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27 results on '"Allensworth-James, Melody"'

2. Maternal undernutrition results in transcript changes in male offspring that may promote resistance to high fat diet induced weight gain.

Author

Miles, Tiffany K., Allensworth-James, Melody L., Odle, Angela K., Moreira, Ana Rita Silva, Haney, Anessa C., LaGasse, Alex N., Gies, Allen J., Byrum, Stephanie D., Riojas, Angelica M., MacNicol, Melanie C., MacNicol, Angus M., and Childs, Gwen V.

Subjects
WEIGHT gain, HIGH-fat diet, NON-alcoholic fatty liver disease, MATERNAL nutrition, EMBRYOLOGY, MALNUTRITION, LOW-calorie diet
Abstract

Maternal nutrition during embryonic development and lactation influences multiple aspects of offspring health. Using mice, this study investigates the effects of maternal caloric restriction (CR) during mid-gestation and lactation on offspring neonatal development and on adult metabolic function when challenged by a high fat diet (HFD). The CR maternal model produced male and female offspring that were significantly smaller, in terms of weight and length, and females had delayed puberty. Adult offspring born to CR dams had a sexually dimorphic response to the high fat diet. Compared to offspring of maternal control dams, adult female, but not male, CR offspring gained more weight in response to high fat diet at 10 weeks. In adipose tissue of male HFD offspring, maternal undernutrition resulted in blunted expression of genes associated with weight gain and increased expression of genes that protect against weight gain. Regardless of maternal nutrition status, HFD male offspring showed increased expression of genes associated with progression toward nonalcoholic fatty liver disease (NAFLD). Furthermore, we observed significant, sexually dimorphic differences in serum TSH. These data reveal tissue- and sex-specific changes in gene and hormone regulation following mild maternal undernutrition, which may offer protection against diet induced weight gain in adult male offspring. [ABSTRACT FROM AUTHOR]

Published
2024
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3. Leptin: A Metabolic Signal for the Differentiation of Pituitary Cells

Author

V., Childs, Gwen, K., Odle, Angela, C., MacNicol, Melanie, L., Allensworth-James, Melody, K., Miles, Tiffany, Noor, Akhter, M., Syed, hsin, and M., cNicol, Angus

Subjects
hormones, hormone substitutes, and hormone antagonists
Abstract

Pituitary cell function is impacted by metabolic states and therefore must receive signals that inform them about nutritional status or adiposity. A primary signal from adipocytes is leptin, which recent studies have shown regulates most pituitary cell types. Subsets of all pituitary cell types express leptin receptors and leptin has been shown to exert transcriptional control through classical JAK/STAT pathways. Recent studies show that leptin also signals through post-transcriptional pathways that involve the translational regulatory protein Musashi. Mechanistically, post-transcriptional control would permit rapid cellular regulation of critical pre-existing pituitary transcripts as energy states change. The chapter will review evidence for transcriptional and/or post-transcriptional regulation of leptin targets (including Gnrhr, activin, Fshb, Gh, Ghrhr, and Pou11f1) and the consequences of the loss of leptin signaling to gonadotrope and somatotrope functions.

Published
2022

9. Control of the Anterior Pituitary Cell Lineage Regulator POU1F1 by the Stem Cell Determinant Musashi

Author

Allensworth-James, Melody, primary, Banik, Jewel, additional, Odle, Angela, additional, Hardy, Linda, additional, Lagasse, Alex, additional, Moreira, Ana Rita Silva, additional, Bird, Jordan, additional, Thomas, Christian L, additional, Avaritt, Nathan, additional, Kharas, Michael G, additional, Lengner, Christopher J, additional, Byrum, Stephanie D, additional, MacNicol, Melanie C, additional, Childs, Gwen V, additional, and MacNicol, Angus M, additional

Published
2020
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17. Control of the Anterior Pituitary Cell Lineage Regulator POU1F1 by the Stem Cell Determinant Musashi.

