doi: 10.1161/hc5001.101061
(Circulation. 2001;104:3052.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Plasma Leptin and the Risk of Cardiovascular Disease in the West of Scotland Coronary Prevention Study (WOSCOPS)
From the Department of Pathological Biochemistry (A.M.W., C.J.P., A.K., J.S., N.S.), Clinical Trials Unit (A.G.), Glasgow Royal Infirmary, and Robertson Centre for Biostatistics (A.D.M.), University of Glasgow, Glasgow, Scotland.
Correspondence to Dr Naveed Sattar, Department of Pathological Biochemistry, 4th Floor QEB, Glasgow Royal Infirmary, Glasgow G31 2ER, UK. E-mail nsattar{at}clinmed.gla.ac.uk
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Abstract |
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Background— Leptin plays a role in fat metabolism and correlates with insulin resistance and other markers of the metabolic syndrome, independent of total adiposity. Therefore, we hypothesized that raised leptin levels may identify men at increased risk of a coronary event in the West of Scotland Coronary Prevention Study (WOSCOPS).
Methods and Results— Plasma leptin levels were measured at baseline in 377 men (cases) who subsequently experienced a coronary event and in 783 men (controls) who remained free of an event during the 5-year follow-up period of the study. Controls were matched to cases on the basis of age and smoking history and were representative of the entire WOSCOPS cohort. Leptin levels were significantly higher in cases than controls (5.87±2.04 ng/mL versus 5.04±2.09 ng/mL, P<0.001). In univariate analysis, for each 1 SD increase in leptin, the relative risk (RR) of an event increased by 1.25 (95% confidence interval [CI], 1.10 to 1.43; P<0.001). There was minimal change in this RR with correction for body mass index (RR, 1.24; 95% CI, 1.06 to 1.45; P=0.006) or with further correction for classic risk factors, including age, lipids, and systolic blood pressure (RR, 1.20; 95% CI, 1.02 to 1.42; P=0.03). Leptin correlated with C-reactive protein (r=0.24, P<0.001) and, even with this variable added to the model, leptin retained significance as a predictor of coronary events (RR, 1.18; 95% CI, 1.00 to 1.39; P=0.05) at the expense of C-reactive protein.
Conclusions— We show, for the first time, in a large prospective study that leptin is a novel, independent risk factor for coronary heart disease.
Key Words: adipocytes • insulin resistance • inflammation • cardiovascular diseases
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Introduction |
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Since the discovery that the adipocyte ob gene encodes leptin, a secreted protein that regulates body weight in mice,1 there has been intense interest in its potential metabolic role in humans. Leptin is hypothesized to be an "adiposity signal" for the long-term regulation of body weight by the brain. In accordance with this postulated role, leptin concentrations increase with obesity and correlate strongly with percent body fat in men and women.2
As a result of leptin’s role in fat metabolism and obesity, its potential association with insulin action has undergone intense investigation. Data from several different populations suggest strong positive correlations between leptin and insulin concentrations,3–5 and insulin-resistant men have higher leptin concentrations than those who are insulin-sensitive, independent of body fat mass.6 Similarly, a large epidemiological study of 2537 men and women from Mauritius showed a strong association between fasting insulin level and leptin concentration, independent of obesity (body mass index [BMI] and waist-hip ratio).7 Leptin also seems to correlate with other markers of the metabolic syndrome, such as plasma triglyceride and apolipoprotein B levels, and with systolic blood pressure, independent of BMI and glucose disposal rate.8 It is also positively associated with markers of impaired fibrinolysis.9 Further, preliminary data from our group10 have linked leptin to C-reactive protein (CRP), a marker of low-grade chronic inflammation and a robust predictor of risk for coronary heart disease (CHD). Finally, higher leptin levels predict subsequent development of obesity or type 2 diabetes in Japanese-Americans.11,12
In light of these observations, we hypothesized that raised leptin levels might signal an increased risk of vascular events; however, to date this relationship has been sparsely studied. We examined whether plasma leptin levels were linked with the risk of a coronary event in the West of Scotland Coronary Prevention Study (WOSCOPS), a landmark primary prevention trial that demonstrated the effectiveness of pravastatin in preventing coronary morbidity and mortality. We also determined whether such a link, if present, was independent of BMI, other classic risk factors (age, lipids, blood pressure), and CRP.
