The effect of obesity-induced cytokine elevation on the molecular regulation of protein turnover and carbohydrate metabolism in human skeletal muscle

Lead Research Organisation: University of Nottingham
Department Name: School of Life Sciences

Abstract

Obesity in humans has been shown to result in the increased release of small inflammatory-inducing proteins, called cytokines, from the fat cells of the body. We are interested in the effects of these cytokines on the mechanisms that control muscle mass and metabolism in the obese human. Previous research from work in cells and animals has shown the cytokines reduce the synthesis of muscle proteins and simultaneously enhance their rate of breakdown, resulting in a loss of muscle mass. Furthermore, research suggests that the same cytokines may inhibit carbohydrate oxidation, a pivotal step in muscle metabolism. However, despite these potential negative consequences for skeletal muscle function, the effect of low-level and persistent inflammation as seen in obese humans, remains largely unknown. Our animal based work demonstrated, for the first time, that the molecular events that occur in muscle to reduce muscle mass and inhibit carbohydrate oxidation operate, at least following statin-induced myopathy and sepsis, in unison. Moreover, these events appear to be dependent on the inactivation of a single enzyme, called AKT. Interestingly, the molecular events that result in increased activity of AKT also appear inhibited by the cytokines. Given the findings from cell and animal research, we believe that in obese individuals, where levels of cytokines in the blood are elevated, synthesis of muscle proteins and carbohydrate oxidation may be reduced and breakdown of muscle proteins increased, and that these observations are due to cytokine inactivation of the AKT enzyme. In the current application, we therefore wish to measure the rates of synthesis and breakdown of muscle proteins in conjunction with rates of carbohydrate oxidation in obese individuals, and compare them to rates determined in healthy non-obese individuals. We intend to make these measurements by utilising stable isotope techniques and determining O2 uptake and CO2 production by the subject. Furthermore, we intend to obtain tissue samples from the thigh muscles of volunteers, allowing us to examine the molecular signalling events that underpin these processes and thus determine for the first time the effect of obesity associated low-dose chronic inflammation on essential muscle events. Following these initial determinations, we will start the subjects on a 12-week course of either pioglitazone, an insulin-sensitiser often prescribed to type II diabetics, or a placebo. Pioglitazone and similar compounds have been shown to increase the activity of AKT in obese and diabetic patients and normalise the levels of cytokines in the blood of the former. By repeating the initial measurements described above, and by accurately determining the levels of the cytokines, we hope to elucidate their role in the instigation of any molecular or functional effect in the obese individual. Furthermore, we wish to determine if an insulin sensitising agent can reverse purported effects of obesity on molecular events in muscle and moreover, lead to functional improvements in synthesis and breakdown of muscle proteins and muscle carbohydrate metabolism. The proposed experiments will be performed in the Centre for Integrated Systems Biology and Medicine (CISBM; www.nottingham.ac.uk/cisbm) at the University of Nottingham Medical School, where integrated human physiology is a major research focus. This work is essential because it will further our understanding of the health consequences of obesity which is all the more important given the purported obesity epidemic threatening to face the Western World in future years. Furthermore, this work may have implications for other disease states characterised by low-grade chronic inflammation. This work therefore falls within the strategic plan of the Diet and Health theme of the BBSRC Agri-Foods Committee.

Technical Summary

Obesity is associated with chronic low-grade inflammation and elevated circulating levels of the cytokines TNFa and IL-6. In vitro and animal based evidence has shown TNFa and IL6 to negatively impact upon protein synthesis, protein degradation and fuel metabolism in skeletal muscle. Interestingly, despite the increasing incidence of obesity and the potential negative connotations on muscle function, the effect of obesity-induced elevations of the cytokines on muscle protein turnover and carbohydrate oxidation in humans is largely unknown. Utilising contemporary isotope and respiratory gas exchange methodologies during insulin clamp conditions in obese and non-obese individuals, we will determine the consequences of obesity on muscle protein turnover and carbohydrate metabolism. The taking of muscle samples will enable us to examine by RT-PCR and Western blot the transcriptional and translational changes to the signalling pathways thought to underpin these processes, namely the AKT/mTOR pathway (protein synthesis), the ubiquitin proteasome system, including the MAFbx and MuRF1 ubiquitin ligases (protein degradation), and PDC activity and PDK expression (carbohydrate metabolism). Furthermore, recent evidence suggests that these three processes may be intrinsically linked via the activity of AKT, whose own activity is known to be negatively impacted by the action of the cytokines. To investigate this further, we will administer to the subjects a course of pioglitazone, a compound known to normalise cytokine levels and increase muscle AKT activity in the obese, and follow up by repeating our initial functional and molecular measurements, thereby allowing us to determine whether any effect of pioglitazone on protein turnover and carbohydrate metabolism occurs in a fashion that is consistent with the proposed central role of AKT in the regulation of these processes, and whether this leads to functional improvements in muscle protein turnover and carbohydrate oxidation.

