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Because this endocrine organ releases hormones like leptin, which are important in reproductive physiology, we investigated the reproductive phenotype of<jats:italic>\u03b1<\/jats:italic>\u2212\/\u2212 males. Compared to controls,<jats:italic>\u03b1<\/jats:italic>\u2212\/\u2212 males displayed delayed onset of puberty accompanied by a reduction in plasma LH levels and testicular weight. At postnatal day 30,<jats:italic>\u03b1<\/jats:italic>\u2212\/\u2212 mice exhibited normal body weight but elevated fasted plasma leptin levels. Testicular leptin gene expression was increased, whereas expression of the cholesterol transporter StAR and of P450 cholesterol side chain cleavage enzyme was decreased. Adult<jats:italic>\u03b1<\/jats:italic>\u2212\/\u2212 males were infertile and exhibited hyperandrogenemia with normal basal LH, FSH, and estradiol levels. However, neither sperm counts nor sperm motility was different between genotypes. The mRNA levels of leptin and of 17-beta-dehydrogenase 3, and enzyme important for testosterone production, were significantly higher in the testis of adult<jats:italic>\u03b1<\/jats:italic>\u2212\/\u2212 males. The mRNA levels of ER<jats:italic>\u03b1<\/jats:italic>, an important regulator of intratesticular steroidogenesis, were lower in the testis of adult and peripubertal<jats:italic>\u03b1<\/jats:italic>\u2212\/\u2212 males. We propose that chronic hyperleptinemia contributes to the negative impact that disrupting PI3K signaling in adipocytes has on puberty onset, steroidogenesis, and fertility in males.<\/jats:p>","DOI":"10.1155\/2017\/3756089","type":"journal-article","created":{"date-parts":[[2017,3,5]],"date-time":"2017-03-05T16:01:50Z","timestamp":1488729710000},"page":"1-13","source":"Crossref","is-referenced-by-count":10,"title":["Loss of PI3K p110<i>\u03b1<\/i>in the Adipose Tissue Results in Infertility and Delayed Puberty Onset in Male Mice"],"prefix":"10.1155","volume":"2017","author":[{"given":"Victoria L. 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