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Methods |
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The design of the original WOSCOPS and the prospective, nested, case-control study drawn from it have been previously described in detail.13,14 Briefly, moderately hypercholesterolemic men (LDL cholesterol, 4.5 to 6.0 mmol/L) who had not had a myocardial infarction and who did not exhibit other major clinical manifestations of coronary artery disease were randomized to a 5-year trial of pravastatin versus placebo. Pravastatin treatment significantly reduced a range of coronary events, including morbidity (myocardial infarction) and mortality and the need for revascularization.
In the case-control study, men who experienced a coronary event (n=580) during the trial were compared with age- and smoking-matched controls (on a 1:2 basis; hence, n=1160) in a series of studies designed to identify novel risk factors.14–16 In the present study, a reduced set of samples was available for leptin analysis (the remainder were exhausted); therefore, we used samples from 377 of the 580 cases (65%) and 783 of the 1160 controls (68%). The characteristics of the truncated groups of cases and controls were virtually identical to those seen in the complete set (compare Table 1 with Table 1 in reference 14). Again, the controls seemed to be a representative sample of the entire WOSCOPS cohort (Table 1). Plasma samples from all subjects were taken at screening (immediately before randomization) and stored frozen at -70°C. Aliquots of these were used for the measurement of potentially novel risk factors, including CRP and leptin, as described here.
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Laboratory Analyses
Major risk factors were assessed during recruitment. Plasma total cholesterol, triglyceride, very low-density lipoprotein (VLDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein (HDL) cholesterol levels were measured before randomization, and the baseline level was taken as the average.14 Plasma leptin was measured by an in-house radioimmunoassay that was validated thoroughly against the commercially available Linco assay.17 The intra-assay and interassay coefficients of variation were <7% and <10%, respectively, over the sample concentration range. The detection limit of the assay was 0.5 ng/mL. Details of the CRP assay are given in Reference 14.
Statistical Analyses
The baseline factors were compared individually between cases and controls using means and SDs for continuous variables and counts and percentages for categorical variables. Both leptin and CRP values were log-transformed to correct their skewed distributions. Univariate analyses were carried out by conditional logistic regression, which was suitable for the matched design. Results are presented in the form of relative risks (RR) and 95% confidence intervals (CI) for an incident coronary event over the 5 years of follow-up. For continuous variables, this is the change in risk for a 1 SD change, as calculated from the distribution of the variable in control subjects. In addition, RRs were calculated for quintiles of leptin at baseline (the cut-off points were calculated from the control subjects). The quintile of lowest leptin level was used as reference. Multivariate conditional regression models were also generated to test the independence of leptin as a predictor of risk. Associations of both leptin and CRP with the other risk factors were calculated for the control subjects using Spearman rank correlations. Adjusted partial correlations were also used.
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Results |
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The baseline characteristics of the cases and controls in the present study are shown in Table 1. Subjects who experienced a coronary event during the 5 years of trial follow-up were older, more likely to be smokers, had higher blood pressures and LDL cholesterol levels, and lower HDL cholesterol levels. A history of hypertension and nitrate use predicted coronary events in the trial itself, and the number of subjects with these characteristics differed between cases and controls in the present study (Table 1). Baseline leptin levels were 16% higher in the cases than controls (P<0.001). Further, in addition to BMI, lipids, systolic blood pressure, and CRP, leptin was found to be a univariate predictor of risk of a coronary event when tested as a continuous variable (Table 2). In univariate analysis, the RR of log leptin was identical in those given pravastatin and in those given placebo (RR=1.27; data not shown).
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When the group was divided into quintiles of baseline leptin level, it can be seen that risk rose 
2-fold when comparing the highest 2 quintiles with the lowest quintile (Figure 1). Risk levels associated with quintiles 4 and 5 remained significant at 1.68 (95% CI, 1.08 to 2.62) and 1.70 (95% CI, 1.05 to 2.76) after adjustment for classic risk factors. The possibility of a threshold effect on risk cannot be excluded by the present analysis because no increment in risk was evident between the lowest quintile (quintile 1) and the subsequent 2 cohorts (quintiles 2 and 3).
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Plasma leptin levels correlated strongly (P<0.001) with BMI, as expected, but they also correlated with plasma triglycerides, CRP, and fasting plasma glucose (Table 3). The associations of leptin with CRP, glucose, and triglycerides remained significant after adjustment for BMI (data not shown). Both leptin and CRP were weakly associated with systolic blood pressure (Table 3).
