ArticleMolecular metabolism2015
SOCS3 deficiency in leptin receptor-expressing cells mitigates the development of pregnancy-induced metabolic changes.
Article in Molecular metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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
25 citing papers in PubMed, 50 citations in OpenAlex.
- Reduced melanocortin tone modulates feeding during pregnancy in mice.Nature communications · 2026Article
- Reproductive experience promotes permanent body growth independently of growth hormone.bioRxiv : the preprint server for biology · 2026Article
- Leptin Resistance and Cardiometabolic Disorders: Bridging Molecular Pathways, Genetic Variants, and Therapeutic Innovation.Current cardiology reviews · 2025Review
- New findings on brain actions of growth hormone and potential clinical implications.Reviews in endocrine & metabolic disorders · 2024Review
- The Interplay between Maternal Nutrition and Oxidative Stress.Nutrients · 2023Article
- Placental Transcriptome Profiling in Subtypes of Diabetic Pregnancies Is Strongly Confounded by Fetal Sex.International journal of molecular sciences · 2022Article
- Hepatokine Fetuin B expression is regulated by leptin-STAT3 signalling and associated with leptin in obesity.Scientific reports · 2022Article
- SOCS3 Ablation in Leptin Receptor-Expressing Cells Causes Autonomic and Cardiac Dysfunctions in Middle-Aged Mice despite Improving Energy and Glucose Metabolism.International journal of molecular sciences · 2022Article
- Epigenetic Profiling in the Saliva of Obese Pregnant Women.Nutrients · 2022Observational
- Modelling gestational diabetes mellitus: large animals hold great promise.Reviews in endocrine & metabolic disorders · 2021Review
- Review
- Deletion of growth hormone receptor in hypothalamic neurons affects the adaptation capacity to aerobic exercise.Peptides · 2021Article
- Exploring the causes and consequences of maternal metabolic maladaptations during pregnancy: Lessons from animal models.Placenta · 2020Review
- Under-carboxylated osteocalcin regulates glucose and lipid metabolism during pregnancy and lactation in rats.Journal of endocrinological investigation · 2020Article
- Central growth hormone action regulates metabolism during pregnancy.American journal of physiology. Endocrinology and metabolism · 2019Article
- Maternal β-Cell Adaptations in Pregnancy and Placental Signalling: Implications for Gestational Diabetes.International journal of molecular sciences · 2018Review
- Leptin Signaling in the Control of Metabolism and Appetite: Lessons from Animal Models.Journal of molecular neuroscience : MN · 2018Review
- Maternal metabolic adaptations are necessary for normal offspring growth and brain development.Physiological reports · 2018Article
- Hypertriglyceridemia in female rats during pregnancy induces obesity in male offspring via altering hypothalamic leptin signaling.Oncotarget · 2017Article
- The role of leptin in health and disease.Temperature (Austin, Tex.) · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveDuring pregnancy, women normally increase their food intake and body fat mass, and exhibit insulin resistance. However, an increasing number of women are developing metabolic imbalances during pregnancy, including excessive gestational weight gain and gestational diabetes mellitus. Despite the negative health impacts of pregnancy-induced metabolic imbalances, their molecular causes remain unclear. Therefore, the present study investigated the molecular mechanisms responsible for orchestrating the metabolic changes observed during pregnancy.
methodsInitially, we investigated the hypothalamic expression of key genes that could influence the energy balance and glucose homeostasis during pregnancy. Based on these results, we generated a conditional knockout mouse that lacks the suppressor of cytokine signaling-3 (SOCS3) only in leptin receptor-expressing cells and studied these animals during pregnancy.
resultsAmong several genes involved in leptin resistance, only SOCS3 was increased in the hypothalamus of pregnant mice. Remarkably, SOCS3 deletion from leptin receptor-expressing cells prevented pregnancy-induced hyperphagia, body fat accumulation as well as leptin and insulin resistance without affecting the ability of the females to carry their gestation to term. Additionally, we found that SOCS3 conditional deletion protected females against long-term postpartum fat retention and streptozotocin-induced gestational diabetes.
conclusionsOur study identified the increased hypothalamic expression of SOCS3 as a key mechanism responsible for triggering pregnancy-induced leptin resistance and metabolic adaptations. These findings not only help to explain a common phenomenon of the mammalian physiology, but it may also aid in the development of approaches to prevent and treat gestational metabolic imbalances.
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.