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Catalunya as Centre de Recerca de Catalunya (CERCA)","award":["CB15\/00071"],"award-info":[{"award-number":["CB15\/00071"]}]},{"name":"Generalitat de Catalunya as Centre de Recerca de Catalunya (CERCA)","award":["CB07\/08\/0016"],"award-info":[{"award-number":["CB07\/08\/0016"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nutrients"],"abstract":"<jats:p>This study investigated the effect of nicotinamide (NAM) supplementation on the development of brain inflammation and microglial activation in a mouse model of type 1 diabetes mellitus. C57BL\/6J male mice, which were made diabetic with five consecutive, low-dose (55 mg\/kg i.p.) streptozotocin (STZ) injections. Diabetic mice were randomly distributed in different experimental groups and challenged to different doses of NAM (untreated, NAM low-dose, LD, 0.1%; NAM high-dose, HD, 0.25%) for 25 days. A control, non-diabetic group of mice was used as a reference. The NAD+ content was increased in the brains of NAM-treated mice compared with untreated diabetic mice (NAM LD: 3-fold; NAM HD: 3-fold, p-value &lt; 0.05). Immunohistochemical staining revealed that markers of inflammation (TNF\u03b1: NAM LD: \u221235%; NAM HD: \u221246%; p-value &lt; 0.05) and microglial activation (IBA-1: NAM LD: \u221229%; NAM HD: \u221250%; p-value &lt; 0.05; BDKRB1: NAM LD: \u221236%; NAM HD: \u221237%; p-value &lt; 0.05) in brains from NAM-treated diabetic mice were significantly decreased compared with non-treated T1D mice. This finding was accompanied by a concomitant alleviation of nuclear NF\u03baB (p65) signaling in treated diabetic mice (NF\u03baB (p65): NAM LD: \u221238%; NAM HD: \u221253%, p-value &lt; 0.05). Notably, the acetylated form of the nuclear NF\u03baB (p65) was significantly decreased in the brains of NAM-treated, diabetic mice (NAM LD: \u221248%; NAM HD: \u221263%, p-value &lt; 0.05) and inversely correlated with NAD+ content (r = \u22120.50, p-value = 0.03), suggesting increased activity of NAD+-dependent deacetylases in the brains of treated mice. Thus, dietary NAM supplementation in diabetic T1D mice prevented brain inflammation via NAD+-dependent deacetylation mechanisms, suggesting an increased action of sirtuin signaling.<\/jats:p>","DOI":"10.3390\/nu15143083","type":"journal-article","created":{"date-parts":[[2023,7,10]],"date-time":"2023-07-10T00:47:35Z","timestamp":1688950055000},"page":"3083","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Nicotinamide Prevents Diabetic Brain Inflammation via NAD+-Dependent Deacetylation Mechanisms"],"prefix":"10.3390","volume":"15","author":[{"given":"Jeimy Katherine","family":"Torres-M\u00e9ndez","sequence":"first","affiliation":[{"name":"Institut d\u2019Investigaci\u00f3 Biom\u00e8dica Sant Pau (IIB Sant Pau), 08041 Barcelona, 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