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The independence of leptin as a predictor of coronary events is explored in Table 4 and Figure 2. Adjustment for BMI hardly attenuated the association with risk for leptin (RR, 1.24; 95% CI, 1.06 to 1.45; P=0.006; Figure 2). Further adjustment for baseline lipids and systolic blood pressure also had only a minor effect (RR, 1.21; 95% CI, 1.02 to 1.42; P=0.02; Table 4 and Figure 2), as did adding glucose to this model (RR, 1.20; 95% CI, 1.02 to 1.42; P=0.03; Table 4). The addition of CRP to the model including classic risk factors and leptin (model A) resulted in the association of leptin with coronary risk shifting to borderline significance (RR, 1.18; 95% CI, 1.00 to 1.39; P=0.05; Table 4 and Figure 2). Finally, although CRP achieved borderline significance (P=0.05) as a predictor of CHD in a model including other major risk factors but excluding leptin (data not shown), the addition of leptin into the model resulted in CRP’s loss as an independent predictor (P=0.12; Table 4).
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Discussion |
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This is the first prospective study to show that higher plasma leptin concentrations in hypercholesterolemic men are associated with an increased risk of a future coronary event. This was true whether leptin was considered as a continuous variable or in quintiles of baseline value. Indeed, the significance of leptin was as strong as classic risk factors in univariate analysis (P<0.001), and the RR for a 1 SD change was as high as the RR for a 1 SD change in systolic blood pressure or HDL cholesterol. More importantly, we found that the predictive value of leptin was hardly altered by adjustment for BMI and was even maintained after adjustment for classic CHD risk factors. Finally, we note that after further adjustment for CRP, a marker of low-grade chronic inflammation, leptin retained a borderline significant association with risk, at the expense of CRP.
The results of this prospective study concur with a recent small, retrospective, case-control study from Northern Europe that reported plasma leptin concentration as an independent risk factor for first-ever acute myocardial infarction and first-ever hemorrhagic stroke.18,19 In contrast to the results of our study, a high plasma leptin concentration was not a predictor for ischemic heart disease in the Quebec cardiovascular study.20 The reason for this difference is unclear. However, it is noteworthy that although only cases with events (myocardial infarction or coronary revascularization) were included in our analysis, the Quebec study included "softer" end points, such as effort angina and coronary insufficiency. These may not be as strongly associated with leptin. The Quebec study was also smaller (86 cases and 95 controls).
We originally speculated that leptin might predict the risk of future coronary events after adjustment for BMI because, as noted previously, leptin correlates with established risk factors, such as plasma triglycerides and systolic blood pressure, independently of BMI.8 It is more surprising, however, that leptin retains its significance as a predictive marker once these traditional risk factors and fasting glucose are included in a multivariate analysis (model A). Part of the explanation for this latter observation may relate to the association of leptin with insulin resistance. Several investigators have reported correlations between plasma leptin and fasting plasma insulin independent of BMI,7,21,22 whereas others have shown that hyperleptinemia correlates with insulin resistance independent of changes in body weight.23 In line with these observations, leptin seems to predict subsequent development of type 2 diabetes, at least in populations tested thus far.12 Of course, associations between insulin resistance, diabetes, and cardiovascular risk are well-established.24 It would be of interest in future studies to examine leptin as a predictor of vascular risk in models incorporating more direct markers of insulin resistance, such as fasting insulin, although because of the needs for rapid sample centrifugation, separation, and storage, such studies are much more difficult to execute.
Leptin is an extremely robust circulating marker of percent fat mass (correlation coefficient >0.8 in many studies). Thus, its correlation with CRP is biologically plausible because both leptin and cytokines such as interleukin-6 (which promotes CRP secretion) are produced by adipocytes.2 Alternatively, because leptin increases as part of the acute phase response,25 hyperleptinemia may also be a sequel to low-grade chronic inflammation. In that regard, recent evidence suggests that CRP, like leptin, correlates with insulin resistance independently of BMI26 and that markers of inflammation predict risk of diabetes.27 Whatever the mechanism, leptin’s continued significance as a predictor of risk in the multivariate model at the expense of CRP is of considerable interest.
The mechanistic implications of our results are that leptin, perhaps as a circulating marker of percent fat mass or an independent correlate of insulin resistance or as a marker of some as-yet-unknown activity of adipose tissue, may yield important information with respect to risk of vascular disease. It is unlikely that leptin has direct atherogenic properties. Because our report represents a post-hoc analysis in an albeit large database, our results do not currently justify adding leptin to risk factor assessment. Instead, our data must be confirmed and extended to different sectors of the population, such as women, individuals with existing CHD, those with diabetes, and different ethnic groups. With respect to the latter, it is noteworthy that immigrant South Asian men and women have significantly higher leptin concentrations relative to individuals of European descent with similar BMIs. Thus, high leptin levels may be a part of the explanation for the high rates of CHD in this population. Our data also reinforce the benefits of exercise and improved diet, because both measures have been shown to reduce plasma leptin concentrations, independent of changes in body mass or, indeed, fat mass.28 Extension of our findings to other cohorts is readily possible because leptin is an extremely stable protein in serum or plasma, is not influenced by thawing, and is stable over long periods of time.
