Ask about this productRelated genes to: G6pc antibody
- Gene:
- G6PC NIH gene
- Name:
- glucose-6-phosphatase catalytic subunit
- Previous symbol:
- G6PT
- Synonyms:
- GSD1a, G6PC1
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-05
- Date modifiied:
- 2019-04-23
Related products to: G6pc antibody
Related articles to: G6pc antibody
- The prolonged cold season on the Qinghai-Tibet Plateau poses substantial challenges for most animals, including limited access to natural pasture, reduced appetite, and subsequent weight loss. The polysaccharides that are contained in yeast cell wall (YCW) act as prebiotics, promoting the action and development of beneficial gut microbiota while inhibiting the proliferation of pathogens, thereby maintaining normal gastrointestinal function in animals. - Source: PubMed
Publication date: 2026/05/18
Han XiaoxiaLiu TingZeng HanfangLiu JianbinLu ZengkuiXu JianfengWang JingYang XinhuiZhu ShengxinRan HangAn LijingPan FamingZheng Chen - Nephrolithiasis is increasingly prevalent worldwide. Although metabolic dysregulation has emerged as an important feature of the disease, the specific metabolic programs within tubular epithelial cells that drive stone formation remain poorly understood. Here, we use single-cell transcriptomics to profile mouse models of nephrolithiasis and identify a marked suppression of gluconeogenesis in renal proximal tubular epithelial cells, driven by downregulation of the rate-limiting enzyme glucose-6-phosphatase (G6PC) and associated with lactate accumulation. We further show that loss of G6PC or lactate accumulation is sufficient to activate TGF-β/SMAD3 signaling, driving epithelial-mesenchymal transition (EMT) and a profibrotic epithelial program associated with enhanced crystal deposition. Mechanistically, lactate induces lactylation of the transcription factor SNAIL1 at lysine 206, facilitating its nuclear localization and transcriptional activation of TGF-β. Together, these findings establish a G6PC-lactate-SNAIL1 axis linking metabolic dysregulation to epithelial remodeling during nephrolithiasis. - Source: PubMed
Publication date: 2026/05/10
Liu KaiZhang BomingFan RuixinDuan ChenZhang YangjunWu HuahuiYao XiangyangMao XiongminLi BoZeng YoumiaoXu ZhenzhenWang YangLuo MengchengXu XinyuFeng NinghanLi HengXu Hua - While lactate accumulation in muscles contributes to fatigue, its efficient clearance-primarily hepatic gluconeogenesis (Cori cycle)-is vital for recovery and sustained performance. This study investigates whether taurine and betaine can enhance this hepatic lactate clearance capacity by modulating gluconeogenesis in canine hepatocytes. The results showed that taurine and betaine significantly promoted lactate clearance in canine hepatocytes. In addition, taurine and betaine significantly increased the levels of phosphoenolpyruvate and glucose in hepatocytes. Meanwhile, taurine and betaine increased the mRNA and protein expression levels of gluconeogenesis-related gene, including pyruvate carboxylase (PC), phosphoenolpyruvate carboxykinase (PEPCK), fructose-1,6-bisphosphatase (FBP1) and glucose-6-phosphatase (G6PC). Consistently, the enhanced activities of PEPCK and G6PC provide functional evidence that taurine and betaine boost the gluconeogenic flux in hepatocytes. Taken together, this study reveals the potential regulatory effects of taurine and betaine on lactate metabolism and gluconeogenesis in canine hepatocytes, providing new insights for recovery strategies in canines after exercise. - Source: PubMed
Publication date: 2026/04/13
