Human Interleukin 1 Delta (IL1d)ELISA Kit
- Known as:
- Human Interleukin 1 Delta (IL1d)Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-2762
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Interleukin 1 Delta (IL1d)ELISA Kit
Related genes to: Human Interleukin 1 Delta (IL1d)ELISA Kit
- Gene:
- DLK1 NIH gene
- Name:
- delta like non-canonical Notch ligand 1
- Previous symbol:
- -
- Synonyms:
- FA1, pG2, Pref-1, ZOG, Delta1
- Chromosome:
- 14q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-09
- Date modifiied:
- 2019-04-23
Related products to: Human Interleukin 1 Delta (IL1d)ELISA Kit
Related articles to: Human Interleukin 1 Delta (IL1d)ELISA Kit
- Childhood obesity is consistently associated with earlier pubertal timing, particularly in girls, whereas its relationship with true central precocious puberty (CPP), defined by premature activation of the hypothalamic-pituitary-gonadal (HPG) axis, is less clearly established. An increased frequency of CPP diagnoses and referrals was reported during the COVID-19 pandemic, alongside changes in body weight, lifestyle, sleep, and psychosocial exposures. Human studies link excess adiposity to hyperleptinemia, insulin resistance, reduced adiponectin, altered sex-steroid bioavailability, and systemic low-grade inflammation, and associate these features with earlier pubertal development-consistently in girls, less so in boys. However, such associations do not establish that obesity directly induces premature hypothalamic activation. Mechanistic understanding of how these peripheral signals may influence pubertal timing derives predominantly from experimental models. The arcuate nucleus kisspeptin/neurokinin B/dynorphin (KNDy) network, a key component of the gonadotropin-releasing hormone (GnRH) pulse generator, interacts with hypothalamic metabolic circuits. In animal models of obesity and overnutrition, altered leptin and insulin signaling, mitochondrial reactive oxygen species generation, and activation of microglia and astrocytes remodel the mediobasal hypothalamus through inflammatory and stress-responsive pathways, including IKKβ/NF-κB and JNK signaling and altered Nrf2-mediated antioxidant defenses. At the molecular level, metabolic status interacts with the epigenetic machinery governing Kiss1 expression: in rodent models of overnutrition, accelerated loss of SIRT1-mediated repression at the Kiss1 promoter facilitates pubertal activation. Human genetic evidence establishes MKRN3 and DLK1 as causes of familial CPP, but evidence that obesity modifies these pathways to induce sporadic CPP is insufficient. Similarly, gut microbial metabolites have been linked experimentally to pubertal timing, and antioxidant micronutrients such as selenium, zinc, and vitamins C and E may be altered in pediatric obesity, yet a specific role in CPP remains unproven. Collectively, current evidence supports a working model in which metabolic, inflammatory, redox, glial, and epigenetic pathways may converge on hypothalamic reproductive circuits to influence pubertal timing in susceptible children. Direct evidence in children with CPP-of hypothalamic oxidative stress, glial activation, Nrf2 dysfunction, SIRT1 remodeling, or microbiome-mediated activation-remains limited or absent. Lifestyle optimization is appropriate for improving metabolic health in children with obesity, whereas antioxidant, micronutrient, and microbiome-targeted interventions should be considered investigational with respect to CPP. Longitudinal pediatric studies that distinguish earlier pubertal timing from true CPP, and that integrate metabolic phenotyping with validated measures of HPG-axis activation, are needed to test this framework. - Source: PubMed
Publication date: 2026/09/13
Bizerea-Moga Teofana-OtiliaChișavu FlaviaChișavu LazărPitulice LauraMoga Tudor VoicuBugi Meda-AdaFoghiș Cornel FlaviusIsac RalucaMărginean OtiliaBalica Nicolae Constantin - Is sperm DNA methylation variability, referred here as sperm Epigenetic Variability Outliers and Stochasticity (EVOS), associated with time-to-pregnancy (TTP) and pregnancy outcomes in couples attempting to conceive naturally? - Source: PubMed
Publication date: 2026/09/25
Nowak KarolinaNobles Carrie JOluwayiose Oladele ABertolla Ricardo PSuvorov AlexanderPilsner J Richard - Chronic lymphocytic leukemia (CLL) is a heterogeneous B-cell malignancy in which B-cell receptor signaling, microenvironmental interactions, genomic lesions, and epigenetic deregulation cooperate to shape disease behavior. The imprinted DLK1-DIO3 locus at chromosome 14q32 contains the largest human miRNA cluster and has been implicated in cancer-related regulatory networks; however, its contribution to CLL remains incompletely defined. - Source: PubMed
Publication date: 2026/09/03
Markopoulos Georgios SSimos Yannis VTsamis Konstantinos ILakkas LamprosHatzimichael EleftheriaKapsali EleniPeschos DimitriosBenetatos Leonidas - Non-coding RNAs from the Dlk1-Dio3 locus are critical for the maturation of metabolic tissues in early stages of postnatal development; however, their role in the mature organs remains elusive. Herein, we show that microRNAs from the miR-379/miR-410 cluster are robustly upregulated in livers of subjects with obesity and various mouse models of metabolic dysfunction. Adult-onset, combinatorial inhibition of this miRNA cluster by hepatocyte-specific expression of a decoy sequence reduces triglyceride, total and LDL cholesterol circulating levels, decreases basal glycemia and improves glucose tolerance and insulin sensitivity irrespective of sex. Consistent with the decoy-triggered enhancement of PI3K/mTOR signaling in these mice, hepatocytes expressing the combinatorial decoy show augmented mitochondrial mass and function. Notably, decoy therapy also ameliorates glucose and lipid homeostasis in both type 1 diabetic and diet-induced, type 2 pre-diabetic, obese male animals. Collectively, our results demonstrate that microRNAs from the miR-379/miR-410 cluster are critical regulators of metabolic homeostasis in the mature liver. Given the preservation of miRNA dysfunction in human obesity, hepatocyte-specific combinatorial inhibition of a large miRNA cluster represents an approach towards multi-parameter improvements in diabetes and obesity. - Source: PubMed
Publication date: 2026/09/21
Gil-Lozano ManuelSimoes EstefaníaWu MoyaWiedemann TobiasKwon YunSekar RevathiMorigny PaulineTroullinaki MariaMerl-Pham JulianeBuettner MichaelFeuchtinger AnnetteJouffe CelineMaida AdrianoHass DanielaSamaga DanielWolff GretchenMachado JulianoGiroud MaudeKlepac KatarinaCummins Carolyn LRíos García MarcosWeber PeterZeigerer AnjaUhlenhaut N HenrietteSzendroedi JuliaBlüher MatthiasHerzig Stephan - is a major human pathogen that can elicit immune-inflammatory responses and infections, largely driven by its broad repertoire of antigenic proteins. Understanding these factors is valuable for elucidating mechanisms of infection. - Source: PubMed
Publication date: 2026/09/02
Dalloul Rajaa S DSohail Muhammad UChennakkandathil SareenaSawarth HinaAl-Noubi MunaChoi SunkyuSchmidt Frank