In conclusion, we have shown, for the first time, in a large prospective study that plasma leptin concentration is a novel, independent risk factor for coronary events. Our data provide further support for a link between adipocyte function and/or mass (rather than total BMI) and cardiovascular disease.
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Appendix |
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WOSCOPS Executive Committee
J. Shepherd, Department of Pathological Biochemistry, Glasgow Royal Infirmary; S.M Cobbe, Department of Medical Cardiology, Glasgow Royal Infirmary; I. Ford, Robertson Center for Biostatistics, Glasgow University; C.G Isles, Department of Medicine, Dumfries and Galloway Royal Infirmary; A.R. Lorimer, Department of Medical Cardiology, Glasgow Royal Infirmary; P.W. Macfarlane, Department of Medical Cardiology, Glasgow Royal Infirmary; J.H. McKillop, Department of Medicine, Glasgow Royal Infirmary; C.J. Packard, Department of Pathological Biochemistry, Glasgow Royal Infirmary.
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Acknowledgments |
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This work was supported by a project grant (PG 97/160) from the British Heart Foundation. The study Data Centre was supported by a grant from Bristol-Myers Squibb.
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Footnotes |
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This report was prepared on behalf of the WOSCOPS Executive Committee; members of this committee can be found in the Appendix.
Received August 13, 2001; revision received October 16, 2001; accepted October 17, 2001.
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References |
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S. Taleb, O. Herbin, H. Ait-Oufella, W. Verreth, P. Gourdy, V. Barateau, R. Merval, B. Esposito, K. Clement, P. Holvoet, et al. Defective Leptin/Leptin Receptor Signaling Improves Regulatory T Cell Immune Response and Protects Mice From Atherosclerosis Arterioscler Thromb Vasc Biol, December 1, 2007; 27(12): 2691 - 2698. [Abstract] [Full Text] [PDF]
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 B. B. McCormick and J. M. Bargman Noninfectious Complications of Peritoneal Dialysis: Implications for Patient and Technique Survival J. Am. Soc. Nephrol., December 1, 2007; 18(12): 3023 - 3025. [Abstract] [Full Text] [PDF]
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P. F. Bodary Links Between Adipose Tissue and Thrombosis in the Mouse Arterioscler Thromb Vasc Biol, November 1, 2007; 27(11): 2284 - 2291. [Abstract] [Full Text] [PDF]
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P. Singh, M. Hoffmann, R. Wolk, A. S.M. Shamsuzzaman, and V. K. Somers Leptin Induces C-Reactive Protein Expression in Vascular Endothelial Cells Arterioscler Thromb Vasc Biol, September 1, 2007; 27(9): e302 - e307. [Abstract] [Full Text] [PDF]
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 G. D. Lopaschuk, C. D.L. Folmes, and W. C. Stanley Cardiac Energy Metabolism in Obesity Circ. Res., August 17, 2007; 101(4): 335 - 347. [Abstract] [Full Text] [PDF]
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 R. Muniyappa, M. Montagnani, K. K. Koh, and M. J. Quon Cardiovascular Actions of Insulin Endocr. Rev., August 1, 2007; 28(5): 463 - 491. [Abstract] [Full Text] [PDF]
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H. Katagiri, T. Yamada, and Y. Oka Adiposity and Cardiovascular Disorders: Disturbance of the Regulatory System Consisting of Humoral and Neuronal Signals Circ. Res., July 6, 2007; 101(1): 27 - 39. [Abstract] [Full Text] [PDF]
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P. D. Anderson, N. N. Mehta, M. L. Wolfe, C. C. Hinkle, L. Pruscino, L. L. Comiskey, J. Tabita-Martinez, K. F. Sellers, M. R. Rickels, R. S. Ahima, et al. Innate Immunity Modulates Adipokines in Humans J. Clin. Endocrinol. Metab., June 1, 2007; 92(6): 2272 - 2279. [Abstract] [Full Text] [PDF]
