Ask about this productRelated genes to: SIRT1 antibody
- Gene:
- SIRT1 NIH gene
- Name:
- sirtuin 1
- Previous symbol:
- -
- Synonyms:
- SIR2L1
- Chromosome:
- 10q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-20
- Date modifiied:
- 2016-10-05
Related products to: SIRT1 antibody
Related articles to: SIRT1 antibody
- Identifying physiological changes during the transition period is essential for improving the health and productivity of dairy goats. This study evaluated hematological, biochemical, hormonal, oxidative stress, and molecular alterations in Shami goats during the pre-pregnancy, late pregnancy, and early lactation periods. Eighty clinically healthy goats were examined, and blood samples were analyzed for hematological indices, metabolic and hormonal profiles, oxidative stress biomarkers, and relative expression of genes associated with energy metabolism, antioxidant defense, inflammation, and autophagy. Late pregnancy was characterized by significant ( < 0.05) increases in red blood cell count (RBCs), hemoglobin concentration (Hb), neutrophils, albumin, globulin, urea, insulin-like growth factor-1 (IGF-I), and malondialdehyde (MDA), accompanied by decreased glucose, cholesterol, total protein (TP), antioxidant markers, total leukocyte count, packed cell volume, and monocytes. Early lactation was associated with higher non-esterified fatty acid, triiodothyronine (T3), and thyroxine (T4) levels. Genes involved in lipid mobilization and oxidation, ketogenesis, inflammation, cellular stress, and autophagy; , , , , , , , , , , , , , and were significantly upregulated, whereas antioxidant- and glucose transport-related genes , , , , and were downregulated during the transition period. The results indicate well-orchestrated metabolic and molecular adaptations that can be employed as biological indicators to track the physiological status of Shami goats. These findings fulfilled the study objective and identified potential biomarkers of the transition period in Shami goats. - Source: PubMed
Publication date: 2026/08/04
Alqhtani Haifa AliAl-Hazani Tahani M ISayed Ahmed ElAteya AhmedGhonaim Ahmed HZarah Rowa KSafhi Fatmah AAlmubarak AdelBabiker HusseinElkhidr Rasha YassinEl-Deeb Wael MKhalid Ahmed MagzoubAlkuwayti Mayyadah AbdullahMarzok Mohamed - Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder involving metabolic impairment, neuroinflammation, synaptic failure, and comorbidities. Hence, therapeutic development for AD is rapidly shifting from a single-target approach, centred on amyloid-beta (Aβ) reduction, to multi-target strategies. In this study, we investigated the neuroprotective profile of two acetanilide derivatives, SG-22 and SG-23, originated from the halogen-free thyronamine-like lead compound SG-2. Their efficacy was evaluated through an integrated approach combining in vitro cellular models, in vivo phenotypic screening in a AD model, and comprehensive ADME-Tox profiling. In U87MG cells, both SG-22 and SG-23 effectively prevented Aβ-induced cytotoxicity and restored autophagy-related gene expression, including LC3, SIRT1, and SIRT6, while reducing mTOR and SIRT5 levels. Furthermore, all compounds exhibited anti-inflammatory effects in activated HMC3 microglial cells, reducing IL-6 and increasing IL-10 levels, with evidence suggesting partial involvement of TAAR1 signalling. ADME-Tox analyses revealed improved safety and metabolic profiles for the tested compounds, particularly SG-22, which showed reduced ERG liability and enhanced cytochrome P450 stability. However, in vivo studies demonstrated that only SG-2 and SG-23 improved motility and fitness in the AD model, consistent with their ability to activate autophagy, whereas SG-22 was ineffective due to limited organismal uptake. Ultimately, the monoacetylated analogue SG-23 emerges as a promising candidate, balancing neuroprotective efficacy and drug-like properties, and supporting thyronamine-like analogues as multi-target agents for AD. - Source: PubMed
Publication date: 2026/08/14
Runfola MassimilianoPolini BeatriceMazzierli AnnaRaffellini LorenzoDi Ricco FabioCirone ItaloSagona SimonaGul SherazLessi MarcoCuzzola Angela RosaD'Orsi RosaritaBellina FabioManera ClementinaChiellini GraziaRapposelli Simona - Quercetin is a plant-derived flavonol positioned at the interface of metabolic health and food preservation. This review integrates quercetin chemistry, plant biosynthesis and metabolism, production-relevant extraction and microbial synthesis, bioavailability, mechanisms of action, preclinical and clinical evidence in metabolic syndrome (MetS), and applications in clean-label food preservation. Experimental studies indicate that quercetin modulates obesity-associated inflammation, dyslipidemia, hepatic steatosis, insulin resistance, hypertension, endothelial dysfunction, and gut-barrier impairment through interconnected Nrf2/HO-1, NF-κB/NLRP3, AMPK/SIRT1, PI3K/Akt, eNOS/NO, lipid metabolism, and microbiota-related pathways. Human evidence is narrower and heterogeneous: modest reductions in systolic blood pressure constitute the most consistent signal, whereas effects on fasting glucose, lipids, inflammatory