Related Experiment Video
Updated: Jan 11, 2026

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
Published on: October 25, 2019
Systemic and Local Leptin Resistance in Patients with Cardiovascular Diseases
Olga Gruzdeva1, Evgeniya Gorbatovskaya1, Yulia Dyleva1
1Research Institute for Complex Issues of Cardiovascular Diseases, Academician Barbarash Blvd., 6, 650002 Kemerovo, Russia.
Insights
Leptin resistance (LR) is common in myocardial infarction (MI) and chronic coronary heart disease (CHD) patients. Changes in epicardial adipose tissue (EAT) contribute significantly to developing LR in these cardiovascular disease (CVD) patients.
Area of Science:
- Cardiovascular Disease Research
- Metabolic Syndrome Studies
- Adipose Tissue Biology
Background:
- Leptin resistance (LR) mechanisms in cardiovascular disease (CVD) are poorly understood.
- Investigating adipose tissue characteristics in CVD patients may elucidate LR pathogenesis.
- This study addresses the prevalence and tissue-specific factors of LR in various CVD forms.
Purpose of the Study:
- To evaluate systemic and local markers of leptin resistance (LR) in patients with myocardial infarction (MI), chronic coronary heart disease (CHD), and acquired heart disease (AHD).
- To determine the prevalence of LR across different CVD patient groups.
- To identify tissue-specific expression patterns of leptin and its receptors contributing to LR.
Main Methods:
- Included 108 MI, 96 chronic CHD, and 96 AHD patients.
- Measured serum leptin, leptin receptor, and free leptin index (FLI) for LR definition (>6.45 ng/mL and FLI >25).
- Assessed gene expression (LEP, LEPR variants) and protein secretion in subcutaneous (SAT), epicardial (EAT), and perivascular (PVAT) adipose tissue for chronic CHD and AHD patients.
Main Results:
- High prevalence of LR (elevated leptin and FLI) observed in MI and chronic CHD patients, unlike AHD patients.
- LR was most pronounced in EAT and moderate in SAT among chronic CHD patients.
- Reduced leptin sensitivity in EAT linked to decreased LEPR variant expression and increased leptin production by adipocytes.
Conclusions:
- High rates of leptin resistance (LR) were detected in patients with myocardial infarction (MI) and chronic coronary heart disease (CHD).
- Specific alterations within epicardial adipose tissue (EAT) are identified as key contributors to the development of LR in chronic CHD patients.
- Findings highlight EAT's role in systemic leptin resistance within the context of cardiovascular disease.
Abstract:
Background/Objectives: The causes and mechanisms underlying the development of leptin resistance (LR) in patients with cardiovascular disease (CVD) remain unknown. Investigating the characteristics of adipose tissue in patients with CVD is a relevant scientific problem that may help to uncover the missing links in the pathogenesis of LR. This study aimed to evaluate systemic and local markers of LR in patients with different forms of CVD, and to determine the prevalence and tissue-specific expression patterns that contribute to LR. Methods: The study included 108 patients with myocardial infarction (MI), 96 patients with chronic coronary heart disease (CHD), and 96 patients with acquired heart disease (AHD). On day 1 of admission to the hospital, leptin and leptin receptor concentrations and the serum-free leptin index (FLI) were measured. Leptin resistance (LR) was defined as a leptin level of >6.45 ng/mL and FLI of >25. In chronic CHD and AHD patients, LEP, LEPR1, LEPR2, LEPR2/2, LEPR3, LEPR3/2, and LEPR4 expression as well as leptin and soluble leptin receptor secretion were assessed in subcutaneous (SAT), epicardial (EAT), and perivascular (PVAT) adipose tissue. Results: MI and chronic CHD patients are characterized by elevated leptin levels and high FLI values in the blood serum, which indicates a high prevalence of LR, in contrast to AHD patients. In chronic CHD, the LR level was highest in EAT and moderate in SAT. Reduced leptin sensitivity in EAT is underlied by decreased expression of LEPR1, LEPR2, LEPR2/2, LEPR3, LEPR3/2, and LEPR4, and increased leptin production by epicardial adipocytes, which contributes to enhancement of leptin resistance at the systemic level. Conclusions: A high LR rate was detected in patients with MI and chronic CHD. The identified changes in EAT lead to the development of leptin resistance in chronic CHD patients.
More Related Videos
09:48Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
Published on: February 17, 2023
03:05Influence of Emotional Factors on the Efficacy of Acupuncture Treatment for Overweight Complicated with Hyperlipidemia: A Retrospective Cohort Study
Published on: November 21, 2025
Related Concept Videos
Pharmacokinetics in Obese Patients: Drug Absorption and Distribution
Heart Failure II: Pathophysiology
Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
Pathophysiology of Heart Failure
Obesity
Cholesterol: Significance and Regulation
Considering cholesterol and...