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I. M. Wahba and R. H. Mak Obesity and Obesity-Initiated Metabolic Syndrome: Mechanistic Links to Chronic Kidney Disease Clin. J. Am. Soc. Nephrol., May 1, 2007; 2(3): 550 - 562. [Abstract] [Full Text] [PDF]
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S. G. Wannamethee, G. D.O. Lowe, A. Rumley, L. Cherry, P. H. Whincup, and N. Sattar Adipokines and Risk of Type 2 Diabetes in Older Men Diabetes Care, May 1, 2007; 30(5): 1200 - 1205. [Abstract] [Full Text] [PDF]
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 G. M. Howard-Alpe, J. W. Sear, and P. Foex Methods of detecting atherosclerosis in non-cardiac surgical patients; the role of biochemical markers Br. J. Anaesth., December 1, 2006; 97(6): 758 - 769. [Abstract] [Full Text] [PDF]
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 A. U. Momin, N. Melikian, A. M. Shah, D. J. Grieve, S. B. Wheatcroft, L. John, A. El Gamel, J. B. Desai, T. Nelson, C. Driver, et al. Leptin is an endothelial-independent vasodilator in humans with coronary artery disease: evidence for tissue specificity of leptin resistance Eur. Heart J., October 1, 2006; 27(19): 2294 - 2299. [Abstract] [Full Text] [PDF]
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R. Wolk and V. K. Somers Leptin and vascular function: friend or foe? Eur. Heart J., October 1, 2006; 27(19): 2263 - 2265. [Full Text] [PDF]
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I. Mertens, R. V Considine, M. Van der Planken, and L. F Van Gaal Hemostasis and fibrinolysis in non-diabetic overweight and obese men and women. Is there still a role for leptin? Eur. J. Endocrinol., September 1, 2006; 155(3): 477 - 484. [Abstract] [Full Text] [PDF]
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M.-H. Gannage-Yared, S. Khalife, M. Semaan, F. Fares, S. Jambart, and G. Halaby Serum adiponectin and leptin levels in relation to the metabolic syndrome, androgenic profile and somatotropic axis in healthy non-diabetic elderly men. Eur. J. Endocrinol., July 1, 2006; 155(1): 167 - 176. [Abstract] [Full Text] [PDF]
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C. Langenberg, J. Bergstrom, C. Scheidt-Nave, J. Pfeilschifter, and E. Barrett-Connor Cardiovascular Death and the Metabolic Syndrome: Role of adiposity-signaling hormones and inflammatory markers. Diabetes Care, June 1, 2006; 29(6): 1363 - 1369. [Abstract] [Full Text] [PDF]
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 F. Taneli, S. Yegane, C. Ulman, H. Tikiz, A. R. Bilge, Z. Ari, and B. S. Uyanik Increased Serum Leptin Concentrations in Patients with Chronic Stable Angina Pectoris and ST-Elevated Myocardial Infarction Angiology, May 1, 2006; 57(3): 267 - 272. [Abstract] [PDF]
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R. Furuya, M. Odamaki, H. Kumagai, and A. Hishida Beneficial effects of icodextrin on plasma level of adipocytokines in peritoneal dialysis patients Nephrol. Dial. Transplant., February 1, 2006; 21(2): 494 - 498. [Abstract] [Full Text] [PDF]
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K. Nishio, M. Sakurai, T. Kusuyama, M. Shigemitsu, T. Fukui, K. Kawamura, S. Itoh, N. Konno, and T. Katagiri A Randomized Comparison of Pioglitazone to Inhibit Restenosis After Coronary Stenting in Patients With Type 2 Diabetes Diabetes Care, January 1, 2006; 29(1): 101 - 106. [Abstract] [Full Text] [PDF]
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M. Pladevall, B. Singal, L. K. Williams, C. Brotons, H. Guyer, J. Sadurni, C. Falces, M. Serrano-Rios, R. Gabriel, J. E. Shaw, et al. A Single Factor Underlies the Metabolic Syndrome: A confirmatory factor analysis Diabetes Care, January 1, 2006; 29(1): 113 - 122. [Abstract] [Full Text] [PDF]
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B. Canavan, R. O. Salem, S. Schurgin, P. Koutkia, I. Lipinska, M. Laposata, and S. Grinspoon Effects of Physiological Leptin Administration on Markers of Inflammation, Platelet Activation, and Platelet Aggregation during Caloric Deprivation J. Clin. Endocrinol. Metab., October 1, 2005; 90(10): 5779 - 5785. [Abstract] [Full Text] [PDF]
