Drug Database
YY

YY-3130 (YY 3130 / YY3130)

✓ Approved

YuYu Pharma · 小分子 · 小分子

什么是 YY-3130?

YY-3130 是一种小分子,由YuYu Pharma研发。该药已获批,用于治疗相关适应症,给药途径:Unknown。

药物档案

商品名YY 3130, YY3130
公司YuYu Pharma
药物类别小分子
给药途径Unknown
状态Approved

治疗适应症

YY-3130 针对 1 个适应症,涉及 1 个治疗领域。

治疗领域疾病/病症分期
Metabolism and nutrition disordersHypercholesterolaemia✓ Approved

相关研究文献

PubMedClinical science (London, England : 1979)2026-09-10

How lipid ingestion is sensed: the mechanisms underlying intestinal hormone secretion.

Santos-Hernández Marta M, Gribble Fiona M FM, Reimann Frank F

Dietary lipids are potent stimulators of intestinal hormone secretion, which plays a central role in the regulation of digestion, appetite, glucose homeostasis, and lipid metabolism. Following digestion in the intestinal lumen, lipid-derived molecules are detected through complementary mechanisms involving lipid transporters, nutrient-sensing receptors, intracellular metabolic pathways, and bile acid signaling. These pathways couple nutrient availability to the secretion of enteroendocrine hormones, including glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), peptide YY (PYY), cholecystokinin (CCK), ghrelin and serotonin, thereby coordinating local and systemic metabolic responses. In the small intestine, CD36 contributes to lipid uptake and sensing, while intracellular lipid processing and chylomicron formation influence hormone secretion. Bile acids facilitate lipid digestion and absorption and further regulate enteroendocrine function through receptor-mediated signaling pathways. This review examines the cellular and molecular mechanisms underlying intestinal lipid sensing, with particular emphasis on the roles of CD36, chylomicron formation, bile acid signaling, and nutrient-sensing receptors in the regulation of enteroendocrine hormone secretion.

PMID 42719962
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PubMedJournal of pediatric endocrinology & metabolism : JPEM2026-09-10

Physical development, hormonal and peptide status in preschool and school-age children born to mothers with obesity.

Firsova Liudmila L, Novikova Valeria V, Evdokimova Nina N, Gurina Olga O et al.

To determine features of physical development and hormonal status in preschool- and school-age children born to mothers with obesity. A case-control single-center study included a group of 69 children (29 aged 5-6 years; 40 aged 14-16 years) born to mothers with body mass index (BMI)≥30 kg/m2 before and during pregnancy (MO group). The control group included 61 children (27 aged 5-6 years; 34 aged 14-16 years) born to mothers with steady normal BMI (18.5-24.9 kg/m2). Anthropometric measurements were analyzed using the World Health Organization (WHO) AnthroPlus program. In 59 children, insulin-like growth factor 1 (IGF-1), insulin-like growth factor 2 (IGF-2), peptide YY (PYY), serotonin, leptin, and ghrelin levels were evaluated using enzyme-linked immunosorbent assay. Statistical analysis was performed. We did not find any differences in height among children aged 5-6 years (p=0.42) and 14-16 years (p=0.12). Children in the MO group had higher weight Z-score and BMI Z-score (p<0.001). In children aged 5-6 years in the MO group, serum leptin was higher (p=0.03) and had a positive correlation with body weight and BMI. Ghrelin level was higher in adolescents of the MO group (p=0.03); however, there were no correlations with body weight (p>0.05). IGF-1, IGF-2, serotonin, and PYY did not show significant differences between the two groups (p>0.05). Children born to mothers with obesity are more likely to suffer from obesity. However, more comprehensive studies on hormonal profiles are needed, incorporating an analysis of additional factors.

PMID 42720320
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PubMedPeerJ2026-09-08

Associations between gut microbiota on carcass traits and meat quality in Neijiang pigs, Yorkshire pigs, and their hybrids.

Hao Ziling Z, Yang Yiting Y, Yan Zhijuan Z, Du Yong Y et al.

This study was designed as an exploratory analysis to compare carcass performance, meat quality traits, and gut microbiota of Neijiang pigs (NN), Yorkshire pigs (YY), and Yorkshire × Neijiang hybrid pigs (YN), with the goal of generating testable hypotheses regarding potential links between gut microbial composition and production phenotypes. Compared with NN pigs, YN hybrids exhibited improved carcass performance while inheriting the favorable meat quality characteristics of Neijiang pigs. The results of 16S rRNA sequencing analysis showed that the relative abundance of the microbiota was similar to that of NN pigs. LDA effect size (LEfSe) results showed that Streptococcus, Treponema, probable_genus_10 and Fibrobacter were the differentially enriched taxa in YN pigs (p < 0.05). Correlation analysis was performed on carcass, meat quality and intestinal microbiota screened out by LEfSe. The results showed that Akkermansia tended to positively associate with body length and oblique length in YN pigs; Dialister correlated positively with dressing rate and pH45min; Treponema showed positive trends with a*45min and a*24h (p < 0.05). Finally, the correlation network model preliminarily mapped associations among production traits, gut microbiota, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways for exploratory screening. Nine core microbial taxa exhibited close correlations with phenotypic indicators, which implied that these microbes might modulate metabolic pathways to shape pig performance. Overall, hybrids inherited superior parental carcass and meat quality but harbored unique gut microbial communities relative to purebreds-these preliminary correlative observations generate new hypotheses that gut microbiota may contribute to heterosis-associated phenotypic advantages, which require further targeted validation.

PMID 42708027
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PubMedClinical nutrition (Edinburgh, Scotland)2026-09-04

Postprandial metabolic responses to a glycomacropeptide-based protein substitute in different meal contexts - Implications for phenylketonuria (PKU).

