Professor Justin Rochford
The Rochford Lab is a member of the Obesity and Metabolic Health theme at the Rowett Institute
2015: Reader, Rowett Institute of Nutrition and Health, University of Aberdeen.
2013-2015: Senior Lecturer, Rowett Institute of Nutrition and Health, University of Aberdeen.
2009-2012: Senior Research Associate (MRC-NIRG), IMS-MRL, University of Cambridge.
2006-2009: BHF Intermediate Research Fellow, Dept. of Clinical Biochemistry, University of Cambridge.
2000-2006: Research Associate, Dept. of Clinical Biochemistry, University of Cambridge.
1998-2000: INSERM Poste Vert Fellow, INSERM Unit 145, Nice, France.
1994-1998: PhD , Department of Biochemistry and Genetics, University of Newcastle upon Tyne.
Memberships and Affiliations
- Internal Memberships
Justin Rochford co-led the Rowett Institute's successful application for an Athena SWAN bronze award in 2016 and remains a member of the Equality and Diversity Team at the Rowett.
Member of the School of Medicine, Medical Sciences and Nutrition Biological Safety Committee.
- External Memberships
Executive Board Member of European Consortium for the Study of Lipodystrophies (ECLip). https://www.eclip-web.org/
Associate Editor, Current Research in Physiology. https://www.journals.elsevier.com/current-research-in-physiology
Editorial Board Member, Diabetes. https://diabetes.diabetesjournals.org/
Grants Panel Member for Diabetes UK. https://www.diabetes.org.uk/
Society for Endocrinology
Gene therapy restores adipose tissue and metabolic health in a pre-clinical mouse model of lipodystrophyMolecular Therapy - Methods & Clinical Development, vol. 27, pp. 206-216Contributions to Journals: Articles
Guanidinoneomycin-Maleimide Molecular Transporter: Synthesis, Chemistry and Cellular UptakeOrganic & Biomolecular Chemistry, vol. 19, no. 29, pp. 6513-6520Contributions to Journals: Articles
Phosphoprotein enriched in astrocytes (PEA)-15 is a novel regulator of adipose tissue expansionScientific Reports, vol. 11, 6949Contributions to Journals: Articles
Bscl2 Deficiency Does Not Directly Impair the Innate Immune Response in a Murine Model of Generalized LipodystrophyJournal of Clinical Medicine, vol. 10, no. 3, 441Contributions to Journals: Articles
Neurochemical characterization of brainstem Pro-opiomelanocortin cellsEndocrinology, vol. 161, no. 4, pp. 1-13Contributions to Journals: Articles
My group focuses on the molecular mechanisms controlling adipocyte differentiation and the functions of mature fat cells generated by this process. Humans turn over adipocytes at a rate of approximately 10% each year so adipocyte development is a process relevant throughout life. Having appropriately functioning fat cells is critical for human health as these cells provide an essential safe store for dietary nutrients, particularly lipids, and protect other tissues in the body from their harmful effects. This is perhaps most clearly demonstrated by individuals with severe forms of lipodystrophy who fail to appropriately develop or maintain adipose tissue and suffer severe insulin resistance and metabolic disease as a consequence. Lipid is stored in adipocytes in a large fat droplet mainly comprised of triglyceride. The storage and release of this lipid is highly regulated and is a defining function of mature adipocytes. In addition adipocytes secrete many factors that affect appetite, insulin sensitivity and metabolic health. In obesity, despite abundant adipose tissue, the adipocytes appear to be dysfunctional and their lipid storage capacity may be exceeded, leading to overflow of lipids to other tissues. For this reason obese individuals may suffer similar metabolic problems to patients with lipodystrophy. Overall, this means that understanding the development and function of adipocytes may lead us to new therapies by which these can be modified to treat both rare lipodystrophies and common obesity.
Lipodystrophy genes as critical regulators of human fat development:
Dr George Mcilroy, Post-doctoral Fellow
Ahlima Roumane, PhD student
Nadine Sommer, Research Assistant
A key approach we are taking is to investigate the functional roles of genes known to cause lipodystrophy in humans, particularly those whose disruption causes severe loss of adipose tissue. Evidently the products of these genes are critical for the development of adipose tissue in humans, however, relatively little is known about their molecular role in developing adipocytes. We use a range of techniques to understand the function of these proteins including immunofluorescence/confocal microscopy to examine subcellular localisation and trafficking, transcriptional and protein analyses to determine their importance in adipogenesis, binding studies and proteomics to identify and characterise novel binding partners and lipidomics to investigate their involvement in lipid biosynthesis, a key component of adipocyte differentiation.
This work is exemplified by our studies of the protein seipin, encoded by the gene BSCL2. Patients with disruption of seipin have almost no detectable adipose tissue and we were the first to show that this may result from an inability to make new fat cells from stem cells lacking seipin. However, the precise function of seipin has remained unknown until very recently. We have previously shown that seipin acts as a binding protein for known regulators of adipogenesis which may at least partly explain why it is needed for adipocyte development. However, we have also identified multiple other binding proteins, both in developing and in mature adipocytes. A major component of our research is to investigate these further both in vitro and in vivo.