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H. S. Elbatarny and D. H. Maurice Leptin-mediated activation of human platelets: involvement of a leptin receptor and phosphodiesterase 3A-containing cellular signaling complex Am J Physiol Endocrinol Metab, October 1, 2005; 289(4): E695 - E702. [Abstract] [Full Text] [PDF]
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P. F. Bodary, S. Gu, Y. Shen, A. H. Hasty, J. M. Buckler, and D. T. Eitzman Recombinant Leptin Promotes Atherosclerosis and Thrombosis in Apolipoprotein E-Deficient Mice Arterioscler Thromb Vasc Biol, August 1, 2005; 25(8): e119 - e122. [Abstract] [Full Text] [PDF]
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L. Perego, P. Pizzocri, D. Corradi, F. Maisano, M. Paganelli, P. Fiorina, M. Barbieri, A. Morabito, G. Paolisso, F. Folli, et al. Circulating Leptin Correlates with Left Ventricular Mass in Morbid (Grade III) Obesity before and after Weight Loss Induced by Bariatric Surgery: A Potential Role for Leptin in Mediating Human Left Ventricular Hypertrophy J. Clin. Endocrinol. Metab., July 1, 2005; 90(7): 4087 - 4093. [Abstract] [Full Text] [PDF]
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J. D. Knudson, U. D. Dincer, C. Zhang, A. N. Swafford Jr., R. Koshida, A. Picchi, M. Focardi, G. M. Dick, and J. D. Tune Leptin receptors are expressed in coronary arteries, and hyperleptinemia causes significant coronary endothelial dysfunction Am J Physiol Heart Circ Physiol, July 1, 2005; 289(1): H48 - H56. [Abstract] [Full Text] [PDF]
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J. E. Ostberg, M. J. H. Attar, V. Mohamed-Ali, and G. S. Conway Adipokine Dysregulation in Turner Syndrome: Comparison of Circulating Interleukin-6 and Leptin Concentrations with Measures of Adiposity and C-Reactive Protein J. Clin. Endocrinol. Metab., May 1, 2005; 90(5): 2948 - 2953. [Abstract] [Full Text] [PDF]
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E. M. Stuveling, S. J. L. Bakker, H. L. Hillege, P. E. de Jong, R. O. B. Gans, and D. de Zeeuw Biochemical risk markers: a novel area for better prediction of renal risk? Nephrol. Dial. Transplant., March 1, 2005; 20(3): 497 - 508. [Full Text] [PDF]
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D. M. Purdham, M.-X. Zou, V. Rajapurohitam, and M. Karmazyn Rat heart is a site of leptin production and action Am J Physiol Heart Circ Physiol, December 1, 2004; 287(6): H2877 - H2884. [Abstract] [Full Text] [PDF]
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R. Wolk, P. Berger, R. J. Lennon, E. S. Brilakis, B. D. Johnson, and V. K. Somers Plasma leptin and prognosis in patients with established coronary atherosclerosis J. Am. Coll. Cardiol., November 2, 2004; 44(9): 1819 - 1824. [Abstract] [Full Text] [PDF]
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S. S. Daskalopoulou, D. P. Mikhailidis, and M. Elisaf Prevention and Treatment of the Metabolic Syndrome Angiology, November 1, 2004; 55(6): 589 - 612. [Abstract] [PDF]
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B. E. Wisse The Inflammatory Syndrome: The Role of Adipose Tissue Cytokines in Metabolic Disorders Linked to Obesity J. Am. Soc. Nephrol., November 1, 2004; 15(11): 2792 - 2800. [Abstract] [Full Text] [PDF]
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K. Tsuda, I. Nishio, A. S.M. Shamsuzzaman, M. Winnicki, R. Wolk, A. Svatikova, D. E. Davison, V. K. Somers, B. G. Phillips, and P. B. Berger Leptin, C-Reactive Protein, and Nitric Oxide Production in Healthy Humans * Response Circulation, September 28, 2004; 110(13): e330 - e330. [Full Text] [PDF]
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F.-P. Xu, M.-S. Chen, Y.-Z. Wang, Q. Yi, S.-B. Lin, A. F. Chen, and J.-D. Luo Leptin Induces Hypertrophy via Endothelin-1-Reactive Oxygen Species Pathway in Cultured Neonatal Rat Cardiomyocytes Circulation, September 7, 2004; 110(10): 1269 - 1275. [Abstract] [Full Text] [PDF]
