Human uncoupling protein 1, UCP1 ELISA Kit
- Known as:
- Human uncoupling protein 1, UCP1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-2173
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human uncoupling protein 1 UCP1 ELISA Kit
Related genes to: Human uncoupling protein 1, UCP1 ELISA Kit
- Gene:
- UCP1 NIH gene
- Name:
- uncoupling protein 1
- Previous symbol:
- UCP
- Synonyms:
- SLC25A7
- Chromosome:
- 4q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-19
- Date modifiied:
- 2016-04-28
Related products to: Human uncoupling protein 1, UCP1 ELISA Kit
Related articles to: Human uncoupling protein 1, UCP1 ELISA Kit
- Sleeve gastrectomy (SG) effectively improves metabolic disorders in individuals with obesity and type 2 diabetes (T2DM), but its molecular mechanism remains unclear. Interleukin 27 (IL-27) improves obesity, insulin resistance and white adipose tissue browning; however, its role in SG-mediated metabolic improvement is unconfirmed. This study aimed to explore the role of IL-27 in metabolic disorders improved by SG in obese T2DM rats. Obese T2DM rats were established and randomly divided into an SG group and a sham operation (control) group. Body weight, food intake, fasting blood glucose levels and insulin resistance indicators were dynamically monitored. Enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qRT‒PCR) and immunohistochemistry were used to measure the levels of IL-27 and adiponectin in rat plasma, as well as the expression levels of related molecules in epididymal white adipose tissue (eWAT) and inguinal white adipose tissue (iWAT); 3T3-L1 adipocyte experiments were performed to clarify the regulatory relationship between IL-27 and adiponectin. Compared with the control group, SG significantly reduced body weight, food intake, fasting blood glucose, and insulin resistance in obese T2DM rats (all P < 0.05); it also significantly increased the IL-27 levels in plasma, eWAT, and iWAT, and upregulated the expression of the IL-27 receptor (IL-27Rα) in eWAT, and the expression of p38 mitogen-activated protein kinase (p38 MAPK), peroxisome proliferator-activated receptor α (PPAR-α), peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), and uncoupling protein 1 (UCP-1) in eWAT, as well as UCP-1 in iWAT (all P < 0.05). In vivo experiments revealed a significant positive correlation between IL-27 and adiponectin levels (P < 0.05); in vitro experiments confirmed that IL-27 directly promoted adiponectin expression, whereas adiponectin did not significantly affect IL-27 expression (P > 0.05). SG is associated with elevated IL-27 levels and activation of the eWAT p38 MAPK-PGC-1α pathway in obese T2DM rats, accompanied by improved metabolic parameters, suggesting that IL-27 may play a role in SG-induced metabolic improvement. - Source: PubMed
Publication date: 2026/07/06
Jiao YangDong ShuohuiLiu ZitianZhao XiangWang Kexin - Obesity remains a global health challenge, with limited therapeutic options. Berberine (BBR) shows promise as an anti-obesity agent. However, its clinical application is hampered by modest efficacy and poor bioavailability. - Source: PubMed
Publication date: 2026/07/04
Zhang WenqingFeng YanhongGao ChunyiZhong LinhaiWang WenjunXu MinyingZheng BowenZhang YuehuaWang ShengyuYi ShaoxiongWu ZufangLin YongqingXu BeibeiCheng SijieZhan Yan-YanZhang ShaoliangHong XiaotingHu Tianhui - Brown adipose tissue (BAT) regulates whole-body energy balance through uncoupling protein 1 (UCP1)-dependent thermogenesis and secretion of metabolic factors. Recent studies suggest UCP1-independent mechanisms contribute to energy balance, with UCP1 being conditionally dispensable. However, how adaptation to UCP1 deficiency is regulated remains unclear. Our single-nucleus RNA sequencing of BAT from cold-exposed Ucp1 knockout mice reveals a distinct brown adipocyte subpopulation (U2). U2 adipocytes exhibit a secretory profile enriched in batokines like growth differentiation factor 15 (GDF15), suggesting a shift toward an endocrine role. Functional analyses reveal that GDF15-GFRAL signaling is required to sustain energy expenditure in adipose tissue (AT). The Ucp1/Gfral knockout increased food intake to compensate for decreased energy expenditure in AT. Additionally, a conserved UCP1-GDF15 regulatory axis in human AT is observed. These findings identify a regulatory brown adipocyte subpopulation emerging in response to UCP1 deficiency, representing a compensatory mechanism for maintaining energy homeostasis in mammals. - Source: PubMed
