Abstract:BackgroundClinical studies have demonstrated that adipocytokines play an important role
in developing atherosclerotic cardiovascular diseases.ObjectiveThe aim of study was to evaluate the relationship between serum resistin and
leptin levels with obesity and coronary artery disease (CAD).MethodsIn a cross-sectional study, we assessed the levels of serum resistin and
leptin, C-reactive protein (CRP), lipid profile and cardiac enzyme tests
(AST, CPK, LDH, CK-MB) in 40 CAD patients compared to 40 healthy controls… Show more
“…Consistent with our studies, several studies have reported serum leptin levels to be significantly elevated in CAD patients [4, 25-27], suggesting the role of leptin as a mediator in human atherosclerotic. A large prospective study was conducted to examine that the raised leptin levels may identify men at increased risk of a coronary event in the West of Scotland Coronary Prevention Study [26].…”
Section: Discussionsupporting
confidence: 81%
“…Leptin is a cytokine, which is released from the adipose tissue and it acts on the hypothalamus to promote weight loss, both by reducing appetite and food intake and by increasing energy expenditure [3, 4]. Leptin contributes to the inflammatory processes related to obesity in both vascular and non-vascular tissues [5, 6], and activates endothelial cells [6].…”
Background/Aims: Previous studies have suggested that leptin was associated with atherosclerosis and involved in inflammation. Gender differences between leptin and inflammatory markers have been evaluated less in untreated patients with stable coronary artery disease (CAD). Methods: In this study, a total of 394 consecutive Chinese patients who received coronary artery angiography were enrolled, including 243 patients with CAD and 151 non-CAD controls. The baseline clinical characteristics were collected and serum leptin levels were determined using ELISA. Results: The relation of serum leptin levels to inflammatory markers was found only in female patients. Leptin and white blood cell count (WBCC) as well as its subsets were significantly higher in female patients than female controls. In female patients, leptin was positively associated with C-reactive protein (CRP; r = 0.28, p = 0.016), WBCC (r = 0.261, p = 0.02), neutrophil, r = 0.268, p = 0.018, and monocyte, r = 0.228, p = 0.044. Multivariable regression analysis revealed that leptin was significantly and independently associated with CRP (β = 0.317, p = 0.004), WBCC (β = 0.278, p = 0.020), neutrophil (β = 0.262, p = 0.032), and monocyte (β = 0.245, p = 0.032). Conclusions: The serum leptin levels were higher in female patients and independently associated with CRP, WBCC, and its subsets, suggesting a potential interaction between leptin and inflammation in female CAD patients.
“…Consistent with our studies, several studies have reported serum leptin levels to be significantly elevated in CAD patients [4, 25-27], suggesting the role of leptin as a mediator in human atherosclerotic. A large prospective study was conducted to examine that the raised leptin levels may identify men at increased risk of a coronary event in the West of Scotland Coronary Prevention Study [26].…”
Section: Discussionsupporting
confidence: 81%
“…Leptin is a cytokine, which is released from the adipose tissue and it acts on the hypothalamus to promote weight loss, both by reducing appetite and food intake and by increasing energy expenditure [3, 4]. Leptin contributes to the inflammatory processes related to obesity in both vascular and non-vascular tissues [5, 6], and activates endothelial cells [6].…”
Background/Aims: Previous studies have suggested that leptin was associated with atherosclerosis and involved in inflammation. Gender differences between leptin and inflammatory markers have been evaluated less in untreated patients with stable coronary artery disease (CAD). Methods: In this study, a total of 394 consecutive Chinese patients who received coronary artery angiography were enrolled, including 243 patients with CAD and 151 non-CAD controls. The baseline clinical characteristics were collected and serum leptin levels were determined using ELISA. Results: The relation of serum leptin levels to inflammatory markers was found only in female patients. Leptin and white blood cell count (WBCC) as well as its subsets were significantly higher in female patients than female controls. In female patients, leptin was positively associated with C-reactive protein (CRP; r = 0.28, p = 0.016), WBCC (r = 0.261, p = 0.02), neutrophil, r = 0.268, p = 0.018, and monocyte, r = 0.228, p = 0.044. Multivariable regression analysis revealed that leptin was significantly and independently associated with CRP (β = 0.317, p = 0.004), WBCC (β = 0.278, p = 0.020), neutrophil (β = 0.262, p = 0.032), and monocyte (β = 0.245, p = 0.032). Conclusions: The serum leptin levels were higher in female patients and independently associated with CRP, WBCC, and its subsets, suggesting a potential interaction between leptin and inflammation in female CAD patients.