Publications

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Atherton PJ (2016) Control of skeletal muscle atrophy in response to disuse: clinical/preclinical contentions and fallacies of evidence. in American journal of physiology. Endocrinology and metabolism

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Marimuthu K (2011) Mechanisms regulating muscle mass during disuse atrophy and rehabilitation in humans. in Journal of applied physiology (Bethesda, Md. : 1985)

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Murton AJ (2010) Physiological control of muscle mass in humans during resistance exercise, disuse and rehabilitation. in Current opinion in clinical nutrition and metabolic care

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Murton AJ (2011) Muscle atrophy; more than one string to MuRF1's bow? in The Journal of physiology

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Murton AJ (2009) Muscle atrophy in immobilization and senescence in humans. in Current opinion in neurology

 
Description To examine the effects of obesity in old age on muscle protein turnover, carbohydrate (CHO) metabolism, and the underlying mechanisms responsible, we performed a detailed set of metabolic experiments on lean and obese men aged 55-75; conducted in accordance with the protocol detailed in the grant proposal. From this work, we made the following observations:



Under experimentally induced fasting conditions, muscle protein synthesis and leg breakdown rates were equivalent between lean healthy subjects and obese individuals, the latter in a confirmed low-grade inflammatory state. In contrast, the anticipated enhancement of fractional protein synthetic rate (FSR) to elevated serum amino acid and insulin concentrations was blunted in obese participants (37% increase (NS) vs. 108% in the lean (P<0.05)), with a negative linear correlation between leg fat mass and change in FSR with feeding (r2= 0.18; P<0.05). These differences could not be explained by a discord in hypertrophy signalling, with similar enhancements of AKT and mTOR phosphorylation between groups in response to amino acid and insulin provision.



In spite of anabolic resistance in the obese, net leg protein balance, leg lean mass and quadriceps isometric strength were equivalent between groups, due in large part to a reciprocal fall in leg proteolysis in obese, but not lean subjects (decreased by 54%; P<0.05). This occurred in parallel to a fall in proteasome-mediated protein breakdown in obese subjects, where a 24% decrease (P<0.05) in chymotrypsin-like activity was observed, but this was not the result of changes in nuclear Foxo1/3 phosphorylation or MAFbx and MuRF1 protein levels which remained constant throughout the study.



In muscle biopsy specimens obtained at baseline, we observed a significant (FDR<0.1) downregulation of mRNA transcripts associated with oxidative phosphorylation and mitochondrial content in obese subjects. In keeping with the perceived reduction in muscle oxidative capacity in the obese, a hyperinsulinemic euglycaemic clamp failed to elevate the respiratory exchange ratio unlike the lean subjects where a significant elevation was observed (0.72+0.02 to 0.82+0.03; P<0.05). Similarly, leg glucose uptake was significantly greater in the lean compared to obese subjects (lean 156.0+15.3 AUC under steady state conditions vs. obese 56.6+7.5; P<0.001), suggesting CHO oxidation was impaired.



As hypothesised, PPAR gamma agonist administration normalised obesity-induced elevations in circulating IL-6, TNFalpha and resistin to lean levels. The treatment also promoted a 1.3-fold enhancement in the response of mTOR phosphorylation to feeding in obese subjects (P<0.05), but this was not mirrored by changes in other measured signalling processes. Importantly, a trend persisted between leg fat mass and change in FSR with feeding following PPAR gamma agonist administration (p=0.095; r2=0.35) and the drug had no effect on leg lean mass, suggesting that the anabolic resistance to feeding in obese elderly individuals was not the result of chronic low-grade inflammation. Likewise, the treatment was ineffective at restoring whole-body CHO oxidation following feeding, although a partial restoration of leg glucose uptake to lean values was observed (53.4+11.7 pre-treatment AUC vs. 84.0+12.9 post-treatment; P<0.05).