Publication date: 2026/07/04
Wu ChunyanWang TongtongGong SonglinZhang JingMann Charlotte GLi MinLiu ZiyuSun YizhiShi ShenweiLiu ZhenghongDe Bock KatrienBalaz MiroslavSpeakman JohnWolfrum Christian - Sepsis causes muscle wasting and cachexia but mechanisms remain unclear. Cachexia in cancer and burn injury is partly attributed to 'browning'; where white adipose tissue (WAT) develops a catabolic, thermogenic brown adipose tissue-like phenotype. We hypothesised that sepsis-induced muscle wasting is caused by browning. 58 male Wistar rats were randomised to sham (n = 17) or experimental sepsis induced by intraperitoneal zymosan (n = 41). Tibialis anterior mass was measured on Days 3 and 14. Browning was sought using whole body and WAT respirometry, RNA-sequencing, immunoblot, thermal imaging and multi-photon microscopy of WAT. Fourteen-day mortality in rats receiving zymosan was 17%. In survivors, body mass loss peaked at day 3 and persisted to day 14 with associated tibialis anterior muscle mass loss. Zymosan peritonitis caused hypermetabolism during the late recovery phase (Days 11-14), but no difference in epididymal white adipose tissue temperature nor oxygen flux. At Day 14 transcriptomics showed inflammation but no increase in uncoupling protein (UCP)-1 at transcript or protein levels. SERCA2 protein was however increased fourfold in retroperitoneal WAT at day 14 (p = 0.016). Rats recovering from zymosan peritonitis developed muscle wasting and cachexia associated with WAT inflammation and whole-body hypermetabolism. No evidence of browning was seen at functional, transcriptomic or protein levels, therefore our data do not support the hypothesis of classical browning as a driver of sepsis-induced muscle wasting and cachexia. SERCA2 protein expression was however increased in retroperitoneal WAT at day 14. - Source: PubMed
Publication date: 2026/07/03
Tidswell RobertAlqallaf AliHarris JosephFalconer JonathanGolforoush Pelin AArulkumaran NishkanthaKleyman AnnaBrealey DavidRodeheffer Matthew SPatel KetanDuchen Michael RSinger Mervyn - β-Adrenergic receptors (β-ARs) drive the induction of beige adipocytes in rodents and humans, yet the dominant human subtype, β2-AR or β3-AR, remains debated. This study aimed to confirm whether human adipose-derived mesenchymal stem cell (hADSCs)-derived adipocytes can serve as a beiging-competent model under human-relevant browning stimuli and to compare the involvement of β2-AR and β3-AR in hADSCs-derived beige adipocyte differentiation. hADSCs were differentiated into adipocytes using an adipogenic cocktail in the presence or absence of human-relevant browning stimuli or β2-AR/β3-AR-selective agonists with or without β2-AR/β3-AR-selective antagonists. Non-selective β-AR activation induces beige adipogenesis along with mRNA and/or protein expression of beiging markers, including uncoupling protein 1 (UCP1), appearance of multilocular adipocytes, and enhanced mitochondrial respiratory readouts. Moreover, norepinephrine, forskolin, and trigonelline increased mRNA and/or protein expression of UCP1. Pharmacological dissection with subtype-selective agonists and antagonists revealed that activation of β2-AR, but not β3-AR, is necessary and sufficient for inducing UCP1. The β2-AR blockade abolished UCP1 upregulation, whereas the β3-AR blockade had minimal effects. β2-selective stimulation recapitulated the beiging response. This study establishes hADSCs-derived adipocytes as a practicable, human-relevant platform for screening pharmacological agents and food-derived compounds and identifies β2-AR as a translationally actionable target for inducing beige adipocytes in humans. - Source: PubMed
Publication date: 2026/07/03
Maekawa KazukiYokoyama FumikaTsutsumi RieTateishi AkikoMaeda AkifumiTateishi Norifumi