“…In fact, Montazerifar et al indicated that Leptin levels were significantly higher in abdominal obese patients than those in patients without abdominal obesity or in the control group. This result was partly consistent with earlier reports …”
Adipose tissue is an important endocrine organ that secretes a number of adipokines, like Leptin (LEP). The aim this study was to investigate the prevalence of single nucleotide polymorphisms in LEP gene (LEP 3'UTR A/C, -2548 G/A) and LEPR (K109R and Q223R) and their association with Leptin level and obesity. We recruited 169 non-obese (body mass index [BMI] = 24.51-3.69 kg/m ) and 160 obese (BMI = 36-4.78 kg/m ) patients. Genotyping was performed using polymerase chain reaction-restriction fragment length polymorphism, BMI was calculated, and Leptin level was measured by ELISA. Statistical analyses were performed by spss19.0. According to LEP 3'UTR A/C polymorphism, AC and CC genotype carriers had higher Leptin levels than AA genotype carriers, respectively, 31[0.05-148.8] (P = .008) vs 41[0.05-111.6] (P = .003). The K109R polymorphism was associated with obesity (P = .025) and seems to significantly decrease the LEP levels (P < .001). Concerning LEP G2548A polymorphism, our results showed that the OR of obesity associated with 2548 AA/GG was 1.87[1.106-2.78] P = .028 vs 1.41[1.035-1.85] P = .045 for 223AA/GG polymorphism. In our haplotype analysis, one haplotype seems to be the more protective and one other seems to be the highest risk to obesity. LEP 3'UTR A/C and LEPR K109R polymorphisms were associated with Leptin level and obesity.
“…High serum leptin levels have been observed in patients with CHD (33). There is a strong correlation between both circulating and adipose tissue levels of leptin and serum c-reactive protein (CRP) in obese women (34).…”
Background We used a multiplex proteomics assay with the aim to discover novel associations between leptin and 88 circulating proteins in order to provide additional insights into the role of leptin in the development of CVD in patients with type 2 diabetes (T2DM). Material and methods In a discovery phase, we investigated associations between 88 plasma proteins, assessed with a proximity extension assay, and plasma leptin in a cohort of middle-aged patients with T2DM (CARDIPP, n=661). Associations that passed the significance threshold of a False discovery rate of 5% (corresponding to p <0.0017) were replicated in diabetes patients in an independent cohort (PIVUS, n=116). We also investigated if proteins mediated the longitudinal association between plasma leptin and the incidence of major cardiovascular events (MACE). Results Two proteins were significantly associated with leptin in the discovery phase, adipocyte fatty acid binding protein (A-FABP) (regression coefficient .118, 95% CI (.064, .173) p =0.000024) and adrenomedullin ( p =0.000002) but only A-FABP was significantly associated with leptin in the replication cohort (regression coefficient .0254, 95% CI (.119, .39) p =0.0003). Multiplicative interaction analyses in the two cohorts suggest a stronger association between A-FABP and leptin in men than in women. In longitudinal analyses, the association between leptin and MACE was slightly attenuated after adding A-FABP to the multivariate model. Conclusions Our analysis identified a consistent association between leptin and A-FABP in two independent cohorts of patients with T2DM, particularly in men. Our data encourage future large-scale proteomics analyses for additional insights into leptin biology.
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