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Last Updated: 3 years ago

Possible Interaction: Glucose and Nitric Oxide

supplement:

Glucose

Research Papers that Mention the Interaction

Specifically, insulin-mediated production of nitric oxide from the vascular endothelium leads to increased blood flow enhancing disposal of glucose.
Metabolism: clinical and experimental  •  2021  |  View Paper
Nitric oxide inhibits the mitochondrial oxidation of glucose resulting in an impairment of insulin secretion.
Vitamins and hormones  •  2014  |  View Paper
In intact cells, through cGMP and … protein kinase signaling, physiological levels of NO acutely stimulate uptake … oxidation of glucose and fatty acids by skeletal muscle, heart, liver, and adipose tissue, while inhibiting the synthesis … glucose, glycogen and fat in the insulin‐sensitive tissues, and enhancing lipolysis in white adipocytes.
BioFactors  •  2013  |  View Paper
ResultsTreatment with 50 mmol/L glucose markedly increased the level of IL-1β, IL-18, TNF-α, PGE2, NO , TGF-β1, MCP-1, MIP-1α, and RANTES.
Inflammation Research  •  2010  |  View Paper
Objective—Previous studies suggest that nitric oxide NO ) may modulate insulin-induced uptake of glucose in insulin-sensitive tissues.
Arteriosclerosis, thrombosis, and vascular biology  •  2008  |  View Paper
Emerging evidence shows that NO regulates the metabolism of glucose , fatty acids and amino acids in mammals.
However, as a signaling molecule, physiological levels of NO stimulate glucose uptake as well as glucose and fatty acid oxidation in skeletal muscle, heart, liver and adipose tissue; inhibit the synthesis of glucose , glycogen, and fat in target tissues (e.g., liver and adipose); and enhance lipolysis in adipocytes.
The Journal of nutritional biochemistry  •  2006  |  View Paper
High glucose induces oxidative and nitrosative stress in many cell types causing the generation of species such as superoxide, nitric oxide and peroxynitrite and their derivatives.
The Journal of nutritional biochemistry  •  2005  |  View Paper
In HAEC culture, d-glucose stimulated AM and nitric oxide production and they were suppressed by addition of AM antisense oligodeoxynucleotides.
Kidney international  •  2004  |  View Paper
As these effects were blocked by an SGLT1 inhibitor and further analyses indicated that SGLT1 is expressed in macula densa cells, the researchers suggest that tubular glucose inhibits TGF and stimulates NO generation via SGLT1.
Using microperfusion and micropuncture techniques, they show that tubular glucose inhibits the TGF response in vitro and in vivo and stimulates the generation of nitric oxide (NO) at the macula densa.
Nature Reviews Nephrology  •  2019  |  View Paper
Physiologically, NO is known to regulate the transport of insulin and uptake of glucose by several tissues including the endothelium, liver, pancreas, and skeletal muscle.
The Journal of physiology  •  2016  |  View Paper
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