weakened the associations with the haemostatic factors although they remained significant, but made minor differences to the associations with inflammatory markers. CONCLUSION: Plasma leptin is associated with insulin resistance, inflammation and disturbances in haemostasis independent of waist circumference, suggesting possible pathways by which leptin may influence risk of cardiovascular disease.

Aged↗
PubMed2006

Microvascular function, metabolic syndrome, and novel risk factor status in women with cardiac syndrome X.

To characterize microvascular function, candidate risk pathways, and metabolic syndrome prevalence in women with cardiac syndrome X, 52 nondiabetic women with angiographically normal epicardial arteries but >1 mm of planar ST depression during exercise testing (patients) and 24 healthy controls of similar age were recruited. In addition to fasting blood samples and anthropometric measurements, forearm cutaneous microvascular function after iontophoresis of acetylcholine and sodium nitroprusside was assessed by laser Doppler imaging. Despite body mass index correction and a larger proportion on statin therapy, patients had high levels of insulin (p=0.016), triglycerides (p=0.018), intercellular adhesion molecule-1 (p=0.021), von Willebrand factor (p=0.005), and leptin (p=0.005) and lower levels of high-density lipoprotein cholesterol (p=0.042) compared with controls. Consistent with these data, 30% of patients but only 8% of controls fulfilled criteria for the metabolic syndrome as defined by the National Cholesterol Education Program (p=0.015). Endothelium-dependent and -independent microvascular functions were markedly impaired in patients (p<0.001), and the odds ratio for cardiac syndrome X was 7.38 (95% confidence interval 2.2 to 24.7) if the acetylcholine response was <8,710 flux units. In conclusion, women with cardiac syndrome X more commonly have metabolic syndrome and related adiposity, metabolic, and inflammatory derangements. They also have significantly impaired skin microvascular function as assessed by laser Doppler imaging, consistent with generalized vascular dysfunction, a finding with potential diagnostic implications.

Acetylcholine↗
PubMed2006

Insight into the nature of the CRP-coronary event association using Mendelian randomization.

BACKGROUND: It is unclear wheather the association between C-reactive protein (CRP) and incident coronary events is free from bias and confounding. Individuals homozygous for a +1444C>T polymorphism in the CRP gene have higher circulating concentrations of CRP. Since the distribution of this polymorphism occurs at random during gamete formation, its association with coronary events should not be biased or confounded. METHODS: We calculated the weighted mean difference in CRP between individuals with variants of the +1444C>T polymorphism in the CRP gene among 4,659 European men from six studies (genotype-intermediate phenotype studies). We used this difference together with data from previous observational studies to compute an expected odds ratio (OR) for non-fatal myocardial infarction (MI) among individuals homozygous for the T allele. We then performed four new genetic association studies (6,201 European men) to obtain a summary OR for the association between the +1444C>T polymorphism and non-fatal MI (genotype-disease studies). RESULTS: CRP was 0.68 mg/l [95% confidence interval (95% CI) 0.31-1.10; P = 0.0001] higher among subjects homozygous for the +1444-T allele, with no confounding by a range of covariates. The expected ORs among TT subjects for non-fatal MI corresponding to this difference in CRP was 1.20 (95% CI 1.07-1.38) using the Reykjavik Heart study data and 1.25 (1.09-1.43) for all observational studies to 2004. The estimate for the observed adjusted-OR for non-fatal MI among TT subjects was 1.01 (95% CI 0.74-1.38), lower than both expected ORs. CONCLUSIONS: A common CRP gene polymorphism is associated with important differences in CRP concentrations, free from confounding. The null association of this variant with coronary events suggests possible residual confounding (or reverse causation) in the CRP-coronary event association in observational studies, though the confidence limits are still compatible with a modest causal effect. Additional studies of genotype (or haplotype) and coronary events would help clarify whether or not the link between CRP and coronary events in observational studies is causal.

