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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. Musashi exerts control of gonadotrope target mRNA translation during the mouse estrous cycle

Author

Moreira, Ana Rita Silva, primary, Lim, Juchan, additional, Urbaniak, Alicja, additional, Banik, Jewel, additional, Bronson, Katherine, additional, Lagasse, Alex, additional, Hardy, Linda, additional, Haney, Anessa, additional, Allensworth, Melody, additional, Miles, Tiffany K, additional, Gies, Allen, additional, Byrum, Stephanie D, additional, Wilczynska, Ania, additional, Boehm, Ulrich, additional, Kharas, Michael, additional, Lengner, Christopher, additional, MacNicol, Melanie C, additional, Childs, Gwen V, additional, MacNicol, Angus M, additional, and Odle, Angela K, additional

Published
2023
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9. 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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