Leptin – ABC CARDIOL

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Original Article

Decreased Collagen Type I is Associated with Increased Metalloproteinase-2 Activity and Protein Expression of Leptin in the Myocardium of Obese Rats

Danielle Cristina Tomaz da Silva-Bertani et al. Danielle Fernandes Vileigas Gustavo Augusto Ferreira Mota Sérgio Luiz Borges de Souza … Loreta Casquel De Tomasi Dijon Henrique Salomé de Campos Adriana Fernandes de Deus Paula Paccielli Freire Carlos Augusto Barnabe Alves Carlos Roberto Padovani Antonio Carlos Cicogna

Abstract

Background

Obesity is a risk factor for medical complications, including the cardiovascular system. There is limited information on collagen in the heart in obesity. Our previous study showed decreased protein levels of myocardial collagen type I in obese rats fed a high-fat diet for 34 weeks. However, the mechanisms responsible for low levels are not fully elucidated.

Objective

The purpose of this study was to test the hypothesis that the reduction in collagen type I is associated with increased metalloproteinase-2 (MMP-2) activity, which is linked to elevated leptin in the myocardium of obese rats.

Methods

Thirty-day-old male Wistar rats were randomized into two groups, control (standard diet) and obese (high-fat diet), and fed for 34 weeks. The general animal characteristics and metabolic and endocrine profiles were evaluated. Myocardial protein expressions of collagen I, leptin, tissue inhibitors of metalloproteinases (TIMP), and MMP-2 activity were assessed. Pearson correlation was employed to determine the associations between variables. The level of significance was 5%.

Results

The obese animals had increased adiposity index compared to control. Comorbidities such as glucose intolerance, hyperinsulinemia, insulin resistance, hyperleptinemia, and hypertension were observed in obese rats. Obesity reduced collagen I, TIMP-1, and TIMP-2, and it increased leptin and MMP-2 in the myocardium. There was a negative correlation between collagen I and MMP-2 and a positive correlation between leptin and MMP-2.

Conclusion

The hypothesis was confirmed; the reduction in collagen type I is associated with increased MMP-2 activity and leptin expression in the myocardium of obese rats. (Arq Bras Cardiol. 2020; 115(1):61-70)

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Original Article

Obesity, Serum Resistin and Leptin Levels Linked to Coronary Artery Disease

Farzaneh Montazerifar et al. Ahmad Bolouri Raheleh Sharifian Paghalea Mahbubeh Khodadadpour Mahani Mansour Karajibani

Abstract

Background:

Clinical studies have demonstrated that adipocytokines play an important role in developing atherosclerotic cardiovascular diseases.

Objective:

The aim of study was to evaluate the relationship between serum resistin and leptin levels with obesity and coronary artery disease (CAD).

Methods:

In 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. Anthropometric measurements including weight and height for calculating of body mass index (BMI), and waist circumference (WC) were performed for evaluation of obesity.

Results:

CAD patients had increased levels of leptin and CRP, (p < 0.001), cholesterol (p < 0.05), triglyceride (p < 0.01), and WC (p < 0.05) compared to healthy controls. There was no statistical difference between CAD and control subjects for resistin (p = 0.058). In a multiple regression analysis, only an association between serum leptin with BMI (β = 0.480, p < 0.05) and WC (β = 1.386, p < 0.05) was found.

Conclusions:

The findings suggest that leptin is a better marker of fat mass value than resistin and may be considered an independent risk factor for cardiac disorders that is largely dependent on obesity. However, further prospective studies are needed to confirm these results.

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Original Article

Obesity does not Lead to Imbalance Between Myocardial Phospholamban Phosphorylation and Dephosphorylation

Paula Paccielli Freire et al. Carlos Augusto Barnabe Alves Adriana Fernandes de Deus Ana Paula Lima Leopoldo … André Soares Leopoldo Danielle Cristina Tomaz da Silva Loreta Casquel de Tomasi Dijon Henrique Salomé Campos Antonio Carlos Cicogna

Background:

The activation of the beta-adrenergic system promotes G protein stimulation that, via cyclic adenosine monophosphate (cAMP), alters the structure of protein kinase A (PKA) and leads to phospholamban (PLB) phosphorylation. This protein participates in the system that controls intracellular calcium in muscle cells, and it is the primary regulator of sarcoplasmic reticulum calcium pump activity. In obesity, the beta-adrenergic system is activated by the influence of increased leptin, therefore, resulting in higher myocardial phospholamban phosphorylation via cAMP-PKA.