C-Reactive Protein↗
PubMed2006

CVD risk factors and ethnicity--a homogeneous relationship?

Current understanding of cardiovascular disease risk (CVD) is derived largely from studies of Caucasians of European origin. However, people of certain ethnic groups experience a disproportionately greater burden of CVD including coronary heart disease (CHD) and stroke. Adoption of a Westernised lifestyle has different effects on metabolic and vascular dysfunction across populations, e.g. South Asians have a higher prevalence of coronary heart disease (CHD) and cardiovascular mortality compared with Europeans. African-Americans demonstrate higher rates of CHD and stroke while African/Caribbeans in the UK have lower CHD rates and higher stroke rates than British Europeans. Other non-European groups such as the Chinese and Japanese exhibit consistently high rates of stroke but not CHD, while Mexican Americans have a higher prevalence of both stroke and CHD, and North American native Indians also have high rates of CHD. While conventional cardiovascular risk factors such as smoking, blood pressure and total cholesterol predict risk within these ethnic groups, they do not fully account for the differences in risk between ethnic groups, suggesting that alternative explanations might exist. Ethnic groups show differences in levels of visceral adiposity, insulin resistance, and novel risk markers such as C-reactive protein (CRP), adiponectin and plasma homocysteine. The marked differences across racial and ethnic groups in disease risk are likely due in part to each of genetic, host susceptibility and environmental factors, and can provide valuable aetiological clues to differences in patterns of disease presentation, therapeutic needs and response to treatment. Ongoing studies should increase understanding of ethnicity as a potential independent risk factor, thus enabling better identification of treatment targets and selection of therapy in specific populations.

Biomarkers↗
PubMed2006

Vitamin antioxidants, lipid peroxidation and the systemic inflammatory response in patients with prostate cancer.

The relationship between lipid soluble antioxidant vitamins, lipid peroxidation, disease stage and the systemic inflammatory response were examined in healthy subjects (n = 14), patients with benign prostate hyperplasia BPH (n = 20), localized (n = 40) and metastatic (n = 38) prostate cancer. Prostate cancer patients had higher concentrations of malondialdehyde (p < 0.05) and lower circulating concentrations of lutein (p < 0.05), lycopene (p < 0.001) and beta-carotene (p < 0.05). Patients with metastatic prostate cancer, when compared with patients having localized disease, had a higher Gleason score (p < 0.01) and had more hormonal treatment, but lower concentrations of PSA (p < 0.05), alpha-tocopherol (p < or = 0.05), retinol (p < 0.01), lutein (p < 0.05) and lycopene (p < 0.01). In the prostate cancer patients, PSA was correlated with the concentrations of the lipid peroxidation product, malondialdehyde (rs= 0.353, p = 0.002). C-reactive protein was not correlated with the vitamin antioxidants nor malondialdehyde. In contrast, there was a negative correlation between malondialdehyde concentrations and both lutein (rs= -0.263, p = 0.020) and lycopene (rs= -0.269, p = 0.017). These results indicate that lower concentrations of carotenoids, in particular, lycopene reflect disease progression rather than the systemic inflammatory response in patients with prostate cancer.

Aged↗
PubMed2006

Effects of acquired obesity on endothelial function in monozygotic twins.

