Fig. 1: Hyperglycemia increases prostaglandin production derived from phospholipids.

a, b Representative results of imaging mass spectrometry (IMS) showing distributions of hypothalamic fatty acids (a) and phospholipids (b) from untreated RCD-fed mice. The dashed black line shows the position of the VMH. Scale bar: 500 μm. c–h Distributions of phospholipids and fatty acids in the hypothalamus 30 min after injection of saline (Sal) or glucose (Glc; 2 g/kg). c, f Representative results of IMS on hypothalamic phosphatidyl-inositol (PI; 18:1/20:4) (c) and arachidonic acid (AA) (f) from mice i.p. injected with saline (left half) or glucose (right half). Scale bar: 500 μm. d, e Relative intensities of phospholipids in the VMH (d) and ARC (e) after injection with saline (n = 4) or glucose (n = 4). (two-tailed t test for each molecule, VMH: p = 0.0268 in PI (18:0/20:4), p = 0.0005 in PI (18:1/20:4), and p = 0.0491 in PE (18:0/20:4); ARC: p = 0.0073 in PI (18:0/20:4), p = 0.0347 in PI (18:1/20:4), p = 0.0106 in PE (18:0/20:4), and p = 0.0331 in PS(18:0/16:0), Glc vs Sal g, h Relative intensities of fatty acids in the VMH (g) and ARC (h) after injection with saline (n = 4) or glucose (n = 4). i–m LC-MS results showing the effects of glucose injection on AA metabolites in the whole hypothalamus. i Relative amounts of hypothalamic prostaglandins mediated by cyclooxygenase. Major prostaglandins were underlined. j 6-keto-PGF1α, k PGD2, l 13,14-dihydro-15-keto-PGF2α and m PGE2 were increased by glucose injection (two-tailed t test, p = 0.0009 in j, p = 0.0244 in k, p = 0.0011 in l, p = 0.0099 in m, n = 5/each, Glc vs Sal). d–h and j–m represent the mean ± SEM; *p < 0.05; **p < 0.01; ***p < 0.001. i represents the mean fold change in color. PA palmitic acid, SA stearic acid, AA arachidonic acid, DHA docosahexaenoic acid, PE phosphatidyl-ethanolamine, PI phosphatidyl-inositol, PS phosphatidyl-serine.