To conclude, obesity in old age is characterised by the development of anabolic resistance to feeding, but net protein balance and muscle mass is preserved as a result of a reciprocal fall in muscle proteolysis. These changes cannot be rationalised by changes in hypertrophic signalling processes and provides an example where AKT signalling does not reflect the overlaying processes it is thought to regulate. Crucially, we show (i) obesity-induced inflammation plays a minor role in these processes or in the dysregulation of CHO metabolism, and (ii) the phenomenon of sarcopenic obesity does not appear to exist, i.e. muscle mass was not reduced in obese older volunteers compared to non-obese older volunteers. These findings therefore make significant contributions to the science of ageing and research translation
Exploitation Route We have shown obesity-induced inflammation plays only a minor role in the dysregulation of muscle protein balance and carbohydrate metabolism in older people. Furthermore, the phenomenon of sarcopenic obesity does not appear to exist, i.e. muscle mass was not reduced in obese older volunteers compared to non-obese older volunteers. Our findings therefore make significant contributions to our understanding human ageing. Importantly, obesity will not accelerate the loss of muscle mass and development of frailty with ageing. This is a clear public health message. A formal collaboration was instigated between Abbott Nutrition and the University of Nottingham on a project aimed at minimising muscle weakness and frailty in the elderly via long-term nutritional intervention.



Partly as a consequence of this BBSRC funded project, a non-disclosure agreement has been signed and formal discussions have begun concerning research collaboration between the PI's laboratory and GlaxoSmithKline, Research Triangle Park, USA focussed on muscle inflammation and adaptation.



A research grant was submitted to Arthritis Research UK aimed at using protocols/strategies developed in this project to blunt muscle inflammation in older people with arthritis.



Data/sequences to be lodged in public access databases were not anticipated to be generated by the project and none were generated.



Licenses and/or patents were not anticipated to be generated by the project and none were generated.



No spin-out company has been generated or associated with the project.
Sectors Healthcare

URL http://www.birmingham.ac.uk/research/activity/mds/centres/mrc-musculoskeletal-ageing/index.aspx
 
Description Effort has gone into quantifying the impact of adiposity on muscle insulin resistance and protein metabolism in older people, and the impact of interventions to alleviate any added burden of adiposity. New data demonstrate obesity in older adults is associated with systemic (but not muscle) inflammation compared to healthy weight control volunteers, but this has no impact upon rates of post-absorptive muscle protein synthesis. However, obesity in older people is associated with diminished muscle metabolic quality, evidenced by the blunting of muscle protein synthesis and leg glucose uptake in the post-prandial state. Nonetheless this is not associated with lower leg lean mass or strength, perhaps in part due to a simultaneous decline in LPB in response to nutrients or the increased muscle work performed by obese individuals when moving.
First Year Of Impact 2014
Sector Healthcare
Impact Types Societal

 
Description ARUK: policy statement on physical activity and musculoskeletal decline
Geographic Reach National 
Policy Influence Type Implementation circular/rapid advice/letter to e.g. Ministry of Health
 
Description COPD MAP (extension award), Workpackage 4
Amount £856,574 (GBP)
Funding ID G1001362/1 
Organisation Medical Research Council (MRC) 
Sector Academic/University
Country United Kingdom
Start 08/2012 
End 09/2015
 
Description MRC COPD MAP G1001362
Amount £426,854 (GBP)
Funding ID G1001362 
Organisation Medical Research Council (MRC) 
Sector Academic/University
Country United Kingdom
Start 01/2011 
End 06/2012
 
Description NIHR Nottingham BRC
Amount £23,000,000 (GBP)
Organisation National Institute for Health Research 
Department NIHR Biomedical Research Centre
Sector Academic/University
Country United Kingdom
Start 04/2017 
End 03/2022
 
Description Vice Chancellor Scholarship
Amount £48,000 (GBP)
Organisation University of Nottingham 
Sector Academic/University
Country United Kingdom
Start 10/2015 
End 09/2018
 