Rodrigues Catarina C, Jácome-Pacheco Dúnio D, Barreiros-Mota Inês I, Ismael Shámila S et al.

Casein glycomacropeptide supplemented with amino acids (CGMP-AA) is used in the treatment of phenylketonuria (PKU). However, its acute metabolic effects when consumed with other foods remain poorly understood. This study investigated the impact CGMP-AA consumed alone or with two low-protein meals providing carbohydrates with either fibre or fat. In this randomised crossover trial, fifteen healthy adults (27.0 ± 7.9 y; 7 females) consumed: A) CGMP-AA alone; B) CGMP-AA with low-protein bread and unpeeled apple; or C) CGMP-AA with low-protein bread and olive oil. Blood samples were collected over 120 min to assess glucose, insulin, C-peptide, amino acids, and appetite-related hormones (glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), and peptide YY (PYY)). Co-ingestion with low-protein foods had limited effects on total essential and large neutral amino acid concentrations over 120 min, but increased Tyr incremental area under the curve (iAUC(0-120min)) and peak concentration (Cmax) compared with CGMP-AA alone. Meal B elicited the highest glucose, insulin, and C-peptide iAUC(0-120min) and Cmax, followed by meal C, whereas meal A induced minimal glycaemic and insulinaemic excursions. Meal C produced the greatest GIP response, whereas GLP-1 and PYY did not differ between test meals. In healthy adults, CGMP-AA elicited distinct acute postprandial responses depending on whether it was consumed alone or with low-protein foods. CGMP-AA consumed with food is not metabolically equivalent to CGMP-AA consumed alone, and carbohydrate-with-fibre and carbohydrate-with-fat meal contexts affect distinct aspects of the postprandial response. These findings should be confirmed in individuals with PKU before being translated into dietary recommendations.

PMID 42696856
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PubMedJournal of ethnopharmacology2026-09-01

Yunpi Xiaoji Formula Restores Gut-Brain Axis Homeostasis in Infantile Anorexia by Targeting the SCFAs-GPR43 Signaling Pathway.

Zhao Binyuan B, Tian Wenxia W, Chen Jing J, He Yuezhen Y et al.

Infantile anorexia (IA) represents a complex feeding disorder with limited therapeutic options currently available. The traditional Chinese medicine (TCM) formula Yunpi Xiaoji Formula (YPXJF) has demonstrated clinical efficacy in ameliorating IA symptoms; however, its underlying mechanisms, particularly those associated with the gut-brain axis, remain to be systematically elucidated. This study aimed to determine the association between anorexia and the SCFAs-GPR43-PYY/GLP-1 pathway, to investigate whether YPXJF ameliorates IA via modulation of this pathway, and to elucidate its role in gut-brain axis crosstalk. The phytochemical profile of YPXJF and its absorbed serum constituents was characterized using UHPLC-MS. An integrative approach combining in vivo IA rat models and in vitro cell systems was employed. Interventions included the GPR43 agonist 4-CMTB and antagonist GLPG0974. Genetic techniques involved GPR43 knockdown and overexpression in GLUTag L-cells. Gut-brain axis communication was modeled using a Transwell co-culture system of GLUTag L-cells and POMC neurons. Analytical methods comprised H&E staining, immunohistochemistry, immunofluorescence, Western blotting, RT-PCR, and ELISA. A total of 883 compounds were detected in YPXJF, with 130 absorbed constituents (82 prototypes and 48 metabolites) identified in serum, primarily phenolic acids, alkaloids, and flavonoids. The pathogenesis of IA was driven by aberrant activation of the gut-brain axis. In IA rats, elevated levels of fecal SCFAs (acetate, propionate, and butyrate) activated G protein-coupled receptor 43 (GPR43) on colonic L-cells, leading to excessive secretion of the anorexigenic hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY). These hormones subsequently acted on the hypothalamus to upregulate anorexigenic POMC/CART neurons and downregulate orexigenic NPY/AGRP neurons, ultimately resulting in anorexia. YPXJF treatment effectively reversed this dysregulation by normalizing fecal SCFA profiles and downregulating colonic GPR43 expression, which reduced GLP-1 and PYY secretion. Consequently, YPXJF suppressed hypothalamic POMC neuronal activity and enhanced NPY neuronal activity, restoring appetite and body weight. These findings were confirmed by molecular assays showing that YPXJF efficacy was blunted by GPR43 overexpression or agonist co-administration. YPXJF ameliorates IA by modulating the SCFAs-GPR43 pathway and restores gut-brain axis homeostasis by attenuating pathological anorexigenic signaling and restoring physiological appetite regulation. This study provides a mechanistic basis for YPXJF's clinical application and identifies GPR43 as a promising therapeutic target.

PMID 42680126
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PubMedOncology reports2026-08-28

[Expression of Concern] Inhibition of TMEM45A suppresses proliferation, induces cell cycle arrest and reduces cell invasion in human ovarian cancer cells.

Guo Jing J, Chen Li L, Luo Ning N, Yang Weihong W et al.

Following the publication of the above article, a concerned author drew to the authors' attention that the western blot data showing the TGF β1‑experiments in Fig. 4C and D on p. 3129 for the HO‑8910 and A2780 cell lines were strikingly similar, suggesting that the data in this figure had been assembled incorrectly. In addition, various of the western blots featured in this figure, and also in Fig. 2B on p. 3127, were remarkably similar to data which were subsequently submitted for publication in articles written by different authors at different research institutes to a number of different journals, at least one of which has since been retracted on account of data sharing issues with other papers. The authors have been contacted by the Editorial Office to offer an explanation for the apparent anomalies in the presentation of the western blot data in this paper, and we are awaiting their response. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Oncology Reports 33: 3124‑3130, 2015; DOI: 10.3892/or.2015.3902].

PMID 42663282
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