Ma YanLi JiaxiLi YunliangLv Lei - Myeloid differentiation factor 88 (MyD88) signaling plays a central role in inflammatory pathway activation. Adipose-derived interleukin-10 (IL-10), which is induced by insulin and lipopolysaccharides, suppresses hepatic glucose production. This study investigated the role of MyD88/IL-10 signaling in diabetes-induced systemic inflammation and hepatic gluconeogenesis. Stromal vascular fractions (SVFs) were isolated from the adipose tissue of and MyD88 mice and treated with IL-10 followed by analysis of inflammatory cytokine expression. IL-10 (10 or 50 ng) was injected into adipose tissue of type 2 DM (T2DM) () mice to investigate its effect on blood dipeptidyl peptidase-4 (DPP4) activity, insulin resistance, and hepatic gluconeogenic signaling. Hepatic inflammatory markers, gluconeogenic gene expression, and metabolic parameters were assessed. Compared with wild-type mice, mice exhibited significantly reduced FOXP3 protein expression and IL-10 levels in adipose tissue, accompanied by increased blood DPP4 activity and adiponectin levels, elevated hepatic inflammatory cytokines, and increased and mRNA expression. In contrast, MyD88 mice showed increased Foxp3 protein and mRNA expression, decreased and mRNA expression in SVFs, increased IL-10 levels in adipose tissue, and lower blood adiponectin and ALT levels. MyD88 deletion also attenuated Kupffer cell accumulation, hepatic inflammatory cytokine expression, and gluconeogenic gene expression. In vitro, IL-10 treatment of SVFs from mice significantly reduced and expression and increased mRNA expression. In vivo, adipose IL-10 injection increased and expression, expanded Treg cells in SVFs, and activated hepatic Akt signaling, while suppressing pJNK and pNF-κB signaling. These changes were accompanied by reduced blood DPP4 activity, ALT and adiponectin levels, decreased Kupffer cell-derived inflammatory cytokines, reduced hepatic and expression, and improved glucose tolerance. MyD88 signaling induces adipose and , liver inflammation and gluconeogenesis, and blood DPP4 activity by reducing IL-10 and Foxp3 of adipose tissue in T2DM. Enhancing adipose IL-10 induces Treg expansion, inhibits JNK and NF-κB signaling, and alleviates hepatic gluconeogenesis and insulin resistance. MyD88 inhibition or IL-10 elevation in adipose tissue may represent a novel strategy for metabolic syndrome. - Source: PubMed
Publication date: 2026/03/23
Li Yi-ChengLai Hsiao-ChiChen Pei-HsuanTang Chia-HuaChen Lee-Wei - Long-term nutritional excess causes hepatic steatosis, endoplasmic reticulum (ER) stress, hyperglycemia, and hyperlipidemia. Mitogen-activated protein kinase phosphatase-3 (MKP-3) is a well-established stress-regulated protein and a regulator of gluconeogenesis. Our previous study revealed that acute ER stress reduced gluconeogenesis and MKP-3 protein stability. However, the expression of MKP-3 and its regulatory mechanisms in chronic ER stress remain unclear. The aim of this study was to investigate the effects of chronic ER stress on hepatic MKP-3 expression and its role in the regulation of gluconeogenesis. The results show that long-term administration of thapsigargin (Tg) or palmitic acid promoted gene expression of and gluconeogenic genes , , and in primary mouse hepatocytes. In addition, a long-term high-fat diet (HFD) or Tg administration significantly increased hepatic ER stress and blood glucose level in mice, while inducing the expression of and hepatic gluconeogenic genes , and . Further study revealed that liver-specific knockout ( LKO) reversed the blood glucose level and expression levels of gluconeogenic genes those were induced by long-term HFD in mice. Moreover, activation of the PKR-like ER kinase (PERK) by its agonist increased hepatic expression, whereas inhibitor of PERK suppressed the expression of under Tg administration. These results suggest that chronic high-fat diet might promote hepatic gluconeogenesis via the PERK/MKP-3 pathway. Consequently, this study identified a potential therapeutic target for treating obesity-related hyperglycemia. - Source: PubMed
Publication date: 2026/03/22
Cao ShengDu YanlinFang ZhengfengChe LianqiangLin YanXu ShengyuJiang XuemeiLiu GuangmangZhuo YongHua LunSun MengmengWu DeFeng Bin