L-Glutamine (GMP)

L-Glutamine GMP is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine GMP is taken up in a Na⁺-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine GMP enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine GMP also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine GMP can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity^[1][2][3][4]. In Vitro:L-Glutamine (GMP) is essential for osteoclast differentiation, maturation, and bone-resorbing activity via SLC1A5-mediated uptake and conversion to α-KG for anaplerosis, with hypoxia-stimulated uptake supporting biosynthetic needs^[1].
L-Glutamine (GMP) promotes BMSC proliferation via upregulation of cell cycle regulators, activation of GLS and GDH through mTOR/S6 and MAPK pathways, and amino acid transaminase-dependent α-KG production^[1].
L-Glutamine (GMP) promotes BMSC osteogenic differentiation via GLS-dependent TCA cycle anaplerosis, regulation by ERRα and mTOR signaling pathways, and glutathione-mediated ROS neutralization, but does not contribute to adipocytic differentiation of BMSCs^[1].
L-Glutamine (GMP) (High-dose) enhances the immunosuppressive properties of BMSCs by modulating cytokine production via reduced NF-κB and increased STAT-3 activity, and inhibits lymphocyte and macrophage proliferation in coculture^[1].
L-Glutamine (GMP) improves osteoblast viability, enhances glucose utilization, and promotes matrix mineralization in human osteoblast-like cell lines and mouse calvarial osteoblasts^[1].
L-Glutamine (GMP) supports chondrocyte extracellular matrix synthesis, enhances hypoxia tolerance via HIF-1^α/GLS1-mediated α-KG production, and protects chondrocytes from injury and apoptosis through glutathione and HSP70 upregulation^[1]. In Vivo:L-Glutamine GMP (0.75 g/kg; i.p.; daily; initiated immediately after MCAO and continued for 3 days) reduces the ischemic cerebral infarction volume by approximately 60% in male ICR mice, improves neurobehavioral recovery, upregulates HSP70 expression, enhances antioxidant capacity, reduces neuronal apoptosis, and promotes astrocyte proliferation via an HSP70-dependent mechanism^[3].
Pretreatment with L-Glutamine GMP (1-2 g/kg; p.o.; once every 2 days; for 5 days) significantly attenuates Cantharidin (HY-N0209)-induced body weight loss in female BALB/c mice^[4].
Pretreatment with L-Glutamine GMP (1-2 g/kg; p.o.; once every 2 days; for a total of 5 days) reduces the mortality rate of female BALB/c mice exposed to 3 mg/kg Cantharidin^[4].
Pretreatment with L-Glutamine GMP (1-2 g/kg; p.o.; single dose) significantly normalizes cardiac mass index, cardiac biomarkers, oxidative stress markers, and succinate dehydrogenase activity, and alleviates histopathological damage in female BALB/c mice with acute cardiotoxicity induced by Cantharidin^[4].
Pretreatment with L-Glutamine GMP (1-2 g/kg; p.o.; single dose) reduces Cantharidin-induced ST-segment elevation and alleviates myocardial injury in female BALB/c mice^[4].