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M. P. Reilly, N. Iqbal, M. Schutta, M. L. Wolfe, M. Scally, A. R. Localio, D. J. Rader, and S. E. Kimmel Plasma Leptin Levels Are Associated with Coronary Atherosclerosis in Type 2 Diabetes J. Clin. Endocrinol. Metab., August 1, 2004; 89(8): 3872 - 3878. [Abstract] [Full Text] [PDF]
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J.-C. Fruchart, M. C. Nierman, E. S. G. Stroes, J. J. P. Kastelein, and P. Duriez New Risk Factors for Atherosclerosis and Patient Risk Assessment Circulation, June 15, 2004; 109(23_suppl_1): III-15 - III-19. [Abstract] [Full Text]
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Y. Iwashima, T. Katsuya, K. Ishikawa, N. Ouchi, M. Ohishi, K. Sugimoto, Y. Fu, M. Motone, K. Yamamoto, A. Matsuo, et al. Hypoadiponectinemia Is an Independent Risk Factor for Hypertension Hypertension, June 1, 2004; 43(6): 1318 - 1323. [Abstract] [Full Text] [PDF]
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A. S.M. Shamsuzzaman, M. Winnicki, R. Wolk, A. Svatikova, B. G. Phillips, D. E. Davison, P. B. Berger, and V. K. Somers Independent Association Between Plasma Leptin and C-Reactive Protein in Healthy Humans Circulation, May 11, 2004; 109(18): 2181 - 2185. [Abstract] [Full Text] [PDF]
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K. Ohashi, N. Ouchi, S. Kihara, T. Funahashi, T. Nakamura, S. Sumitsuji, T. Kawamoto, S. Matsumoto, H. Nagaretani, M. Kumada, et al. Adiponectin I164T mutation is associated with the metabolic syndrome and coronary artery disease J. Am. Coll. Cardiol., April 7, 2004; 43(7): 1195 - 1200. [Abstract] [Full Text] [PDF]
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K. Schafer, M. Halle, C. Goeschen, C. Dellas, M. Pynn, D. J. Loskutoff, and S. Konstantinides Leptin Promotes Vascular Remodeling and Neointimal Growth in Mice Arterioscler Thromb Vasc Biol, January 1, 2004; 24(1): 112 - 117. [Abstract] [Full Text] [PDF]
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R. Wolk, B. D. Johnson, and V. K. Somers Leptin and the ventilatory response to exercise in heart failure J. Am. Coll. Cardiol., November 5, 2003; 42(9): 1644 - 1649. [Abstract] [Full Text] [PDF]
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R. Wolk, P. Berger, R. J. Lennon, E. S. Brilakis, and V. K. Somers Body Mass Index: A Risk Factor for Unstable Angina and Myocardial Infarction in Patients With Angiographically Confirmed Coronary Artery Disease Circulation, November 4, 2003; 108(18): 2206 - 2211. [Abstract] [Full Text] [PDF]
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P. Piatti, C. Di Mario, L. D. Monti, G. Fragasso, F. Sgura, A. Caumo, E. Setola, P. Lucotti, E. Galluccio, C. Ronchi, et al. Association of Insulin Resistance, Hyperleptinemia, and Impaired Nitric Oxide Release With In-Stent Restenosis in Patients Undergoing Coronary Stenting Circulation, October 28, 2003; 108(17): 2074 - 2081. [Abstract] [Full Text] [PDF]
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 A. S. M. Shamsuzzaman, B. J. Gersh, and V. K. Somers Obstructive Sleep Apnea: Implications for Cardiac and Vascular Disease JAMA, October 8, 2003; 290(14): 1906 - 1914. [Abstract] [Full Text] [PDF]
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L. Piemonti, G. Calori, A. Mercalli, G. Lattuada, P. Monti, M. P. Garancini, F. Costantino, G. Ruotolo, L. Luzi, and G. Perseghin Fasting Plasma Leptin, Tumor Necrosis Factor-{alpha} Receptor 2, and Monocyte Chemoattracting Protein 1 Concentration in a Population of Glucose-Tolerant and Glucose-Intolerant Women: Impact on cardiovascular mortality Diabetes Care, October 1, 2003; 26(10): 2883 - 2889. [Abstract] [Full Text] [PDF]
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M. P. Reilly and D. J. Rader The Metabolic Syndrome: More Than the Sum of Its Parts? Circulation, September 30, 2003; 108(13): 1546 - 1551. [Full Text] [PDF]
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M. Tomaszewski, F. J. Charchar, M. Przybycin, L. Crawford, A. M. Wallace, K. Gosek, G. D. Lowe, E. Zukowska-Szczechowska, W. Grzeszczak, N. Sattar, et al. Strikingly Low Circulating CRP Concentrations in Ultramarathon Runners Independent of Markers of Adiposity: How Low Can You Go? Arterioscler Thromb Vasc Biol, September 1, 2003; 23(9): 1640 - 1644. [Abstract] [Full Text] [PDF]
