Leptin increase is associated with markers of the hemostatic system in obese healthy women.

J Thromb Haemost

Center of Excellence on Aging and Department of Medicine, University of Chieti G D'Annunzio, School of Medicine, Chieti, Italy.

Published: November 2003

Background: Leptin, a hormone secreted by the adipose tissue, might be a link between obesity and increased morbidity for cardiovascular disease. Leptin exerts proinflammatory, pro-angiogenic actions by activating a specific receptor (Ob-Rb) which is expressed in human endothelial cells. Thus, a link may exist between leptin expression and endothelial dysfunction.

Objectives: We sought to determine whether in obese women there is a correlation between leptin levels, endothelial perturbation and coagulative activation.

Methods: Circulating levels of leptin, von Willebrand Factor (VWF), factor (F)VIIa, prothrombin fragment 1 + 2 (F1+2), were measured in 51 non-diabetic, obese women and in 51 normal-weight subjects, using immunoenzymatic assays.

Results: Obese women had significantly higher levels of leptin, VWF, FVIIa, F1+2 compared with healthy women. Simple correlation coefficients showed significant correlation between leptin and either VWF, FVIIa, or F1+2 concentrations. A multiple linear regression analysis, performed to quantify further the relationship between leptin levels and the above-mentioned variables as well as the inflammatory marker C-reactive protein (CRP) and including age, body mass index (BMI), waist-hip ratio (WHR) and lipid parameters as potential confounders, revealed that only FVIIa and VWF were independently related to leptin levels. Reduction in adipose tissue after weight loss resulted in a decrease in both circulating leptin and endothelial and coagulative activation markers.

Conclusions: We suggest that leptin might have pro-atherogenic effects in vivo, with a mechanism involving endothelial cell activation.

Download full-text PDF

Source
http://dx.doi.org/10.1046/j.1538-7836.2003.00445.xDOI Listing

Publication Analysis

Top Keywords

leptin
12
obese women
12
leptin levels
12
healthy women
8
adipose tissue
8
correlation leptin
8
levels leptin
8
leptin vwf
8
vwf fviia
8
fviia f1+2
8

Similar Publications

Adipsin and Leptin Levels in Type 2 Diabetic Patients on Sitagliptin and Metformin Versus Metformin Therapy.

Sisli Etfal Hastan Tip Bul

December 2024

Department of Pharmacognosy and Medicinal Plants, University of Mosul, College of Pharmacy, Mosul, Iraq.

Objectives: Adipsin and leptin are adipokines that link adipose tissue dysfunction and increased fat accumulation to obesity-related metabolic disorders. This study aimed to assess the effects of sitagliptin/metformin versus metformin monotherapy on the levels of adipsin, leptin, and lipid profile in type 2 diabetic patients.

Methods: This comparative case-control study included 120 participants divided into four groups: healthy participants, newly diagnosed type 2 diabetic patients, metformin-treated patients, and sitagliptin/metformin-treated patients.

View Article and Find Full Text PDF

Background: Chemoresistance is a major cause of treatment failure in advanced colorectal cancer (CRC), severely impacting patient survival and quality of life. While conventional chemotherapy regimens can somewhat control tumor progression, their effectiveness is frequently compromised by the development of drug resistance in cancer cells. The aim of this study is to verify and elucidate the specific mechanisms by which leptin enhances chemosensitivity in CRC, providing valuable insights for the development of new combination chemotherapy options.

View Article and Find Full Text PDF

Maternal circadian rhythms during pregnancy dictate metabolic plasticity in offspring.

Cell Metab

January 2025

Division of Endocrinology, Metabolism, and Nephrology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan; Center for Preventive Medicine, Keio University, Tokyo, Japan. Electronic address:

Tissue-level oscillation is achieved by tissue-intrinsic clocks along with network-dependent signals originating from distal organs and organismal behavior. Yet, it remains unexplored whether maternal circadian rhythms during pregnancy influence fetal rhythms and impact long-term susceptibility to dietary challenges in offspring. Here, we demonstrate that circadian disruption during pregnancy decreased placental and neonatal weight yet retained transcriptional and structural maturation.

View Article and Find Full Text PDF

Neurotensin receptor agonist PD149163 modulates LPS-induced enterocyte apoptosis by downregulating TNFR pathway and executioner caspase 3 in endotoxemic mice: insights from in vivo and in silico study.

Naunyn Schmiedebergs Arch Pharmacol

January 2025

Department of Zoology, University of Allahabad, Senate House, University Road, Old Katra, Prayagraj, Uttar Pradesh, 211002, India.

This study was designed to evaluate the dose-dependent efficacy of neurotensin receptor-1 (NTSR1) agonist PD149163 in the amelioration of the lipopolysaccharide (LPS)-induced apoptosis in the gastrointestinal tract (GIT) of mice. PD149163 is an analogue of NTS, a GIT tri-decapeptide with anti-inflammatory and anti-oxidative effects. Swiss-albino mice (female/8 weeks/25 ± 2.

View Article and Find Full Text PDF

Adipose tissue may not be a major player in the inflammatory pathogenesis of Autism Spectrum Disorder.

Brain Behav Immun Health

February 2025

Institute of Maternal and Child Medicine, Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China.

Purpose: Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder increasingly recognized for its strong association with chronic inflammation. Adipose tissue functions as an endocrine organ and can secrete inflammatory cytokines to mediate inflammation. However, its involvement in ASD-related inflammation remains unclear.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!