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Discover Supplement-Drug Interactions
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Last Updated: 3 years ago
Research Papers that Mention the Interaction
“In this study, glucose homeostasis, as measured by glucose and insulin tolerance tests, was significantly impaired by rapamycin in both inbred (C57BL/6) and genetically heterogeneous (UT-HET3) mice.”
About-face on the metabolic side effects of rapamycin“ Rapamycin had potential to increase cell survival and significantly decreased the total levels of oxidative stress markers after cell exposure to 30mM glucose (p<0.05).”
“ Rapamycin potentially improved the detrimental effect of 30mM glucose on cell migration and tubulogenesis capacity (p<0.05).”
“Analysis of individual strains shows that rapamycin induced higher glucose values at 15 minutes post challenge in 7/9 strains.”
Differential effects of rapamycin on glucose metabolism in 9 inbred strains.“ Rapamycin suppressed levels of fasting triglycerides, insulin, and uric acid in ZO but increased glucose.”
“Our results revealed … intraperitoneal administration of glucose induced hyperglycemia for … vehicle and rapamycin treatments, which peaked at 2 h. Plasma glucose level in vehicle-treated fish was significantly higher than in …-treated fish at 8 and 17 h, whereas it remained at the basal level in rapamycin-treated fish.”
“In direct support of SAD-A as a unique mediator of mTORC1 signaling in islet β-cells, we demonstrate that glucose dramatically stimulated SAD-A protein translation in isolated mouse islets, which was potently inhibited by rapamycin , an inhibitor of mTORC1.”
“ Rapamycin inhibited mitochondrial DNA expression and ATP production as well as insulin secretion in response to glucose.”
“Glucose oxidation, which indicates the velocity of metabolism in the Krebs cycle, was decreased by rapamycin in the presence of 16.7 mM glucose (30.1+/-2.7, rapamycin versus 42.2+/-3.3 pmol/islet per 90 min, control, n=9, P<0.01).”
“The reduction in cellular ATP caused by glucose depletion were exacerbated by the inhibitors but mitigated by rapamycin , suggesting that inhibition of autophagy may accelerate energy depletion, leading to necrosis.”
“Moreover, glucose increased mTORC1 activity and its inhibition by rapamycin decreased β-cell apoptosis under conditions of glucolipotoxicity.”
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