Lymphatic diamine oxidase secretion stimulated by fat absorption is linked with histamine release.

Diamine oxidase (DAO) is abundantly expressed in mammalian small intestine catalyzing the oxidative breakdown of polyamines and histamine. The aim of this study was to determine the relationship between stimulation of intestinal diamine oxidase secretion with intestinal fat absorption and histamine release. Conscious intestinal lymph fistula rats were used. The mesenteric lymph ducts were cannulated and intraduodenal tubes were installed for the infusion of Liposyn II 20% (an intralipid emulsion). Lymphatic DAO activity and protein secretion were analyzed by radiometric assay and Western blot, respectively. Lymphatic histamine concentration was measured by ELISA. Infusion of Liposyn II (4.43 kcal/3 ml) resulted in a ~3.5-fold increase in lymphatic DAO protein secretion and DAO activity, peaking at 1 h and lasting for 3 h. Liposyn II infusion also increased the lymphatic histamine release, a substrate for DAO. To determine the relationship of DAO release with histamine release, histamine was administered intraperitoneally (10 mg/kg) in fasting rats and resulted in a significant doubling in lymphatic DAO activity, supporting a link between histamine and DAO. In addition, ip administration of the histamine H4 receptor antagonist JNJ7777120 significantly reduced the Liposyn II-induced DAO output by 65.9%, whereas H(1) (pyrilamine maleate), H(2) (ranitidine), and H(3) (thioperamide maleate) receptor antagonists had little effect. We conclude that DAO secretion may contribute to the catabolism of histamine released during fat absorption and this is probably mediated through the histamine H(4) receptor.

Moderate folate deficiency influences polyamine synthesis in rats.

Spermidine, spermine and putrescine are polyamines, essential growth factors in mammalian cells. Decarboxylated S-adenosylmethionine (SAM) is an essential precursor in the formation of both spermidine and spermine. SAM is formed from methionine through the addition of adenosine. Because 5-methyltetrahydrofolate donates a methyl group to homocysteine to produce methionine, folate deficiency may decrease polyamine synthesis. Weanling male Sprague-Dawley rats were fed an amino acid-defined diet with 2 mg folic acid/kg diet (control) or no added folic acid (test). Blood, liver, brain, jejunum, ileum and colon samples were collected at the end of 5 wk. Compared with controls, rats fed the test diet had a 72% reduction in plasma folate (123.6 +/- 13.1 vs. 34.6 +/- 2.2 nmol/L, P < 0.001) and a 42% reduction in RBC folate (2834.4 +/- 218.3 vs. 1651.8 +/- 75.9 nmol/L, P < 0.001). Hepatic spermidine and spermine in folate-depleted rats were 58 (P < 0.001) and 67% (P < 0.01) higher, respectively, than in controls. Plasma putrescine was 27% higher (P < 0.05) than in controls. The polyamine concentrations of the jejunum, ileum, colon and brain did not differ. This study suggests that mild folate deficiency influences polyamine synthesis, but contrary to our hypothesis, hepatic spermidine and spermine were increased, as was circulating putrescine. This may have occurred for a number of reasons including increased enzyme activity or overcompensation by the betaine-homocysteine transmethylation pathway in the liver. Further study is necessary to clarify interactions between folate and polyamine metabolism and to determine whether polyamines are involved in the damaging effects of folate deficiency.