Understanding what the products of lipodystrophy genes do, the pathways they influence and the proteins they regulate will give key insights into human adipose tissue development and function. By identifying novel pathways and proteins that can influence adipocyte function, this work may also reveal new therapeutic targets for the treatment of common obesity and metabolic disease. This work is funded by Diabetes UK, the EFSD, The Wellcome Trust and the MRC.
For more about lipodystrophy see our blog post:
Nutrition and Health
Funding and Grants
- Wellcome Trust Institutional Strategic Support Fund pilot grant: "Developing viral therapeutics for the treatment of severe diabetes and metabolic disease in lipodystrophy" Rochford JJ (PI) Mcilroy GD (Co-I) 01/12/20-01/06/21.£17,469.
- Diabetes UK Project Grant: “New Treatments for Severe Type 2 Diabetes in Lipodystrophy” Rochford JJ (PI) Heisler LK (Co-I) 01/02/19-31/04/21. £159,536
- The Instituto de Salud Carlos III (Spanish Institute of Health): “Therapeutic approaches to celia encephalopathy (PELD) in humans and in murine "knock in" BSCL2 Celia / Celia models” PI Araujo Vilar D, Rochford JJ (Co-I) 01/03/19-28/02/22. €99,500.
- BBSRC Project Grant: ”Defining the underpinnings of Neuropeptide Y (NPY)'s control of hunger and body fat” PI Heisler LK, Rochford JJ (Co-I) 15/07/18-14/07/21. £548,427
- NHS Grampian Endowments “Fast Field Cycling/Magnetic Resonance Imaging (FFC-MRI): A New Diagnostic that Reveals Acutely Inflamed Coronary Artery Plaques by Detecting Fat Dysfunction”. PI Dawson D, Rochford JJ (Co-I) 01/04/18-31/03/19. £9,350
- WT Strategic Award to the Institute of Metabolic Science, University of Cambridge. PI O’Rahilly S, Rochford (Co-I, plus 9 others) 01/07/13-30/06/19. £4.7M
- MRC Discovery Award “Defining the role of seipin in the central regulation of energy metabolism”. Rochford JJ (PI), Heisler LK. Start: 11/2017. 6 months. £23,344.
- NHS Research Endowment Trust pilot grant. “The role of joint fat in osteoarthritis.” Roelofs AJ, De Bari C, Rochford JJ (Co-I). Start: 04/2017. 12 months. £11,971.
- Wellcome Trust Institutional Strategic Support Fund pilot grant. “Defining the metabolic properties of mechanical fat, an adipose depot with unexplored therapeutic potential.” Rochford JJ (PI), Roelofs AJ, De Bari C. Start: 04/2016. 6 months. £13,960.
- MRC Project Grant: “Defining the Role of the Human Lipodystrophy Protein Seipin in Adipose Tissue Development and Metabolic Disease”. 01/06/13-01/11/17. £435,613
- BBSRC Project Grant: “Delineating the regulation and function of gamma-synuclein in adipocyte lipid metabolism”. PI: JJ Rochford 01/02/13-31/01/17. £376,972
- MRC New Investigator Research Grant “Elucidating the Function of BSCL2, a Critical Regulator of Human Fat Development” PI: JJ Rochford 01/03/09-31/09/12. £357,799
Course co-ordinator: SR4008 Nutrition, Obesity and Metabolic Health.
BC3503 The Molecular Control of Cell Function
B125M7 Energy for Life
SM2501 Reserach Skills for Medical Sciences
BM5518 Genetics Research Tutorials
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Female adipose tissue-specific Bscl2 knockout mice develop only moderate metabolic dysfunction when housed at thermoneutrality and fed a high-fat dietScientific Reports, vol. 8, 17863Contributions to Journals: Articles
Nucleus of the Solitary Tract Serotonin 5-HT2C Receptors Modulate Food IntakeCell Metabolism, vol. 28, no. 4, pp. 619-630.e5Contributions to Journals: Articles
Adipose specific disruption of seipin causes early-onset generalised lipodystrophy and altered fuel utilisation without severe metabolic diseaseMolecular Metabolism, vol. 10, pp. 55-65Contributions to Journals: Articles
Lorcaserin improves glycemic control via a melanocortin neurocircuitMolecular Metabolism, vol. 6, no. 10, pp. 1092-1102Contributions to Journals: Articles
Sex difference in physical activity, energy expenditure and obesity driven by a subpopulation of hypothalamic POMC neuronsMolecular Metabolism, vol. 5, no. 3, pp. 245-252Contributions to Journals: Articles
Seipin oligomers can interact directly with AGPAT2 and lipin 1, physically scaffolding critical regulators of adipogenesisMolecular Metabolism, vol. 4, no. 3, pp. 199-209Contributions to Journals: Articles
Analyzing the functions and structure of the human lipodystrophy protein seipinMethods in Enzymology, vol. 537, pp. 161-175Contributions to Journals: Articles
Mouse models of lipodystrophy and their significance in understanding fat regulationCurrent topics in developmental biology, vol. 109, pp. 53-96Contributions to Journals: Articles
Analysis of naturally occurring mutations in the human lipodystrophy protein seipin reveals multiple potential pathogenic mechanismsDiabetologia, vol. 56, no. 11, pp. 2498-2506Contributions to Journals: Articles
γ-synuclein is a novel player in the control of body lipid metabolismAdipocyte, vol. 2, no. 4, pp. 276-280Contributions to Journals: Articles