Systemic and Local Leptin Resistance in Patients with Cardiovascular Diseases

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.