OBJECTIVE: To determine whether acquired obesity or accompanying metabolic changes such as adiponectin deficiency, insulin resistance, dyslipidemia, or visceral fat are associated, independent of genetic influences, with endothelial dysfunction by studying young adult monozygotic (MZ) twin pairs discordant for obesity. RESEARCH METHODS AND PROCEDURES: Nine obesity-discordant (intra-pair difference in BMI, 3.8 to 10.1 kg/m(2)) and nine concordant (0 to 2.3 kg/m(2)) 24- to 27-year-old MZ twin pairs were identified from a population-based FinnTwin16-sample. Endothelial function was measured by blood flow responses to intrabrachial infusions of an endothelium-dependent (acetylcholine) and an endothelium-independent (sodium nitroprusside) vasodilator. Whole body insulin sensitivity was measured using the euglycemic insulin clamp technique, and forearm and body composition were measured with magnetic resonance imaging and DXA. In addition, serum levels of adiponectin, high-sensitivity C-reactive protein, and lipids were determined. RESULTS: The heavier co-twins of the discordant pairs had significantly lower whole body insulin sensitivity than the leaner co-twins. Blood flows/muscle volume during infusions of acetylcholine and sodium nitroprusside were not altered by obesity. However, intra-pair differences in serum adiponectin, intra-abdominal fat, and C-reactive protein were significantly correlated with those in endothelial function. Only the relationship between intra-pair differences in adiponectin and endothelial function persisted in multiple linear regression analysis. Obesity-concordant co-twins had comparable insulin sensitivity and endothelial function. DISCUSSION: In young adult MZ twins discordant for obesity, acquired adiponectin deficiency rather than obesity per se is an independent correlate of endothelial dysfunction.

Acetylcholine↗
PubMed2006

"Anti-inflammatory" drugs and their effects on type 2 diabetes.

There is a growing body of evidence for the role of inflammation in type 2 diabetes. In addition to the evidence presented elsewhere, evidence is emerging that many drugs that have apparent "anti-inflammatory" properties may reduce the incidence and/or delay the onset of type 2 diabetes. Statins have been found to lower inflammatory markers, and a post hoc analysis of the West of Scotland Coronary Prevention Study (WOSCOPS) suggested that pravastatin may reduce the risk of developing diabetes, although the Lipid Lowering Arm of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) found no statistically significant effect of atorvastatin on risk of developing diabetes. Fibrates have been found to lower some markers of inflammation, and a prospective trial found that bezafibrate reduces risk of developing diabetes. Angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers appear to reduce some markers of inflammation, and a meta-analysis concluded that ACE inhibitors and angiotensin receptor blockers reduce risk of developing type 2 diabetes. Metformin is known to reduce the risk of developing diabetes, and more recent evidence suggests it also lowers C-reactive protein, in part because of its modest weight-reducing effect. Thiazolidinediones reduce risk of developing diabetes, and consistently lower inflammatory markers independent of adiposity effects. High-dose aspirin inhibits cyclooxygenase and IkappaB kinase-beta and reduces fasting plasma glucose concentration, although there has not, as yet, been a large-scale trial to examine the effect of aspirin on the risk of developing diabetes. We conclude that although many drugs with potential anti-inflammatory properties reduce the risk of developing diabetes, it is difficult to prove that such anti-inflammatory properties contribute to their diabetes prevention since nearly all drugs have other, often more pronounced, actions. Studies with more specific inhibitors of inflammatory pathways (e.g., interleukin- 6 blockers) and mendelian randomization (genetic studies) will help determine whether targeting the inflammation axis is a fertile mechanism to treat or prevent type 2 diabetes.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

The metabolic syndrome: should current criteria influence clinical practice?

PURPOSE OF REVIEW: Many studies have recommended use of metabolic syndrome as an 'alternative' means to assess vascular disease risk, but few have been rigorous, leading to confusion amongst physicians regarding risk screening. This review critically appraises this evidence and also evaluates the data linking metabolic syndrome to type 2 diabetes. RECENT FINDINGS: Although presence of metabolic syndrome predicts vascular events, such prediction is inferior and does not enhance simpler Framingham-based risk scores which can be determined using nonfasting blood samples. The dichotomous nature of metabolic syndrome criteria and lack of age, low-density lipoprotein cholesterol, and smoking in part account for their inferior predictive ability. Metabolic syndrome criteria better predict type 2 diabetes but diabetes screening, if adopted, will likely require a two-stage process, with the first stage not dependent on blood sampling. Nevertheless, recent interest in metabolic syndrome has contributed to greater interaction between diabetologists and cardiologists and highlighted more strongly the relevance of obesity to vascular risk. SUMMARY: Best evidence suggests that current metabolic syndrome criteria should not be used as an alternative to established charts for risk prediction for vascular disease. Clinical focus should remain on established risk factors to determine and reduce risk of vascular events.

