UCP3 C-terminal Blocking Peptide
- Known as:
- UCP3 C-terminal Blocking Peptide
- Catalog number:
- 30r-au002
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- UCP3 C-terminal Blocking Peptide
Related genes to: UCP3 C-terminal Blocking Peptide
- 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 C-terminal Blocking Peptide
Related articles to: UCP3 C-terminal Blocking Peptide
- This study investigates whether, in a mouse model under ad libitum feeding conditions, substituting a wheat-flour-based diet with a rice-flour-based diet influences body-weight- and glucose-related outcomes. Using female KK- mice, we compared diets containing wheat or rice flour. After seven weeks, the rice-flour-based diet was associated with significantly lower body weight (8.5% lower) and improved glucose tolerance compared with the wheat-flour-based diet; however, no significant improvement in insulin sensitivity was observed. Gene expression analysis revealed that mRNA expression in skeletal muscle was significantly higher in the rice-flour-based diet group than in the wheat-flour-based diet group, whereas no significant differences were observed in the expression of genes encoding enzymes involved in pyruvate oxidation and the TCA cycle. These results suggest that the lower body weight and improved glucose tolerance observed in the rice-flour-based diet group may be associated with increased skeletal muscle mRNA expression; however, whether this increase reflects altered UCP3 protein activity or energy expenditure remains unclear and requires further functional validation. Overall, substituting the wheat-flour-based diet with the rice-flour-based diet was associated with lower body weight and improved glucose tolerance in this model. - Source: PubMed
Publication date: 2026/09/10
Yokoyama YokoOsari NanaTaworntawat TanonSekimoto SumitoTsubota KazuoKitamura NahoWatanabe Mitsuhiro - Cold exposure is a major physiological stimulus that promotes adipose tissue browning and enhances thermogenic capacity. As a cold-tolerant breed, may rely on distinct adaptive mechanisms in adipose tissues, but how different adipose depots respond to cold stress remains unclear. This study systematically examines how cold exposure affects adipose tissue morphology, thermogenic gene expression, and the differentiation potential of preadipocytes derived from four adipose depots-cervical, axillary, perirenal, and inguinal-in . Adipose tissues from the four depots were collected and analyzed using infrared thermography, histological staining, scanning electron microscopy, real-time quantitative PCR, Western blotting and in vitro differentiation assays. The results demonstrated that cold stress induced depot-specific remodeling patterns. Infrared thermography showed that the subcutaneous adipose depots including inguinal and axillary depots maintained relatively higher surface temperatures following cold exposure. Histological and ultrastructural analyses revealed typical beige-like characteristics in inguinal depots, including the accumulation of small lipid droplets, whereas changes in other depots were minimal. Molecular analyses further confirmed this heterogeneity: inguinal depots exhibited the strongest beiging response, characterized by significant upregulation of key thermogenic markers (, , and ) and lipolytic genes ( and ) at the mRNA and/or protein levels. In contrast, visceral adipose depots showed weak or suppressed thermogenic activation. In vitro differentiation assays demonstrated that preadipocytes isolated from inguinal depot had the strongest beiging potential, forming tightly packed small lipid droplets and markedly increasing the expression of beige adipose-related genes upon induction. In conclusion, this study demonstrates that cold stress induces distinct beige remodeling across adipose depots in , with the inguinal depot exhibiting the strongest thermogenic response and differentiation potential at morphological, molecular, and cellular levels. These findings identify the inguinal depot as a key site for adaptive thermogenesis and provide novel insights into adipose tissue remodeling and environmental adaptation in large mammals. - Source: PubMed