Author

Allensworth-James, Melody, Banik, Jewel, Odle, Angela, Hardy, Linda, Lagasse, Alex, Moreira, Ana Rita Silva, Bird, Jordan, Thomas, Christian L, Avaritt, Nathan, Kharas, Michael G, Lengner, Christopher J, Byrum, Stephanie D, MacNicol, Melanie C, Childs, Gwen V, and MacNicol, Angus M

Subjects
STEM cells, LEPTIN receptors, SOMATOTROPIN, NUCLEOTIDE sequence, TRANSCRIPTION factors
Abstract

The adipokine leptin regulates energy homeostasis through ubiquitously expressed leptin receptors. Leptin has a number of major signaling targets in the brain, including cells of the anterior pituitary (AP). We have previously reported that mice lacking leptin receptors in AP somatotropes display growth hormone (GH) deficiency, metabolic dysfunction, and adult-onset obesity. Among other targets, leptin signaling promotes increased levels of the pituitary transcription factor POU1F1, which in turn regulates the specification of somatotrope, lactotrope, and thyrotrope cell lineages within the AP. Leptin's mechanism of action on somatotropes is sex dependent, with females demonstrating posttranscriptional control of Pou1f1 messenger RNA (mRNA) translation. Here, we report that the stem cell marker and mRNA translational control protein, Musashi1, exerts repression of the Pou1f1 mRNA. In female somatotropes, Msi1 mRNA and protein levels are increased in the mouse model that lacks leptin signaling (Gh -CRE Lepr -null), coincident with lack of POU1f1 protein, despite normal levels of Pou1f1 mRNA. Single-cell RNA sequencing of pituitary cells from control female animals indicates that both Msi1 and Pou1f1 mRNAs are expressed in Gh -expressing somatotropes, and immunocytochemistry confirms that Musashi1 protein is present in the somatotrope cell population. We demonstrate that Musashi interacts directly with the Pou1f1 mRNA 3′ untranslated region and exerts translational repression of a Pou1f1 mRNA translation reporter in a leptin-sensitive manner. Musashi immunoprecipitation from whole pituitary reveals coassociated Pou1f1 mRNA. These findings suggest a mechanism in which leptin stimulation is required to reverse Musashi-mediated Pou1f1 mRNA translational control to coordinate AP somatotrope function with metabolic status. [ABSTRACT FROM AUTHOR]

Published
2021
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21. Association of Gnrhr mRNA With the Stem Cell Determinant Musashi: A Mechanism for Leptin-Mediated Modulation of GnRHR Expression

Author

Odle, Angela K, primary, Beneš, Helen, additional, Melgar Castillo, Andrea, additional, Akhter, Noor, additional, Syed, Mohsin, additional, Haney, Anessa, additional, Allensworth-James, Melody, additional, Hardy, Linda, additional, Winter, Benjamin, additional, Manoharan, Ragul, additional, Syed, Raiyan, additional, MacNicol, Melanie C, additional, MacNicol, Angus M, additional, and Childs, Gwen V, additional

Published
2017
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27. Leptin : A Metabolic Signal for the Differentiation of Pituitary Cells

Author

Childs, Gwen V., MacNicol, Angus M., Syed, Mohsin M., Akhter, Noor, Miles, Tiffany K., Allensworth-James, Melody L., MacNicol, Melanie C., and Odle, Angela K.

Subjects
Medical
Abstract

Pituitary cell function is impacted by metabolic states and therefore must receive signals that inform them about nutritional status or adiposity. A primary signal from adipocytes is leptin, which recent studies have shown regulates most pituitary cell types. Subsets of all pituitary cell types express leptin receptors and leptin has been shown to exert transcriptional control through classical JAK/STAT pathways. Recent studies show that leptin also signals through post-transcriptional pathways that involve the translational regulatory protein Musashi. Mechanistically, post-transcriptional control would permit rapid cellular regulation of critical pre-existing pituitary transcripts as energy states change. The chapter will review evidence for transcriptional and/or post-transcriptional regulation of leptin targets (including Gnrhr, activin, Fshb, Gh, Ghrhr, and Pou11f1) and the consequences of the loss of leptin signaling to gonadotrope and somatotrope functions.

Published
2020

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