Cardiovascular Diseases↗
PubMed2006

Effects of HRT on liver enzyme levels in women with type 2 diabetes: a randomized placebo-controlled trial.

BACKGROUND: Increasingly strong links are being recognized between diabetes, insulin resistance and liver fat accumulation [e.g. nonalcoholic fatty liver disease (NAFLD)]. Recent data indicating that hormone replacement therapy (HRT) may lessen diabetes risk is intriguing but explanatory mechanisms are unclear. OBJECTIVE: Post hoc investigation of the possibility that HRT may favourably influence liver enzyme levels commonly elevated in patients with diabetes. We examined liver function test data from a 6-month trial of a low-dose continuous combined HRT (1 mg 17beta oestradiol and 0.5 mg norethisterone acetate). DESIGN: Double-blind, randomized placebo-controlled. PATIENTS: Fifty women with type 2 diabetes. MEASUREMENTS: Liver enzyme levels (AST, ALT, gamma-glutamylytransferase [GGT], and alkaline phosphatase [ALP]). RESULTS: Forty-five women completed the study with 19/22 in the active group demonstrating compliance as measured by sex hormone changes. Relative to placebo recipients (n = 23), women randomized and compliant to HRT demonstrated significant reductions in ALT [-14 (-23 to -6) U/l, P = 0.002], AST [-9.2 (-14 to -5) U/l, P < 0.001] and ALP [-60.8 (-80 to -42) U/l, P < 0.001]. Circulating concentrations in GGT were also significantly reduced (P = 0.035). All changes were significant using an intention-to-treat analysis. CONCLUSION: HRT containing low-dose oestradiol and norethisterone reduces serum concentrations of liver function enzymes, potentially due to a lowering of liver fat accumulation. Better understanding of mechanisms by which this HRT improves liver function tests could help the design of new therapies to treat individuals with NAFLD.

Aged↗
PubMed2006

High sensitivity C-reactive protein and cardiovascular disease: an association built on unstable foundations?

There is considerable interest in the inflammatory hypothesis of vascular disease. Markers of inflammation predict vascular events, and inflammatory cells and molecules are critical elements within plaques and are especially prominent in unstable lesions. With respect to screening, concentrations of C-reactive protein (CRP), as determined by high-sensitivity assays, have been consistently shown to predict myocardial infarction and other vascular events independently of traditional risk factors. As a result, some authorities proposed potential inclusion of CRP in risk factor stratification. However, more recent evidence in the last two years from larger studies suggests that CRP concentrations are only around as half as predictive for vascular events as suggested in earlier reports. Furthermore, it now appears as if CRP measurements add little additional predictive value to current coronary heart disease risk prediction charts. The short-term variability of CRP is also problematic for risk factor screening. At the same time, other recent evidence questions the proposed causal role of CRP in atherogenesis. Therefore, the current focus in clinical practice should remain on established risk factors (e.g. smoking, lipids and blood pressure), both to determine coronary heart disease risk and to reduce it.

Biomarkers↗
PubMed2005

Plasma adiponectin levels are associated with insulin resistance, but do not predict future risk of coronary heart disease in women.