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V. Rajapurohitam, X. T. Gan, L. A. Kirshenbaum, and M. Karmazyn The Obesity-Associated Peptide Leptin Induces Hypertrophy in Neonatal Rat Ventricular Myocytes Circ. Res., August 22, 2003; 93(4): 277 - 279. [Abstract] [Full Text] [PDF]
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N. Sattar, J. Ramsay, L. Crawford, H. Cheyne, and I. A. Greer Classic and Novel Risk Factor Parameters in Women With a History of Preeclampsia Hypertension, July 1, 2003; 42(1): 39 - 42. [Abstract] [Full Text] [PDF]
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R. A. Anderson, A. M. Wallace, N. Sattar, N. Kumar, and K. Sundaram Evidence for Tissue Selectivity of the Synthetic Androgen 7{alpha}-Methyl-19-Nortestosterone in Hypogonadal Men J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2784 - 2793. [Abstract] [Full Text] [PDF]
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 N. Sattar, C. G Perry, and J. R Petrie Type 2 diabetes as an inflammatory disorder The British Journal of Diabetes & Vascular Disease, January 1, 2003; 3(1): 36 - 41. [Abstract] [PDF]
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 N. G. Patel, J. C. Holder, S. A. Smith, S. Kumar, and M. C. Eggo Differential Regulation of Lipogenesis and Leptin Production by Independent Signaling Pathways and Rosiglitazone During Human Adipocyte Differentiation Diabetes, January 1, 2003; 52(1): 43 - 50. [Abstract] [Full Text] [PDF]
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M. Kratz, A. von Eckardstein, M. Fobker, A. Buyken, N. Posny, H. Schulte, G. Assmann, and U. Wahrburg The Impact of Dietary Fat Composition on Serum Leptin Concentrations in Healthy Nonobese Men and Women J. Clin. Endocrinol. Metab., November 1, 2002; 87(11): 5008 - 5014. [Abstract] [Full Text] [PDF]
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A. Singhal, I. S. Farooqi, T. J. Cole, S. O'Rahilly, M. Fewtrell, M. Kattenhorn, A. Lucas, and J. Deanfield Influence of Leptin on Arterial Distensibility: A Novel Link Between Obesity and Cardiovascular Disease? Circulation, October 8, 2002; 106(15): 1919 - 1924. [Abstract] [Full Text] [PDF]
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A. J Krentz Type 2 diabetes and atherosclerotic cardiovascular disease: do they share common antecedents? The British Journal of Diabetes & Vascular Disease, September 1, 2002; 2(5): 370 - 378. [Abstract] [PDF]
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A. E. Pontiroli, P. Pizzocri, F. Folli, N. Sattar, P. W. Macfarlane, C. J. Packard, A. Kelly, J. Shepherd, A. Gaw, A. M. Wallace, et al. Plasma Leptin Levels and Coronary Heart Disease * Response Circulation, August 27, 2002; 106 (9): e42 - e42. [Full Text] [PDF]
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F. Corica, A. Corsonello, F. Perticone, P. F. Bodary, and D. T. Eitzman Effects of Leptin on Platelet Function in Obese Patients JAMA, July 17, 2002; 288(3): 313 - 314. [Full Text] [PDF]
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M. Winnicki, V. K. Somers, V. Accurso, B. G. Phillips, M. Puato, P. Palatini, and P. Pauletto Fish-Rich Diet, Leptin, and Body Mass Circulation, July 16, 2002; 106(3): 289 - 291. [Abstract] [Full Text] [PDF]
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C. Bernal-Mizrachi, S. Weng, B. Li, L. A. Nolte, C. Feng, T. Coleman, J. O. Holloszy, and C. F. Semenkovich Respiratory Uncoupling Lowers Blood Pressure Through a Leptin-Dependent Mechanism in Genetically Obese Mice Arterioscler Thromb Vasc Biol, June 1, 2002; 22(6): 961 - 968. [Abstract] [Full Text] [PDF]
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P. F. Bodary, R. J. Westrick, K. J. Wickenheiser, Y. Shen, and D. T. Eitzman Effect of Leptin on Arterial Thrombosis Following Vascular Injury in Mice JAMA, April 3, 2002; 287(13): 1706 - 1709. [Abstract] [Full Text] [PDF]
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