Ask about this productRelated genes to: UCP3 antibody
- Gene:
- UCP3 NIH gene
- Name:
- uncoupling protein 3
- Previous symbol:
- -
- Synonyms:
- SLC25A9
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-11
- Date modifiied:
- 2016-04-28
Related products to: UCP3 antibody
Related articles to: UCP3 antibody
- White adipose tissue (WAT) browning enhances energy expenditure and represents a promising target for metabolic disease. Growth differentiation factor 11 (GDF-11), a circulating member of the TGF-β superfamily, has been implicated in metabolic regulation, but its role in adipose tissue plasticity remains unclear. This study investigated whether GDF-11 regulates WAT browning and the underlying mechanisms. - Source: PubMed
Publication date: 2026/06/16
Sagliocchi SerenaAcampora LuciaMiro CaterinaNappi AnnaritaRestolfer FedericaDentice MonicaCicatiello Annunziata Gaetana - Mitochondrial uncoupling proteins (UCPs) play central roles in vertebrate energy metabolism, with UCP1 specializing as a thermogenic effector in placental mammals. Comparative genomics demonstrated that UCP1, UCP2, and UCP3 originated prior to the emergence of endothermy, suggesting that their ancestral functions evolved in ectothermic vertebrates. Here, we investigated the genomic organization, conserved synteny, and mRNA expression of all three UCP paralogs and homoeologs in the allotetraploid amphibian Xenopus laevis. Comparative genome analyses revealed that all three UCP paralogs and their L and S homoeologs were retained following polyploidization, although local rearrangements were evident for neighboring genes at the UCP2/UCP3 locus. Quantitative expression analyses across adult frog tissues reveal pronounced tissue specificity, with predominant expression of UCP1 and UCP2 in kidney, UCP3 in muscle, and differences in UCP2 homoeolog expression levels. Together, these findings establish a framework for UCPs in an amphibian model organism, primarily linking them to energetically demanding tissues. - Source: PubMed
Publication date: 2026/06/15
Rollwitz ErikJastroch Martin - : Exploiting the metabolic properties of postbiotics is a novel strategy for managing metabolic disorders, including diabetes. Inactivated microorganisms, a major class of postbiotics, improve glycemic control in preclinical and clinical studies. Here, we examined whether heat-killed (HK) () exerts prophylactic or therapeutic anti-hyperglycemic effects in diabetic mice. : Diabetes was induced in male BALB/c mice by streptozotocin (STZ; 150 mg/kg) injection. HK (1 mg) was given orally (three prophylactic doses before STZ) or intradermally (six weekly therapeutic doses after STZ). We assessed glycemic parameters, serum -peptide/insulin (ELISA), and tissue protein expression (Western blot). : Neither route altered body weight or glucose homeostasis in non-diabetic mice. In STZ-diabetic mice, oral prophylactic treatment significantly attenuated hyperglycemia (39-60% reduction weeks 5-8 post-STZ) and showed a trend toward improved serum -peptide, but did not affect dysregulated expression of skeletal muscle (SM), hepatic, pancreatic and renal proteins involved in glucose transport (GLUT2, GLUT4, and SGLT2), glycolysis (α-LDH), mitochondrial uncoupling (UCP2 and UCP3), and antioxidant defense (CAT). Therapeutic intradermal administration significantly decreased blood glucose (~30% at week 5, ~40% at week 6) and modestly enhanced insulin secretion. Hepatic UCP2 and α-LDH and SM UCP3 protein levels were normalized toward non-diabetic levels, whereas hepatic GLUT2 and SM GLUT4 remained largely unchanged. These correlative findings suggest effects independent of insulin-dependent glucose transport, but do not demonstrate direct functional improvement in mitochondrial or redox status. : HK exerts partial anti-hyperglycemic effects in STZ-induced diabetic mice, but the associated protein changes require functional validation before its role as a postbiotic in β-cell dysfunction can be established. - Source: PubMed
Publication date: 2026/05/22
Ali AliHakam Hanin-KhaulaEter AlaaBazzi SamerChahine AmaniAkle CharlesBahr Georges MEchtay Karim S - Coenzyme Q10 (CoQ) is an integral component of the mitochondrial electron transfer system. Most studies have administered the oxidised form of CoQ (ubiquinone) and observed no effects on mitochondrial respiratory function or endurance exercise performance. The reduced form of CoQ, ubiquinol (UQH), has greater bioavailability than ubiquinone, but the effects of UQH supplementation on mitochondrial respiratory function and exercise capacity are unclear. Fifty-four healthy, recreationally active males were randomised to receive either 300 mg·day UQH or placebo (PLA) for 6 weeks in a double-blind independent-group design. Before and after the supplementation period, skeletal muscle mitochondrial respiration variables and protein content of the mitochondrial leak proteins, adenine nucleotide translocase1 + 2 (ANT1 + 2) and uncoupling protein-3 (UCP-3), were assessed. In addition, participants completed a severe-intensity cycle test to exhaustion to assess time to the limit of tolerance (T) and oxygen uptake (V̇O) kinetics. Compared to pre-supplementation and PLA, UQH supplementation increased plasma [CoQ] (P < 0.05), and lowered inverse respiratory control ratio (Pre-PLA: 0.064 ± 0.034 vs. Post-PLA: 0.072 ± 0.026; Pre- UQH: 0.073 ± 0.039 vs. Post-UQH: 0.044 ± 0.019; P < 0.05), suggestive of improved oxidative phosphorylation coupling efficiency. There were no differences in ANT1 + 2 or UCP-3 protein content post-supplementation compared to pre-supplementation between groups (P > 0.05). End-exercise V̇O, change in V̇O between 2 min and end-exercise, and T were not different between groups post-supplementation (P > 0.05). Six-weeks UQH supplementation increased plasma [CoQ] and oxidative phosphorylation coupling efficiency, but did not alter mitochondrial leak proteins, T or V̇O kinetics during severe-intensity exercise in healthy, active males. - Source: PubMed
Publication date: 2026/06/06
Acton Jarred PAlsharif Nehal SBond Jack WCocksedge Stuart PMclellan Abbie GPeden Donald LFunnell Mark PDugdale Hannah FJames Lewis JFerguson Richard AClifford TomBailey Stephen J - Endurance exercise (EXE) has been recognized as a cardioprotective strategy against metabolic diseases, including obesity and type 2 diabetes. However, the precise molecular mechanisms remain incompletely understood, especially in female populations. This study investigates the molecular metabolic signaling nexus in a female mouse model of obese type 2 diabetes (OT2D) induced by a high-fat diet (HFD) and a single dose of streptozotocin (STZ). - Source: PubMed
Publication date: 2026/05/27
Ko JoungboChung EunheeCosio-Lima LudmilaMahmoudian ArmaghanLee Youngil