CONTEXT: Low adiponectin levels predict type 2 diabetes, and one prospective study in men reported its independent prediction of vascular events. Many observers thus already consider adiponectin to be a major part of the "common soil" underpinning diabetes and vascular disease. OBJECTIVE: The objective of this study was to assess the association between adiponectin and incident coronary heart disease (CHD) risk in the British Women's Heart and Health Study. DESIGN: This was a prospective (4 yr) case (n = 167) control (n = 334) study nested within the 4286 women in British Women's Heart and Health Study. SETTING: The study was performed in a primary care setting. PARTICIPANTS: The study consisted of women (n = 4286) randomly selected from 23 British towns between 1999 and 2001, who were 60-79 yr of age at baseline. MAIN OUTCOME MEASURES: Association of adiponectin with CHD risk factors and incident CHD events were the main outcome measures. RESULTS: Among both cases and controls, adiponectin positively correlated with age and high-density lipoprotein cholesterol and inversely correlated with waist to hip ratio, fasting insulin, fasting glucose, homeostasis model assessment of insulin resistance scores, C-reactive protein, and triglycerides. However, despite adequate power and these associations with CHD risk factors, adiponectin did not predict CHD events in unadjusted or adjusted analyses. The relative risk ratio for a doubling of adiponectin was 0.93 (95% confidence interval, 0.78, 1.11). CONCLUSIONS: It is premature to consider adiponectin as a root for vascular disease in women despite its association with insulin resistance and diabetes. Additional prospective studies are required to determine whether there is a true sex difference in the effect of adiponectin on CHD.

Adiponectin↗
PubMed2005

Effects of a moderate exercise session on postprandial lipoproteins, apolipoproteins and lipoprotein remnants in middle-aged men.

Prior moderate exercise reduces postprandial triglyceride concentrations. Its effects on the concentrations, compositions and potential atherogenicity of lipoprotein subfractions were investigated in the present study. Twenty normoglycaemic middle-aged men each underwent two fat tolerance tests (blood taken fasting and for 8 h after a meal containing 80 g fat and 70 g carbohydrate). On the afternoon before one test, subjects performed a 90-min treadmill walk (exercise); no exercise was performed before the control test. Prior exercise significantly reduced postprandial concentrations of chylomicrons (Sf >400) by 28.6% (absolute reduction 14.6 mg dl(-1)), of large VLDL1 (Sf 60-400) by 34.4% (39.7 mg dl(-1)) and of small VLDL2 (Sf 20-60) by 23.0% (9.6 mg dl(-1)). Over 95% of VLDL1 and VLDL2 comprised apolipoprotein (apo) B100-containing particles. Exercise also reduced postprandial remnant-like lipoprotein cholesterol (by 35%) and triglyceride concentrations (by 29%). Postprandial apo CIII/apo B and apo E/apo B ratios in VLDL1 were lower following exercise. Postprandial cholesteryl ester/triglyceride ratios were lower in VLDL1 and VLDL2 and higher in HDL2 following exercise. These data suggest that the effect of prior moderate exercise on VLDL1 is quantitatively greater than its effect on chylomicrons and that, in addition to reducing lipoprotein concentrations, exercise induces compositional changes to lipoprotein species which are likely to influence their metabolism and atherogenicity.

Apolipoproteins↗
PubMed2005

The associations of physical activity and adiposity with alanine aminotransferase and gamma-glutamyltransferase.

The mechanisms linking obesity and inactivity to diabetes mellitus are unclear. Recent studies have shown associations of alanine aminotransferase (ALT) and gamma-glutamyltransferase (GGT) with diabetes. In a random sample of 3,789 British women aged 60-79 years, the authors examined the associations of obesity and physical activity with ALT and GGT (1999-2001). Both body mass index and waist:hip ratio were independently (of each other, physical activity, alcohol consumption, smoking, and childhood and adulthood social class) positively and linearly associated with ALT and GGT. In adjusted models, a one-standard-deviation increase in body mass index was associated with a 0.46-units/liter (95% confidence interval (CI): 0.16, 0.75) increase in ALT and a 2.14-units/liter (95% CI: 0.99, 3.30) increase in GGT. Similar results for a one-standard-deviation increase in waist:hip ratio were 13.96 (95% CI: 10.44, 17.48) for ALT and 39.44 (95% CI: 25.89, 52.98) for GGT. Frequency of physical activity was inversely and linearly associated with GGT in fully adjusted models, but the inverse association with ALT was attenuated towards the null after adjustment for body mass index and waist:hip ratio. Adjustment for ALT and GGT resulted in some attenuation of the strong linear associations of body mass index and waist:hip ratio with diabetes. These findings provide some support for the suggestion that the relation between obesity and diabetes is, at least in part, mediated by liver pathology.