Publication date: 2026/09/15
Yang ShuoMu LinlinHe XinmiaoWang WentaoZhang HaifengTian MingWu SaihuiLiu ZiguangChen HeshuNing SiyuYang XiuqinLiu Di - Genetic causes of early-onset obesity remain undercharacterized in East Asian children. This study evaluated a whole-exome sequencing (WES)-centered diagnostic workflow in Chinese children with obesity onset before 5 years. - Source: PubMed
Publication date: 2026/07/22
Chen SiZhang JingGe LiyuanLi ZhonghuiWang LiuxuCheng Xinran - Cardiometabolic diseases (CMDs) impose a significant global health burden. Although CMDs rarely occur in isolation, most genetic studies have examined individual conditions separately, overlooking shared pathogenic pathways that link them into a continuous cardiometabolic continuum. Moreover, population-specific data for Eastern and Central Europe are scarce, and combined effects of variants in key metabolism-related genes, such as UCP1-UCP3 and FTO, have not been studied within cardiometabolic continuum. In this study, we investigated individual and combinatorial effects of UCP1-UCP3, and FTO variants on risk of CMDs as a continuum in Central Russian and Polish populations. We identified novel risk-increasing combinations: minor alleles of UCP2 c.-866G > A and UCP3 c.-55C > T; and minor alleles of UCP3 c.-55C > T and FTO c.46_23525T > A with wild alleles of four UCP1 and two UCP2 variants. Protective effects were observed for two novel combinations: minor allele of FTO c.46_23525T > A with wild alleles of all studied UCPs variants; and minor allele of UCP2 c.-866G > A with wild allele of UCP2 p.Ala55Val. The FTO variant showed context-dependent effects, shifting from risk to protection depending on genetic background. Increased age, BMI, WtHR, and BF% were also significant predictors, with sex-specific differences. Predictive quality of models integrating genetic and non-genetic factors (AUC up to 0.97) further underscore the potential value of this approach. In silico analysis suggested these variants exhibit regulatory functions across various tissues, which potentially involved in CMD pathogenesis. This is the first study to demonstrate combinatorial UCP1-UCP3 and FTO effects on risk of CMDs as a continuum in Central Russian and Polish populations. - Source: PubMed
Publication date: 2026/09/03
Pravednikova Anna ENikitich AntoninaAndrzejczak AnnaTomkiewicz AnnaKarabon LidiaSkrypnik DamianBogdanski PawelGrebenshchikov Eugene SShulgin BorisShidlovskii Yulii V - Skeletal muscle mitochondrial dysfunction and altered myokine signaling contribute to insulin resistance in type 2 diabetes. This study compared the effects of non-work-matched high-intensity interval training (HIIT) and moderate-intensity interval training (MIIT) on skeletal muscle exerkine/myokine- and mitochondrial biogenesis-related gene expression and systemic metabolic indices in streptozotocin-nicotinamide-induced diabetic rats. Twenty-four male Wistar rats were initially allocated to healthy control, diabetic control, MIIT, or HIIT groups; after predefined treadmill-familiarization exclusions, five animals per group were analyzed. Training was performed for 6 weeks, three sessions per week, with MIIT prescribed at 70% maximal aerobic speed and HIIT at 90% maximal aerobic speed. Gastrocnemius expression of FNDC5, OSTN, PGC-1α, TFAM, CCO, and UCP3 was quantified by RT-qPCR, and fasting glucose, insulin, lipid variables, HOMA-IR, HOMA-β, QUICKI, and TyG index were assessed. Diabetes reduced all targeted transcripts and impaired insulin-related metabolic indices. Both MIIT and HIIT partially restored myokine- and mitochondrial-related transcripts compared with diabetic controls, with no significant differences between training protocols for most molecular outcomes. HIIT produced lower fasting insulin and HOMA-IR than MIIT but imposed a greater estimated cumulative workload. These findings indicate that interval training partly attenuates diabetes-associated transcriptional and insulin-related metabolic disturbances, while intensity-specific conclusions require work-matched designs. - Source: PubMed
Publication date: 2026/08/07
Rezae SaeedMehr Payam AbasianPournemati ParisaLaher IsmailEken ÖzgürAldhahi Monira I