Objective:

To investigate the involvement of proteins which regulate the degree of PLB phosphorylation due to beta-adrenergic activation in obesity. In the present study, we hypothesized that there is an imbalance between phospholamban phosphorylation and dephosphorylation, with prevalence of protein phosphorylation.

Methods:

Male Wistar rats were randomly distributed into two groups: control (n = 14), fed with normocaloric diet; and obese (n = 13), fed with a cycle of four unsaturated high-fat diets. Obesity was determined by the adiposity index, and protein expressions of phosphatase 1 (PP-1), PKA, PLB, phosphorylated phospholamban at serine16 (PPLB-Ser16) were assessed by Western blot.

Results:

Obesity caused glucose intolerance, hyperinsulinemia, hypertriglyceridemia, hyperleptinemia and did not alter the protein expression of PKA, PP-1, PLB, PPLB-Ser16.

Conclusion:

Obesity does not promote an imbalance between myocardial PLB phosphorylation and dephosphorylation via beta-adrenergic system.

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Artigo Original

Leptin and aldosterone in sympathetic activity in resistant hypertension with or without type 2 diabetes

Leandro Boer-Martins et al. Valéria Nasser Figueiredo Caroline Demacq Luiz Cláudio Martins … Ana Paula Cabral de Faria Carolina de Haro Moraes Heitor Moreno Jr.

BACKGROUND: The finding of adipocyte-derived hormone leptin as an overstimulator of sympathetic activity brought a new perspective to the pathophysiological mechanisms of obesity-hypertension. OBJECTIVES: As aldosterone also increases sympathetic activity, we aimed to assess the relationship between sympathetic overactivity and plasma leptin and aldosterone levels in resistant hypertension (RHTN), comparing the groups with and without T2D. METHODS: Twenty-five RHTN patients underwent ambulatory electrocardiography to analyze heart rate variability (HRV) in time and frequency domains, which were stratified into two periods: 24 hours and daytime (DT), comprising the records between 2:00 p.m to 6:00 p.m (time domain) and one hour at 3:00 p.m (frequency domain). RESULTS: T2D group (n=10) had higher serum aldosterone and plasma leptin levels than the non-T2D (n=15) (26.0±11.5 vs. 16.9±7.0 ng/dL – p=0.021; 81.368.7±47.086.1 vs 41.228.1±24.523.1 pg/mL – p=0.048, respectively). Both groups had aldosterone correlated with HRV in frequency domain. Non-T2D had aldosterone correlated with DT low frequency in normalized units (LF nu) (r=0.6 [0.12-0.85] p=0.018) and DT high frequency in normalized units (HF nu) (r=-0.6 [-0.85- -0.12] p=0.018). Type-2-diabetes group had aldosterone correlated with DT LF nu (r=0.72 [0.16-0.93] p=0.019) and DT HF nu (r=-0.72 [-0.93- -0.16] p=0.019). However, despite of the importance of leptin in sympathetic overactivity in hypertension, leptin did not correlate with HRV. CONCLUSION: Aldosterone seems to overdrive sympathetic activity in RHTN with and without T2D. This information combined with the clinical efficacy of mineralocorticoid receptor blocker in RHTN may reinforce that aldosterone is a major player to be a therapeutic target in RHTN. (Arq Bras Cardiol. 2012; [online].ahead print, PP.0-0)

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Decreased Collagen Type I is Associated with Increased Metalloproteinase-2 Activity and Protein Expression of Leptin in the Myocardium of Obese Rats

Abstract

Background

Objective

Methods

Results

Conclusion

Obesity, Serum Resistin and Leptin Levels Linked to Coronary Artery Disease

Abstract

Background:

Objective:

Methods:

Results:

Conclusions:

Obesity does not Lead to Imbalance Between Myocardial Phospholamban Phosphorylation and Dephosphorylation

Background:

Objective:

Methods:

Results:

Conclusion:

Leptin and aldosterone in sympathetic activity in resistant hypertension with or without type 2 diabetes

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