Adipose Tissue↗
PubMed2005

Metformin and weight loss in obese women with polycystic ovary syndrome: comparison of doses.

CONTEXT: Metformin treatment of women with polycystic ovary syndrome (PCOS) is widespread, as determined by studies with diverse patient populations. No comparative examination of weight changes or metabolite responses to different doses has been reported. OBJECTIVE: The aim of this study was to determine whether different doses of metformin (1500 or 2550 mg/d) would have different effects on body weight, circulating hormones, markers of inflammation, and lipid profiles. DESIGN: The study included prospective cohorts randomized to two doses of metformin. SETTING: The study was performed at a university teaching hospital with patients from gynecology/endocrinology clinics. PATIENTS: The patients studied were obese (body mass index, 30 to <37 kg/m2; n = 42) and morbidly obese (body mass index, > or =37 kg/m2; n = 41) women with PCOS. INTERVENTION: Patients were randomized to two doses of metformin, and parameters were assessed after 4 and 8 months. MAIN OUTCOME MEASURES: The main outcome measures were changes in body mass, circulating hormones, markers of inflammation, and lipid profiles. RESULTS: Intention to treat analyses showed significant weight loss in both dose groups. Only the obese subgroup showed a dose relationship (1.5 and 3.6 kg in 1500- and 2550-mg groups, respectively; P = 0.04). The morbidly obese group showed similar reductions (3.9 and 3.8 kg) in both groups. Suppression of androstenedione was significant with both metformin doses, but there was no clear dose relationship. Generally, beneficial changes in lipid profiles were not related to dose. CONCLUSION: Weight loss is a feature of protracted metformin therapy in obese women with PCOS, with greater weight reduction potentially achievable with higher doses. Additional studies are required to determine whether other aspects of the disorder may benefit from the higher dose of metformin.

Administration, Oral↗
PubMed2005

Adiponectin predicts insulin resistance but not endothelial function in young, healthy adolescents.

BACKGROUND: Adiponectin, an adipocyte-derived hormone found in lower concentration with greater adiposity, is suggested to reduce the risk of insulin resistance, atherosclerosis, and cardiovascular disease. We tested this hypothesis in a healthy, nonobese population. METHODS AND RESULTS: Brachial artery flow-mediated endothelial-dependent vasodilation and distensibility, measures of vascular function relevant to the early atherosclerotic process, were determined in 294 adolescents (aged 13-16 yr) using high-resolution vascular ultrasound. Fasting insulin concentration and the homeostasis model assessment of insulin resistance were used to estimate insulin resistance. Fat mass was measured by bioelectric impedance analysis; fasting serum adiponectin concentration by RIA; and lipid profile, fasting insulin, glucose, and C-reactive protein concentrations using standard laboratory techniques. Adiponectin concentration was associated with insulin resistance independent of potential confounding factors (e.g. -1.3% change in fasting insulin concentration per 10% increase in adiponectin concentration; 95% confidence interval, -2.4% to -0.1%; P = 0.03), but not with flow-mediated endothelial-dependent vasodilation or arterial distensibility. CONCLUSIONS: Lower adiponectin concentration was associated with lower insulin sensitivity in a healthy, nonobese population. Our study supports the hypothesis that adiponectin benefits insulin sensitivity from a young age but, in contrast to experimental models and data from older subjects, does not affect vascular changes associated with early atherosclerosis.

Adiponectin↗