markers, endothelial function, liver fat, and body weight vary by population, formulation, dose, and duration. In food systems, quercetin has been investigated as an antioxidant, antimicrobial, antibiofilm agent, and photodynamic photosensitizer. It is incorporated into edible films, coatings, freshness indicators, and controlled-release packaging, although most evidence remains laboratory-scale. Key translational challenges include limited aqueous solubility, variable bioavailability, incomplete long-term safety evidence, matrix-dependent efficacy, sensory constraints, manufacturing scale-up, migration, and regulation. Overall, quercetin is promising, but clinical use and industrial deployment require formulation-specific, adequately powered human studies and validation in clinically relevant populations and under commercially realistic processing conditions. - Source: PubMed
Publication date: 2026/08/12
Jacobo-Velázquez Daniel A - : Impaired glucose tolerance (IGT) is a prediabetic condition affecting over 600 million adults worldwide. Mulberry leaf ( L.) has shown antidiabetic potential, but whether adipose AMPKα1 is required for its effects remains unclear. This study aimed to determine whether mulberry leaf water extract (MLE) ameliorates IGT through adipose AMPKα1-mediated gut microbiota modulation and thermogenesis. : Adipose-specific AMPKα1 knockout (AKO) mice and floxed controls (Flox) were fed a high-fat diet for 12 weeks to establish IGT, then treated with MLE or short-chain fatty acids (SCFAs) for 10 weeks. Metabolic parameters, gut microbiota (16S rRNA sequencing), fecal SCFAs, and AMPKα1/SIRT1/PGC-1α pathway expression were assessed. : In Flox mice, MLE and SCFAs significantly improved glucose tolerance, reduced serum lipids and hepatic steatosis, and enhanced brown adipose tissue activation and white adipose browning. These effects were accompanied by gut microbiota remodeling, elevated fecal acetate/propionate/butyrate, and upregulation of the AMPKα1/SIRT1/PGC-1α pathway. All these metabolic and microbiota benefits were abrogated in AKO mice, in which MLE failed to improve any parameter, with only minimal and functionally insignificant thermogenic gene/protein upregulation. : Adipose AMPKα1 is essential for MLE to improve IGT via gut microbiota/SCFAs and thermogenesis. These findings identify adipose AMPKα1 as a molecular target for dietary intervention in prediabetes. - Source: PubMed
Publication date: 2026/08/05
Yang YangZhao YigeDu YuhangXie JiameiLiu ShuchangLiu GaitingBu SitongWang GuohuaAn YongchengWang MengluShan ZiyiZhao Baosheng - While Sanzi Sijun Formula (SSF) has exhibited preliminary efficacy against metabolic dysfunction-associated steatotic liver disease (MASLD), its mode of action remains undefined. This study therefore aimed to unravel its core therapeutic mechanisms. UPLC-MS was employed to characterize the major components of SSF. Male C57BL/6J mice were fed a high-fat diet combined with high-fructose/glucose drinking water (HFD-HF/G) for 10 weeks to establish a MASLD model, followed by SSF intervention. After 8-week treatment, body and liver weight, hepatic histopathological alterations, serum levels of lipids, transaminase, and inflammatory cytokines were detected, and transcriptomic sequencing was performed on mouse liver tissues for mechanistic exploration. AML12 hepatocytes stimulated with palmitic acid (PA) were treated with SSF alone or in combination with AMPK or SIRT1 specific inhibitors. RT-qPCR and Western blotting were used to detect the expression or activation levels of AMPK, SIRT1, and key lipid metabolism-related molecules. A total of 77 active components were identified in SSF by UPLC-MS analysis. In MASLD model mice, SSF significantly reduced body and liver weight, serum levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-c), and alanine aminotransferase (ALT), suppressed the pro-inflammatory cytokines including TNF-α and IL-6, and elevated adiponectin levels. Histopathological staining demonstrated that SSF effectively alleviated hepatic steatosis, ballooning, and inflammatory cell infiltration. Transcriptomic profiling analysis verified the major regulatory effect of SSF on lipid metabolism and identified the AMPK/SIRT1 signaling pathway as a potential mechanism. Further experiments confirmed that SSF restored the levels of AMPK/ACC phosphorylation and SIRT1 expression, thereby modulating downstream lipid metabolism-related genes in liver tissues. In PA-induced AML12 cells, SSF significantly reduced intracellular accumulation of lipid and reactive oxygen species (ROS), which were partially abrogated by the inhibitors of AMPK or SIRT1. SSF exerts prominent effects against MASLD in both in vivo and in vitro models. Modulation of the AMPK/SIRT1 signaling pathway primarily contributes to its therapeutic mechanism against lipid metabolism disorder and lipotoxic liver injury. These findings provide experimental evidence to support the clinical application of SSF for MASLD treatment. - Source: PubMed
Publication date: 2026/07/29
Ding JunyaoLiu TaoHuang PingYang LiliChen ZhiweiXue YiningHua YunlongSong HaiyanZheng Peiyong