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Protocol to study inter-tissue communication between the hypothalamus and white adipose tissue and lifespan using a chemogenetic approach in aged mice.
STAR Protoc
January 2025
Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address:
Here, we present a protocol for assessing the impact of a chemogenetic manipulation in a subpopulation of the hypothalamic neurons on aging and lifespan control using a mouse model developed specifically for this purpose. We describe steps for stereotaxic viral injection and assess inter-tissue communication between protein phosphatase 1 regulatory subunit 17 (Ppp1r17)-expressing neurons in the dorsomedial hypothalamus and white adipose tissue. We then detail procedures for lifespan measurements following chemogenetic manipulation in aged mice.
View Article and Find Full Text PDFConditional Pten inactivation in pituitary results in sex-specific prolactinoma formation.
Biochim Biophys Acta Mol Basis Dis
January 2025
Unidad de Gestión de Endocrinología y Nutrición, Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Spain. Electronic address:
Pituitary tumors, including prolactinomas, present significant clinical challenges that require a deeper understanding of their molecular roots for improved diagnostics and therapies. Here, we investigate the role of the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K) pathway in pituitary tumorigenesis using a mouse model. Conditional knockout of Pten in all pituitary cell lineages resulted in prolactinoma formation exclusively in female mice, demonstrating the critical role of PTEN in pituitary homeostasis.
View Article and Find Full Text PDFIntestinal gluconeogenesis controls the neonatal development of hypothalamic feeding circuits.
Mol Metab
November 2024
INSERM UMR-S1213, Université Claude Bernard Lyon 1, Lyon, France. Electronic address:
Article Synopsis
- The study investigates the role of intestinal gluconeogenesis (IGN) in regulating energy balance and the development of feeding circuits in the hypothalamus, particularly during the neonatal period.
- Researchers induced IGN in newborn mice by overexpressing the enzyme G6pc1 and studied the impact on hypothalamic feeding circuit development and sympathetic innervation of adipose tissues.
- Results showed that inducing IGN at birth led to changes in key hypothalamic circuits and better protection against metabolic issues from a high-fat diet, while later induction had no effect on these parameters.
βAR-mTOR-lipin1 pathway mediates PKA-RIIβ deficiency-induced adipose browning.
Theranostics
September 2024
Department of Anatomy, Histology and Embryology, School of Basic Medical Sciences, Peking University, Beijing, China.
Enhancing white adipose tissue (WAT) browning combats obesity. The RIIβ subunit of cAMP-dependent protein kinase (PKA) is primarily expressed in the brain and adipose tissue. Deletion of the hypothalamic RIIβ gene centrally induces WAT browning, yet the peripheral mechanisms mediating this process remain unexplored.
View Article and Find Full Text PDFProtein Tyrosine Phosphatase Receptors N and N2 Control Pituitary Melanotroph Development and POMC Expression.
Endocrinology
July 2024
Section on Cellular Signaling, The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.
The neuroendocrine marker genes Ptprn and Ptprn2 encode protein tyrosine phosphatase receptors N and N2, 2 members of protein tyrosine phosphatase receptors void of enzymatic activity, and whose function and mechanism of action have not been elucidated. To explore the role(s) of Ptprn and Ptprn2 on the hypothalamic-pituitary-adrenal axis, we used mice in which both genes were knocked out (DKO). The focus in this study was on corticotrophs and melanotrophs from the anterior and intermediate lobes of the pituitary gland, respectively.
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