Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Fructose metabolism is unregulated in cancers and placentae.
Exp Biol Med (Maywood)
November 2024
Department of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX, United States.
Fructose and lactate are present in high concentrations in uterine luminal fluid, fetal fluids and fetal blood of ungulates and cetaceans, but their roles have been ignored and they have been considered waste products of pregnancy. This review provides evidence for key roles of both fructose and lactate in support of key metabolic pathways required for growth and development of fetal-placental tissues, implantation and placentation. The uterus and placenta of ungulates convert glucose to fructose via the polyol pathway.
View Article and Find Full Text PDFInjection-molded thermoplastic cassava starch modified with single and mixed polyol plasticizers.
Int J Biol Macromol
November 2024
Department of Packaging and Materials Technology, Faculty of Agro-Industry, Kasetsart University, Bangkok 10900, Thailand; Center for Advanced Studies for Agriculture and Food (CASAF), Kasetsart University Institute for Advanced Studies (KUIAS), Kasetsart University, Bangkok 10900, Thailand. Electronic address:
Increasing interest in biodegradable and cost-effective materials derived from renewable resources has led to the development of injection-moldable thermoplastic starch (TPS). Plasticizers constitute an indispensable additive for manufacturing TPS, influencing both its thermomechanical processability and performance. The aim of the current work is thus to study the effect of single and mixed polyol plasticizers on the performance of injection-molded TPS.
View Article and Find Full Text PDFHigh glucose combined with lipopolysaccharide stimulation inhibits cell proliferation and migration of human HaCaT keratinocytes by impacting redox homeostasis and activating the polyol pathway.
Mol Biol Rep
October 2024
Department of Endocrinology, The First Affiliated Hospital of Anhui Medical University, 218 Jixi Road, Hefei City, 230022, Anhui Province, People's Republic of China.
Article Synopsis
- Chronic inflammation and high glucose levels contribute to poor healing in diabetic skin wounds, affecting the function of keratinocytes, which are crucial for skin repair.
- This study investigated the impact of high glucose and lipopolysaccharide on the metabolomic changes in keratinocytes, revealing altered levels of 273 metabolites, especially in redox metabolism.
- The findings indicate that these stressors impair keratinocyte proliferation and migration, potentially suggesting new therapeutic approaches for managing chronic diabetic ulcers.
Exploring fructose metabolism as a potential therapeutic approach for pancreatic cancer.
Cell Death Differ
December 2024
Chinese Medicine Phenome Research Centre, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.
Excessive fructose intake has been associated with the development and progression of pancreatic cancer. This study aimed to elucidate the relationship between fructose utilization and pancreatic cancer progression. Our findings revealed that pancreatic cancer cells have a high capacity to utilize fructose and are capable of converting glucose to fructose via the AKR1B1-mediated polyol pathway, in addition to uptake via the fructose transporter GLUT5.
View Article and Find Full Text PDFAKR1B1-dependent fructose metabolism enhances malignancy of cancer cells.
Cell Death Differ
December 2024
Center for Translational Medicine and Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.
Fructose metabolism has emerged as a significant contributor to cancer cell proliferation, yet the underlying mechanisms and sources of fructose for cancer cells remain incompletely understood. In this study, we demonstrate that cancer cells can convert glucose into fructose through a process called the AKR1B1-mediated polyol pathway. Inhibiting the endogenous production of fructose through AKR1B1 deletion dramatically suppressed glycolysis, resulting in reduced cancer cell migration, inhibited growth, and the induction of apoptosis and cell cycle arrest.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!