Description ARUK Centre for Sport Exercise and Osteoarthritis 
Organisation Nottingham University Hospitals NHS Trust
Department Nottingham University Hospitals Charity
Country United Kingdom 
Sector Charity/Non Profit 
PI Contribution We are undertaking a project investigating the molecular regulation of muscle insulin resistance and mass loss as a result of ankle fracture and subsequent surgery. We are also investigating the impact of early mobilisation of the joint on the restoration of muscle mass, insulin sensitivity and function during rehabilitation following surgery.
Collaborator Contribution All patient and surgical contributions to the project
Impact This project involves clinicians, physiotherapists and scientists. WE have just gained ethical approval for this project.
Start Year 2014
 
Description ARUK/MRC Centre for Musculoskeletal Ageing Research 
Organisation University of Birmingham
Country United Kingdom 
Sector Academic/University 
PI Contribution Joint bid from Universities of Birmingham and Nottingham
Start Year 2012
 
Description Association of British Pharmaceutical Industry/MRC Consortium 
Organisation Glenfield Hospital
Country United Kingdom 
Sector Hospitals 
PI Contribution Association between the MRC and Association of British Pharmaceutical Industries (work package 4) investigating skeletal muscle as a limitation to mobility and quality of life in COPD.
Collaborator Contribution Funding has been provided by the Association and Novartis to undertake a gene array study in COPD vs control volunteers aimed at understanding the molecular basis of the restoration of muscle mass and function in COPD. Funding has been provided to execute a COPD vs young vs old healthy control volunteers to investigate mitochondrial function in COPD and ageing (joint with the MRC/ARUK Centre for Musculoskeletal Ageing Research). We wish to know whether the proposed mitochondrial dysfunction in COPD and ageing is in reality attributable to inactivity. This is important as it offers a viable route for intervention if deemed to be true.
Impact A new EME outline grant application has been submitted between members of the consortium.
Start Year 2011
 
Description Member of EU wide Framework 7 collaborative consortium 
Organisation European Commission
Department Seventh Framework Programme (FP7)
Country European Union (EU) 
Sector Public 
PI Contribution Investigating intermittent training as a modality for improving insulin resistance in overweight inactive people
Start Year 2012
 
Description A departmental lecture, University of Leeds 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach Regional
Primary Audience Postgraduate students
Results and Impact This was an invited lecture at the University of Leeds focussed on muscle metabolic dysregulation with ageing.
Year(s) Of Engagement Activity 2016
 
Description ARUK advisory panel meeting on physical activity 
Form Of Engagement Activity A formal working group, expert panel or dialogue
Part Of Official Scheme? Yes
Geographic Reach National
Primary Audience Public/other audiences
Results and Impact Interaction with ARUK about their policy document relating to exercise and musculoskeletal health in the context of OA.

Stimulated significant interest with ARUK
Year(s) Of Engagement Activity 2014
 
Description Academic seminar, Kennedy Research Institute, University of Oxford 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach Regional
Primary Audience Postgraduate students
Results and Impact A seminar lecture focussed on differentiating the effects of inflammation and inactivity on muscle metabolic dysregulation in ageing.
Year(s) Of Engagement Activity 2016
 
Description Ageing Masterclass 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach Local
Primary Audience Undergraduate students
Results and Impact A masterclass of researchers presenting on ageing and age related disease to undergraduate and postgraduate students across the University of Nottingham
Year(s) Of Engagement Activity 2018
URL https://revl.world/event/interprofessional-masterclass-ageing-population/
 
Description BBC Radio 4 Frontiers programme 
Form Of Engagement Activity A press release, press conference or response to a media enquiry/interview
Part Of Official Scheme? No
Geographic Reach National
Primary Audience Participants in your research or patient groups
Results and Impact Ageing and Muscle wasting

no actual impacts realised to date
Year(s) Of Engagement Activity 2010
URL http://www.ed.ac.uk/news/2013/flowers-130813
 
Description BBC Radio Nottingham Interview 
Form Of Engagement Activity A press release, press conference or response to a media enquiry/interview
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Media (as a channel to the public)
Results and Impact Took part in live-to-air interview to discuss the sarcopenic obesity research.

