301 research outputs found

    Protein Tyrosine Phosphatase 1B (PTP1B) in the immune system

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    Journal not available online when checked 02/04/19. DOI: 10.14800/ics.965Peer reviewedPublisher PD

    Effects of dietary restriction on metabolic and cognitive health

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    M. S. M. is a recipient of the Elphinstone Scholarship of the University of Aberdeen as well as Institute of Medical Sciences postdoctoral studentship. Work in B. P. and M. D. laboratories is funded by Alzheimer's Research UK, British Heart Foundation and Diabetes UK. Tenovus Scotland and BBSRC DTP studentship funded the published work on methionine restriction in M. D. laboratory.Peer reviewedPostprin

    The Role of Inflammation in Diabetic Retinopathy

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    Funding Information: This paper was financially supported by Ministry of Health and Fondazione Roma. Publisher Copyright: © 2020 Verduci Editore s.r.l. All rights reserved. Copyright: Copyright 2020 Elsevier B.V., All rights reserved.Peer reviewedPublisher PD

    How stra(i)nge are your controls? : A comparative analysis of metabolic phenotypes in commonly used C57BL/6 substrains

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    Open Access via the PLOS Agreement Funding: The authors received no specific funding for this work.Peer reviewedPublisher PD

    Regulation of growth hormone induced JAK2 and mTOR signalling by hepatic protein tyrosine phosphatase 1B.

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    Protein tyrosine phosphatase 1B (PTP1B) regulates various signalling pathways including insulin, leptin, IGF-1 and growth hormone (GH) signalling. Transmission of the GH signal depends on Janus kinase 2 (JAK2), which is how PTP1B is thought to modulate GH signalling in the liver, based on studies utilising global PTP1B knockout mice (Ptp1b(-/-)). Here, we investigated the liver-specific role of PTP1B in GH signalling, using liver-specific Ptp1b(-/-) mice (alb-crePtp1b(-/-)), under physiological (chow) or insulin resistant (high-fat diet [HFD]) feeding conditions. Body weight and adiposity were comparable between female alb-crePtp1b(-/-) and Ptp1b(fl/fl) control mice. On chow diet, under 48-hour fasting GH-resistant conditions, GH stimulation in vivo led to a robust stimulation of the JAK-STAT signalling pathway. Alb-crePtp1b(-/-) mice exhibited significantly higher GH-induced JAK2 phosphorylation and SOCS3 gene expression post-GH stimulation. However, STAT3, STAT5 and ERK1/2 phosphorylation and SOCS2 gene expression were similar between groups. Interestingly, GH-induced mTOR phosphorylation was significantly higher in alb-crePtp1b(-/-) mice 5-min post-GH stimulation compared to controls, revealing this part of the pathway under direct control of PTP1B. Under ad lib HFD-fed conditions, GH-induced STAT5 phosphorylation significantly increased in alb-crePtp1b(-/-) mice only, with no alterations in the controls. Overall, our data demonstrate that liver-specific PTP1B deletion leads to significant alterations in GH signalling with increased JAK2, STAT5 and mTOR phosphorylation and SOCS3 gene expression

    Female adipose tissue-specific Bscl2 knockout mice develop only moderate metabolic dysfunction when housed at thermoneutrality and fed a high-fat diet

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    The authors would like to thank the staff at the University of Aberdeen’s Medical Research Facility. We are very grateful for the gift of the Adiponectin-Cre mice from Dr. Evan Rosen (Beth Israel Deaconess Medical Centre and Harvard Medical School, Boston, USA). Work was supported by the Medical Research Council (GDM/JJR; MR/L002620/1, MC/PC/15077), the Biotechnology and Biological Sciences Research Council (JJR; BB/K017772/1), the British Heart Foundation (MD; PG/14/43/30889) and The Agency for Science, Technology and Research, Singapore (A*STAR) (WH). The datasets generated during and/or analysed during the current study are available from the corresponding author on reasonable request.Peer reviewedPublisher PD
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