Hypothesis: can glucose-insulin-potassium regimen in combination with polyunsaturated fatty acids suppress lupus and other inflammatory conditions?
In systemic lupus erythematosus, plasma concentrations of tumor necrosis factor alpha (TNF alpha) and other pro-inflammatory cytokines are elevated and those of transforming growth factor beta (TGF beta) are decreased. TNF alpha prevents lupus nephropathy whereas increased concentration of TGF beta causes glomerulosclerosis. Insulin inhibits TNF alpha and enhances TGF beta production, augments nitric oxide synthesis and blocks superoxide anion generation. Polyunsaturated fatty acids (PUFAs) also have actions similar to insulin. Hence, it is suggested that a combination of insulin (in the form of glucose-insulin-potassium) and PUFAs may be of benefit in lupus and other inflammatory conditions.
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D016207:Cytokines / Q000378:metabolism; D004359:Drug Therapy, Combination; D005231:Fatty Acids, Unsaturated / Q000494:pharmacology*; D005609:Free Radicals; D005947:Glucose / Q000494:pharmacology*; D006801:Humans; D007249:Inflammation / Q000188:drug therapy*; D007328:Insulin / Q000494:pharmacology*; D008177:Lupus Vulgaris / Q000188:drug therapy*; D008233:Lymphotoxin-alpha / Q000097:blood; D008954:Models, Biological; D009569:Nitric Oxide / Q000378:metabolism; D011188:Potassium / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D016207:Cytokines; D005231:Fatty Acids, Unsaturated; D005609:Free Radicals; D007328:Insulin; D008233:Lymphotoxin-alpha; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D005947:Glucose; D011188:Potassium