no actual impacts realised to date
Year(s) Of Engagement Activity 2009
 
Description Community engagement workshop, Nottingham County Council 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach Local
Primary Audience Patients, carers and/or patient groups
Results and Impact Public dissemination of research findings on the impact of obesity and inactivity on healthy ageing.
Year(s) Of Engagement Activity 2015
 
Description Differentiating drivers of muscle mass regulation: ageing, inactivity and inflammation. 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? Yes
Geographic Reach International
Primary Audience Participants in your research or patient groups
Results and Impact MRC Lifecourse Epidemiology Unit, September 2012 - Invited speaker. Invited seminar focussed on the drivers of sarcopenia, including obesity

no actual impacts realised to date
Year(s) Of Engagement Activity 2012
 
Description European College of Sports Science Symposium - control of skeletal muscle mass with ageing: effects of exercise, inactivity and inflammation. 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Participants in your research and patient groups
Results and Impact Talk sparked discussion and interaction

Post talk discussion (students asking for papers and interaction)
Year(s) Of Engagement Activity 2014
 
Description I attended the expert "think-tank" workshop titled "Influencing the trajectories of ageing"at the Academy of Medical Sciences, London 
Form Of Engagement Activity A formal working group, expert panel or dialogue
Part Of Official Scheme? No
Geographic Reach National
Primary Audience Professional Practitioners
Results and Impact This was an expert workshop aimed at exploring the current developments in ageing research and how this science can be used for decision-making by better predicting longevity and health.
Year(s) Of Engagement Activity 2016
URL https://acmedsci.ac.uk/file-download/41227-5746fb4d0f825.pdf
 
Description I delivered a lecture titled "Is there a role of insulin resistance in driving muscle disuse atrophy?" in the symposium "The control of skeletal muscle atrophy in responses to disuse: clinical/ pre-clinical contentions and fallacies of evidence" at Experimental Biology, San Diego (2-6th April 2016) 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Professional Practitioners
Results and Impact Loss of skeletal muscle mass in response to mechanical unloading is associated with prolonged bed-rest, casting of lower-limbs due to broken/fractured bones, and spaceflight. Moreover, a number of catabolic conditions including age-related sarcopenia and numerous diseases associated with muscle wasting i.e. respiratory or organ failure; are exacerbated by interactions between disease(s) pathogenesis (i.e. inflammation) and increasingly sedentary behaviours associated with ill-health. Indeed, the physiological and metabolic consequences of skeletal muscle unloading are profound including: skeletal muscle atrophy, bone loss, whole-body/muscle insulin resistance, fluid shifts and cardio-respiratory de-conditioning. This symposium focussed on the physiological/metabolic disturbances associated with disuse atrophy with contributors conveying knowledge yielded from clinical and pre-clinical studies (and from multi-modal approaches).
Year(s) Of Engagement Activity 2016
 
Description Keynote lecture, American College of Sports Medicine Annual Meeting 2018, Minneapolis, USA 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Other audiences
Results and Impact Keynote lecture, American College of Sports Medicine Annual Meeting 2018, Minneapolis, USA
Year(s) Of Engagement Activity 2018
 
Description Mayfest Community outreach event 
Form Of Engagement Activity Participation in an activity, workshop or similar
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Public/other audiences
Results and Impact An open day held at the University of Nottinghamfor the local community. At the event we presented information related to our sarcopenic obesity research.

no actual impacts realised to date
Year(s) Of Engagement Activity 2011
 
Description Physiological Society Conference 
Form Of Engagement Activity Participation in an activity, workshop or similar
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Other audiences
Results and Impact A symposium on inactivity and musculoskeletal degeneration in Ageing at a Physiological Society meeting in Edinburgh in 2014
Year(s) Of Engagement Activity 2014
 
