ArticleEpigenetics2011
Human leptin tissue distribution, but not weight loss-dependent change in expression, is associated with methylation of its promoter.
Article in Epigenetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Epigenetics and human obesity.International journal of obesity (2005) · 2015Pooled it
- Demethylation of leptin promoter in gestational diabetes mellitus: evidence from a mouse model.Frontiers in cell and developmental biology · 2026Article
- DNA methylation and demethylation in adipocyte biology: roles of DNMT and TET proteins in metabolic disorders.Frontiers in endocrinology · 2025Review
- Review
- A negative feedback loop between TET2 and leptin in adipocyte regulates body weight.Nature communications · 2024Article
- Epigenetics in Precision Nutrition.Journal of personalized medicine · 2022Review
- Leptin production capacity determines food intake and susceptibility to obesity-induced diabetes in Oikawa-Nagao Diabetes-Prone and Diabetes-Resistant mice.Diabetologia · 2020Article
- Molecular Insight into the Interaction between Epigenetics and Leptin in Metabolic Disorders.Nutrients · 2019Review
- Review
- Maternal obesity influences expression and DNA methylation of the adiponectin and leptin systems in human third-trimester placenta.Clinical epigenetics · 2019Article
- Association of Leptin Gene DNA Methylation With Diagnosis and Treatment Outcome of Anorexia Nervosa.Frontiers in psychiatry · 2019Article
- Differential placental DNA methylation of VEGFA and LEP in small-for-gestational age fetuses with an abnormal cerebroplacental ratio.PloS one · 2019Article
- Programming of mouse obesity by maternal exposure to concentrated ambient fine particles.Particle and fibre toxicology · 2017Article
- Lower Placental Leptin Promoter Methylation in Association with Fine Particulate Matter Air Pollution during Pregnancy and Placental Nitrosative Stress at Birth in the ENVIRONAGE Cohort.Environmental health perspectives · 2017Article
- Review
- Leptin and adiponectin DNA methylation levels in adipose tissues and blood cells are associated with BMI, waist girth and LDL-cholesterol levels in severely obese men and women.BMC medical genetics · 2015Article
- Mitigating or exacerbating effects of maternal-fetal programming of female mice through the food choice environment.Endocrinology · 2015Article
- Maternal obesity and gestational diabetes are associated with placental leptin DNA methylation.American journal of obstetrics and gynecology · 2014Article
- DNA methylation of leptin and adiponectin promoters in children is reduced by the combined presence of obesity and insulin resistance.International journal of obesity (2005) · 2014Article
- The genetics of fat distribution.Diabetologia · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Leptin is a master regulator of energy homeostasis. Its expression, prevalently localized in adipocytes, is positively related to adipose mass. Epigenetics is emerging as an important contributor to the changes in gene expression undergone by adipose tissue during obesity. We herein investigated the involvement of methylation-dependent mechanisms in leptin regulation in humans. We studied the methylation profile of a 305 bp region in the leptin promoter and analyzed the correspondent leptin expression in visceral adipocyte fraction (AF) and stromal vascular fraction (SVF) of white adipose tissue (WAT) and liver. We found an inverse relationship between methylation and leptin expression with AF displaying a lower methylation density (8%) than SVF and liver (18%, 21%). We evidenced a hot spot region, which mostly differentiates AF versus liver. This includes C15 and 21, which are within the recognition sequences for the transcription factors Sp1 and C/EBP, and C22-23/24, flanking a TATA box. In vitro studies demonstrated that demethylation (by decitabine) increase or de novo activate leptin expression in primary fibroblasts and HeLa cells, respectively. A longitudinal study carried out in patients analyzed before and after bariatric surgery-induced weight loss indicated that in this case decrease in WAT leptin expression (about 50%) does not correspond to changes in promoter methylation density. In conclusion, methylation density in the leptin promoter constitutes one control level for cell type specific leptin expression, whereas weight-loss induced changes in leptin expression does not seem to be methylation-dependent.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.