Leptin, the adipocyte-secreted hormone, exerts its main function as regulator of food intake and energy expenditure through central effects at the hypothalamic level. However, it appeared that this cytokine-like peptide has also direct effects on other peripheral tissues and cell types. Remarkable effects have been demonstrated on the immune function in vivo and in vitro. Monocytes are one of the target cells of leptin, and we have demonstrated that secretion of L-1Ra, an IL-1 receptor antagonist, is induced by leptin. In human obesity leptin and IL-1Ra levels are elevated, and these levels are decreased after weight loss. It is discussed that IL-1Ra may contribute to central leptin resistance.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/s0303-7207(02)00191-0 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Quantitative determination of leptin hormone using gold nanoparticle-based lateral flow assay.
Mikrochim Acta
January 2025
Science and Technology Research and Application Center (BITAM), Necmettin Erbakan University, Konya, Türkiye.
A lateral flow assay (LFA) has been developed that can be used in point-of-care (PoC) use for the sensitive determination of leptin hormone. The limit of detection value was 0.158 ng/mL and the limit of quantification value was 0.
View Article and Find Full Text PDFCorrelation between obesity and Alzheimers disease and the mechanisms.
Zhong Nan Da Xue Xue Bao Yi Xue Ban
July 2024
Second Ward of Endocrinology Department, First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450000.
Alzheimer's disease (AD) is a progressive central neurodegenerative disorder with an insidious onset. With global aging, the incidence and mortality of AD have been steadily increasing, yet effective treatments remain elusive. Obesity, characterized by excessive or abnormal fat accumulation, is a complex metabolic disorder and a confirmed risk factor for numerous diseases.
View Article and Find Full Text PDFOverfeeding and overweight rapidly reprogram inflammatory signaling.
Clin Immunol
January 2025
Division of Immunology, Boston Children's Hospital, Boston, MA, United States of America. Electronic address:
Epidemiologic studies have shown a continuous increase in mortality risk associated with overweight, thus highlighting the health risks beginning before the onset of obesity. However, early changes in inflammatory signaling induced by an obesogenic diet remain largely unknown since studies of obesity typically utilize models induced by months of continuous exposure to a high-fat diet. Here, we investigated how short-term overfeeding remodels inflammatory signaling.
View Article and Find Full Text PDFBiomarkers.
Alzheimers Dement
December 2024
Division of clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet and Stockholm University, Stockholm, Sweden.
Background: The Cardiovascular risk factors, aging, and dementia (CAIDE) risk score is a validated tool estimating dementia risk. We investigated the association of CAIDE score with 12 markers of glucose and lipid metabolism, in the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) participants.
Methods: The FINGER trial had 1260 participants, aged 60-77 years, with a CAIDE score ≥6, without substantial cognitive impairment.
Public Health.
Alzheimers Dement
December 2024
Herbert and Jacqueline Krieger Klein Alzheimer's Research Center at Rutgers Brain Health Institute, New Brunswick, NJ, USA.
Background: High body mass index (BMI), which poorly represents specific fat depots, is linked to poorer cognition and higher dementia risk, with different associations between sexes. We examined associations of abdominal fat depots with cognition and brain volumes and whether sex modifies this association.
Method: 204 healthy middle-aged Alzheimer's-dementia (AD) offspring (mean age = 59.
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!