Description Physiological Society annual meeting (symposium) 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Postgraduate students
Results and Impact I presented a talk entitled "Physical inactivity and age-related declines in muscle metabolic health" in the symposium "Physiological approaches to study the science of human sedentariness" at Physiology 2016, which was a Joint Meeting of the American Physiological Society and The Physiological Society, 29 - 31 July 2016, Convention Centre Dublin, Ireland.
Non-communicable chronic diseases, such as cardiovascular disease, cancer and type 2 Diabetes account worldwide for ~48% of healthy life years lost (Disability Adjusted Life Years DALYs; ~65% of all current deaths, and are projected to cause over 75% of all deaths by 2030. A substantial body of epidemiological and experimental evidence has established a causal relationship between NCDs and preventable risk factors, with physical inactivity being at the heart of these. Moreover, there is accumulating epidemiological evidence to suggest that sitting time is an independent risk factor, perhaps being even independent of the amount of leisure-time physical activity and body adiposity. The study of sedentariness is an emergent science, meaning we know relatively little about the physiological drivers and mechanisms mediating the metabolic and dysregulation associated with sedentariness or the time-course of their effects with few mechanistic studies to date reliant upon measures that are definitive in terms of muscle protein turnover and insulin resistance. This disconnect will ultimately limit the effectiveness of strategies to combat this burgeoning public health problem.
The purpose of this symposium was to present current information on the metabolic physiology of sedentariness. The senior speakers will provided an overview of current insights gained from human mechanistic studies of acute immobilisation/ inactivity as well as applied studies of the acute effects of sitting time and their influence on cardio-metabolic risk, whilst early career researchers presented their current cutting-edge research utilising both basic and applied science approaches. The seminar was attended by established and early career researchers and news press and has added to the current increase in the sedentariness on human health and sparked further research focussed meetings on ageing and health.
Year(s) Of Engagement Activity 2016
URL http://www.physiology2016.org/scientific-programme/physiological-approaches-study-science-human-sede...
 
Description Presentation to the Birmingham 1,000 Elders group 
Form Of Engagement Activity Participation in an activity, workshop or similar
Part Of Official Scheme? No
Geographic Reach Regional
Primary Audience Study participants or study members
Results and Impact A presentation on the negative impact of obesity and inactivity of metabolic health and ageing processes.
Year(s) Of Engagement Activity 2017
 
Description Press release by The University of Nottingham 
Form Of Engagement Activity A press release, press conference or response to a media enquiry/interview
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Participants in your research or patient groups
Results and Impact Concerning the sarcopenic obesity work funded by the BBSRC grant.

(http://www.nottingham.ac.uk/news/pressreleases/2009/september/helping-the-obese-fight-loss-of-muscle-function.aspx)

no actual impacts realised to date
Year(s) Of Engagement Activity 2009
URL http://www.nottingham.ac.uk/news/pressreleases/2009/september/helping-the-obese-fight-loss-of-muscle...
 
Description Protein intake, muscle function and aging 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Postgraduate students
Results and Impact 8th International Congress of Taste, Nutrition and Health, Dijon France, March 2013. Invited speaker.

no actual impacts realised to date
Year(s) Of Engagement Activity 2013
 
Description School outreach event 
Form Of Engagement Activity Participation in an activity, workshop or similar
Part Of Official Scheme? No
Geographic Reach Local
Primary Audience Schools
Results and Impact Hosting of local sixth-form students for a day in Human Physiology Labs with workshops for the students aimed at exploring the possibility of a career in Physiology.

After this visit students requested placements
Year(s) Of Engagement Activity 2010
 
Description The impact of immobilization and inflammation on muscle mass regulation and insulin resistance 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Participants in your research and patient groups
Results and Impact Presentation to GlaxoSmithKline "Muscle Group" at GSK, Research Triangle, North Carolina, USA Providing an overview of how obesity related inflammation, amongst other physiological drivers, influences muscle protein turnover and insulin resistance.

Research funding secured from collaboration with GSK
Year(s) Of Engagement Activity 2012,2013,2014
 
Description The impact of immobilization and inflammation on muscle mass regulation and insulin resistance. 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Postgraduate students
Results and Impact Invited seminar to the "Harvard Muscle Group" Part of the presentation involved focus on obesity and muscle mass regulation and data pertaining to this grant were presented

Research collaboration
Year(s) Of Engagement Activity 2012
 
Description Universities of Ghent and Leuven Inter-university Doctoral Training School 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Participants in your research and patient groups
Results and Impact Talking sparked discussion amongst PhD students attending the doctoral training course

Change way of thinking about inflammation amongst young scientists
Year(s) Of Engagement Activity 2014