ADRB3
- Known as:
- ADRB3
- Catalog number:
- 001246A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADRB3
Related genes to: ADRB3
- Gene:
- ADRB3 NIH gene
- Name:
- adrenoceptor beta 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8p11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-04
- Date modifiied:
- 2015-10-15
Related products to: ADRB3
Related articles to: ADRB3
- Epicardial adipose tissue (EAT) has been linked to cardiac conduction through direct myocardium interaction and endocrine activity. We investigated sex-specific associations between ventricular electrical activity and the molecular composition of EAT. - Source: PubMed
Publication date: 2026/09/07
Ahmed Nadeem ASánchez-López DavidBasdas RumeysaNúñéz-Caamaño José RamónMartínez-Cereijo José ManuelReija-López LauraFernández Ángel LGarcía-Seara JavierRodriguez-Mañero MoisésGonzález-Juanatey José REiras Sonia - Polymorphisms in genes involved in obesity-related metabolic pathways are associated with metabolic syndrome (MetS). We hypothesized that variants in FTO, LEP, LEPR, ADRB3, ADIPOQ, TCF7L2, ENPP1, APOA5, PPARG, and CYP11B2 are associated with MetS and obesity-related traits. - Source: PubMed
Publication date: 2026/09/21
Stefani Tamiris Invencioni MoraesHirata Thiago Dominguez CrespoCerda Alvarode Oliveira RaquelDos Santos Marina AparecidaFajardo Cristina MorenoDorea Egídio LimaBernik Márcia Martins SilveiraHirata Mario HiroyukiHirata Rosario Dominguez Crespo - Human seminal vesicle (hSV) contractions contribute to seminal emission, but regulation of spontaneous oscillatory contractions (SOCs) between ejaculations remains incompletely understood. We examined how pharmacological enhancement of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) signaling affects hSV contractile activity. - Source: PubMed
Publication date: 2026/08/28
Okada TatsunoriTozaki-Saitoh HidetoshiKajioka ShunichiKato KenichiShiota MasakiKashiwagi EijiEto Masatoshi - Leptin, secreted by adipocytes, conveys the status of peripheral energy stores to the brain to regulate appetite and metabolism. Although sympathetic activation via β3-adrenergic receptors (β3-ARs) has been shown to suppress leptin expression, it remains unclear whether this regulation arises directly within adipocytes or through other populations. In addition, it is unclear whether β3-AR signaling contributes to the fasting-induced reduction in leptin. To address this, we generated a novel transcriptional block mouse () enabling global β3-AR inactivation and adipocyte-specific reexpression (; -Cre). Global loss of increased plasma leptin levels, whereas reexpression in adipocytes normalized leptin and restored β3-AR agonist-induced leptin suppression. Analysis of mRNA revealed depot-specific regulation, with β3-AR signaling predominantly affecting gonadal and subcutaneous white adipose tissue, whereas brown adipose tissue responses were modest and variable. Despite these effects, fasting for 48 h comparably reduced plasma leptin and mRNA in both wild-type (WT) and mice, indicating that β3-AR signaling is not required for the fasting-induced decline in leptin. Collectively, these findings establish adipocyte β3-AR signaling as a key regulator that constrains leptin synthesis under basal and stimulated conditions in male mice, but not during energy deprivation. Together, these findings clarify the role of adipocyte β3-adrenergic signaling in leptin regulation and provide new insight into the sympathetic control of adipose tissue function. This study introduces a novel Adrb3 transcriptional block mouse model that enables global inactivation or adipocyte-specific reexpression of β3-adrenergic receptor signaling. Using this approach, we demonstrate that adipocyte β3-adrenergic signaling directly restrains leptin production under basal and stimulated conditions but is dispensable for fasting-induced leptin suppression. These findings refine the role of sympathetic signaling in adipose tissue and clarify mechanisms governing leptin regulation. - Source: PubMed
Publication date: 2026/09/01
Heaselgrave Samuel RWyler Steven CThomas ShreyaTinajero ArelyGalvan MarcoMihaila EmmaFan RogerFujikawa TeppeiScherer Philipp EElmquist Joel K - Genetic polymorphisms modulate the risk of metabolic complications of obesity; yet, it remains unclear how genotype reshapes actual dietary intake and why these mechanisms differ between men and women. The aim of this study was to identify sex-specific associations of three common polymorphisms (MTHFR C677T, PPARG Pro12Ala, ADRB3 Trp64Arg) with habitual nutrient intake in patients with obesity, and to explore candidate sex-differentiated dietary hypotheses for future prospective testing. A single-centre cross-sectional study was performed in 348 patients with obesity (83 men, 265 women; BMI ≥ 30 kg/m; age 18-60 years). Genotyping was performed by allele-specific real-time PCR from buccal swabs. Habitual intake of more than 18 nutrients was assessed using a standardised Russian software-based questionnaire. Statistical analysis included Kruskal-Wallis and Mann-Whitney tests with Bonferroni correction (threshold < 0.017), as well as odds ratios (OR) with 95% confidence intervals. Genotype distributions were tested for Hardy-Weinberg equilibrium, and genotype-nutrient associations were additionally examined in models adjusted for age, BMI and total energy intake. Three genotype-phenotype associations remained significant after Bonferroni correction. In men, the dominant-heterozygous MTHFR C/T genotype was associated with a hypercaloric dietary pattern-excess protein, fat, sodium and phosphorus-and with a high risk of arterial hypertension (OR 5.96, 95% CI 1.48-24.08; = 0.010). The sodium load in C/T carriers was a consequence of overall overeating rather than a selective preference for salty foods. In men, ADRB3 Trp64Arg carriage was associated with massive dietary cholesterol overconsumption (+466% vs. +153% in Trp/Trp; = 0.012), whereas in women the opposite direction was observed. The PPARG G/G genotype in women was associated with elevated alanine aminotransferase ( = 0.027), most pronounced under 40 years ( = 0.011), and is considered a marker of hepatic risk without a confirmed dietary target. In women, the MTHFR T/T homozygous genotype showed suggestive associations with excessive mono-/disaccharide intake and a tendency toward hypertension (OR 2.62, 95% CI 1.07-6.43; = 0.035); however, these did not survive FDR correction and require independent validation. Genetic polymorphisms were associated with sex-specific patterns of actual dietary intake, a finding that extends current knowledge beyond biochemical risk associations. Based on these associations, we propose testable hypotheses rather than clinical recommendations: that caloric restriction (with consequent sodium reduction) in men with MTHFR C/T, cholesterol restriction in men with ADRB3 Arg64, and mono-/disaccharide restriction in women with MTHFR T/T might reduce metabolic risk; women with PPARG G/G may warrant ALT monitoring. These findings suggest that genotype-informed dietary strategies may need to be sex-specific, and that the window for intervention may be earlier in life than currently practised. However, these hypotheses require prospective interventional validation before any clinical application. - Source: PubMed
Publication date: 2026/08/04
Lapik Irina ATarmaeva Inna YuNikityuk Dmitry B