Sex steroids effects on the endocrine pancreas

Morimoto, Sumiko; Escobedo-Morales, A.; Zambrano, Elena; Fernández-Mejía, Cristina

doi:10.1016/j.jsbmb.2010.05.003

Cited by 15 publications

(14 citation statements)

References 98 publications

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“…In the BG- EcR - exclusive category includes enrichment of protein transport ( p value 0.003), while endocytosis ( p value 0.01) is enriched in the WPP- EcR - exclusive category. These functions may be clues to the non-genomic effects of the hormone signal (Blackmore 1993; Bramley 2003; Groeneweg et al 2011; Losel et al 2002; McEwen 1991; Morimoto et al 2010; Rafiq et al 2011; Wehling and Losel 2006) and may implicate the receptor in alternate functions and physiological interactions outside of direct gene regulation. However, because we are measuring gene response, these functions must still be modulated on the transcriptional level.…”

Section: Discussionmentioning

confidence: 99%

Genomic analysis of the ecdysone steroid signal at metamorphosis onset using ecdysoneless and EcRnull Drosophila melanogaster mutants

Davis

2013

Genes Genom

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Steroid hormone gene regulation is often depicted as a linear transduction of the signal, from molecule release to the gene level, by activation of a receptor protein after being bound by its steroid ligand. Such an action would require that the hormone be present and bound to the receptor in order to have target gene response. Here, we present data that presents a novel perspective of hormone gene regulation, where the hormone molecule and its receptor have exclusive target gene regulation function, in addition to the traditional direct target genes. Our study is the first genome-wide analysis of conditional mutants simultaneously modeling the steroid and steroid receptor gene expression regulation. We have integrated classical genetic mutant experiments with functional genomics techniques in the Drosophila melanogaster model organism, where we interrogate the 20-hydroxyecdysone signaling response at the onset of metamorphosis. Our novel catalog of ecdysone target genes illustrates the separable transcriptional responses among the hormone, the pre-hormone receptor and the post-hormone receptor. We successfully detected traditional ecdysone target genes as common targets and also identified novel sets of target genes which where exclusive to each mutant condition. Around 12 % of the genome responds to the ecdysone hormone signal at the onset of metamorphosis and over half of these are independent of the receptor. In addition, a significant portion of receptor regulated genes are differentially regulated by the receptor, depending on its ligand state. Gene ontology enrichment analyses confirm known ecdysone regulated biological functions and also validate implicated pathways that have been indirectly associated with ecdysone signaling.Electronic supplementary materialThe online version of this article (doi:10.1007/s13258-013-0061-0) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Genomic analysis of the ecdysone steroid signal at metamorphosis onset using ecdysoneless and EcRnull Drosophila melanogaster mutants

Davis

2013

Genes Genom

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“…The pancreatic β-cell is a direct target of androgen, 51 and the loss of its function is one of the causal factors in androgen-deprivation induced T2DM 52 . The gut-vagus-brain-pancreas axis with its glucagon-like peptide-1 affects β-cell function 53 .…”

Section: Type 2 Diabetes Mellitus (T2dm)mentioning

confidence: 99%

Hypogonadism alters cecal and fecal microbiota in male mice

et al. 2016

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Low testosterone levels increase the risk for cardiovascular disease in men and lead to shorter life spans. Our recent study showed that androgen deprivation via castration altered fecal microbiota and exacerbated risk factors for cardiovascular disease, including obesity, impaired fasting glucose, excess hepatic triglyceride accumulation, and thigh muscle weight loss only in high-fat diet (HFD)-fed male mice. However, when mice were administered antibiotics that disrupted the gut microbiota, castration did not increase cardiovascular risks or decrease the ratio of dried feces to food intake. Here, we show that changes in cecal microbiota (e.g., an increased Firmicutes/Bacteroidetes ratio and number of Lactobacillus species) were consistent with changes in feces and that there was a decreased cecal content secondary to castration in HFD mice. Castration increased rectal body temperature and plasma adiponectin, irrespective of diet. Changes in the gut microbiome may provide novel insight into hypogonadism-induced cardiovascular diseases.

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“…The difference in the kinetics of FP development between males and females may be due to sex hormones since they appear to have an effect on proliferation, survival, and insulin production of β-cells (23). To address this question, we castrated male and female BALB/c mice before transplantation of one FP, eliminating hormones produced by gonads, and quantified insulin produced by the graft 3 weeks later.…”

Section: Resultsmentioning

confidence: 99%

Fetal Pancreas Transplants Are Dependent on Prolactin for Their Development and Prevent Type 1 Diabetes in Syngeneic but Not Allogeneic Mice

et al. 2013

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Transplantation of adult pancreatic islets has been proposed to cure type 1 diabetes (T1D). However, it is rarely considered in the clinic because of its transient effect on disease, the paucity of donors, and the requirement for strong immunosuppressive treatment to prevent allogeneic graft rejection. Transplantation of fetal pancreases (FPs) may constitute an attractive alternative because of potential abundant donor sources, possible long-term effects due to the presence of stem cells maintaining tissue integrity, and their supposed low immunogenicity. In this work, we studied the capacity of early FPs from mouse embryos to develop into functional pancreatic islets producing insulin after transplantation in syngeneic and allogeneic recipients. We found that as few as two FPs were sufficient to control T1D in syngeneic mice. Surprisingly, their development into insulin-producing cells was significantly delayed in male compared with female recipients, which may be explained by lower levels of prolactin in males. Finally, allogeneic FPs were rapidly rejected, even in the context of minor histocompatibility disparities, with massive graft infiltration with T and myeloid cells. This work suggests that FP transplantation as a therapeutic option of T1D needs to be further assessed and would require immunosuppressive treatment.

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Sex steroids effects on the endocrine pancreas

Cited by 15 publications

References 98 publications

Genomic analysis of the ecdysone steroid signal at metamorphosis onset using ecdysoneless and EcRnull Drosophila melanogaster mutants

Genomic analysis of the ecdysone steroid signal at metamorphosis onset using ecdysoneless and EcRnull Drosophila melanogaster mutants

Hypogonadism alters cecal and fecal microbiota in male mice

Fetal Pancreas Transplants Are Dependent on Prolactin for Their Development and Prevent Type 1 Diabetes in Syngeneic but Not Allogeneic Mice

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