Defining the molecular roles of peripheral CB1 and CB2 cannabinoid receptors in age-induced changes in energy and metabolic homeostasis.

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

Abstract

There is immense interest at present in targeting the action of a class of compounds, termed cannabinoids, in the treatment of obesity and metabolic-related disorders. Cannabinoids are present in cannabis, but our bodies naturally create cannabinoid-like chemicals, known as endocannabinoids that lock-on to protein molecules found on the surface of cells called cannabinoid receptors (i.e. CB1 and CB2). During obesity, diabetes and, as we have recently discovered, during ageing the CB1 is notably over-activated by endocannabinoids produced by the body resulting in impaired insulin action and dysregulation of energy balance in metabolically important tissues such as muscle, fat and liver. CB1 over-activation has been linked strongly with development of insulin resistance and increased adiposity. In contrast, emerging data indicates that CB2 may confer a protective physiological effect. In line with this idea, we find that CB2 inhibitors (antagonists) augment the insulin-desensitising effects of the endocannabinoid, anandamide (AEA) in muscle cells, whereas CB2 activators (agonists) ameliorate the loss in insulin signalling. Moreover, it is noteworthy that whilst CB1 expression is enhanced in ageing muscle that of CB2 is significantly decreased, consistent with the reduced insulin sensitivity that prevails in ageing skeletal muscle.

Intriguingly, CB1 antagonists (e.g. rimonabant) promote glucose tolerance, stimulate energy expenditure and reduce body weight in obese animals by mechanisms independent of their appetite-reducing effect. Consistent with such findings, we find rimonabant ameliorates age-related tissue insulin resistance and fat mass gain in older animals. Precisely how CB1 antagonism elicits these beneficial effects is unclear, but our recent work indicates that CB1 blockade induces activation of AMPK - a molecule that not only senses cellular energy but promotes the breakdown and burning of fat in mitochondria (the cell's energy factory). The molecular events linking CB1 blockade to AMPK activation and the effect of the latter on enzymes involved in fat breakdown/burning and mitochondrial dynamics remain poorly understood. The proposed studies will utilise cultured muscle and fat cells to understand how CB1 inhibition or CB2 activation impacts upon molecules implicated in insulin action, energy balance and mitochondrial function and integrity. Our molecular analyses will involve biochemical and state-of-the-art imaging techniques for visualising mitochondrial staining in muscle and fat cells. These cell-based studies will be complemented with analysis of tissues from young and old mice genetically deficient in CB2 or experiments in young and aged mice administered a pharmacologically active dose of a CB1 antagonist or CB2 agonist for two weeks. During this period we will monitor food intake, glucose tolerance, energy expenditure, physical activity and fat mass before sampling blood/tissue for experimental analyses designed to dissect the mechanisms by which CB1 blockade or CB2 activation improves the metabolic status of aged animals. We also aim to test the effects of exercise in aged animals given that physical activity is known to help sustain tissue sensitivity to anabolic hormones such as insulin and preserve tissue functionality during aging. These studies will help unveil whether exercise curtails age-related changes in tissue CB1 and CB2 expression and, if so, whether these correlate favourably with measures of whole body energetics (i.e. body fat, glucose tolerance and energy expenditure).

The proposed research will specifically expand our fundamental understanding of how modulating peripheral CB receptor activity influences energy balance and insulin action. The findings that will emerge will advance our knowledge of these key issues and prove invaluable in designing therapies that selectively target the peripheral ECS for treatment of age and obesity-related metabolic disorders.

Technical Summary

There is growing appreciation that sustained over-activation of the peripheral type I cannabinoid receptor (CB1) contributes significantly to the development of insulin resistance and promotes disturbances in both energy and metabolic homeostasis in tissues such as muscle, liver and adipose tissue. Reduced insulin sensitivity and increased metabolic dysfunction are prominent features of ageing tissue and we have discovered that expression of CB1 is significantly enhanced in aging muscle, liver and fat. Administration of a selective CB1 antagonist (rimonabant) to aged animals not only induces beneficial effects upon tissue insulin signalling and energy balance, but reduces fat mass by mechanisms that are, as yet, poorly understood. Intriguingly, unlike CB1, expression of CB2 is significantly reduced in aging tissue consistent with emerging data suggesting it may confer a protective insulin-sensitising function. Remarkably, we reveal that both CB1 antagonism and CB2 agonism invoke AMPK activation and that this is likely to support greater fat oxidation via enhanced PGC1alpha-induced mitochondrial biogenesis/respiratory capacity, thereby promoting favourable gains in insulin sensitivity and metabolic function within peripheral tissues. The fact that CB1 inhibition suppresses expression of proadipogenic genes (FAS, SREBP-1, PPAR-gamma2) whilst inducing that of the lipolytic enzyme, ATGL in aged animals strongly supports this proposition. This proposal will investigate how CB1 blockade/CB2 stimulation (using peripherally acting receptor antagonists/agonists), activate AMPK and how this impacts mechanistically, at the molecular level, on mitochondrial function/energy homeostasis and insulin sensitivity in muscle, fat and liver during aging. We will also explore whether exercise mitigates age-related changes in tissue CB1 and CB2 receptor expression and, if so, whether these correlate with enhanced retention of insulin sensitivity and metabolic function.

Planned Impact

Who will benefit from this research?
Academics: Our understanding of how the peripheral endocannabinoid (EC) system affects key anabolic responses in tissues such skeletal muscle, liver and adipose tissue is still very much in its infancy. Consequently, our findings will have benefits for other academic researchers, especially those working on ageing research, regulation of fuel/energy homeostasis and insulin action.
Private Sector: Our findings will appeal to pharmaceutical companies with an interest in the EC system, especially with respect to therapies that help maintain tissue response/function during ageing.
Government: The findings may help inform policy on healthy ageing and benefits of exercise in relation to maintenance of tissue mass/function at both national (e.g. DH) and international (e.g. EU Healthy Ageing Initiative, WHO) levels.
Public and Charitable Sectors: Individuals working for public health/sports-related disciplines (e.g. physiotherapists, exercise instructors) and scientific advisors to Medical Charities will benefit from the findings in terms of helping to devise appropriate strategies that alleviate age-related decline in tissue health, as well as advising their clients of recent advances.
General Public: Target beneficiaries include the elderly, especially those presenting with significant insulin resistance or sarcopenia.

How will they benefit from this research?
Our pilot studies have identified significant age-related changes in EC receptor activity in tissues such as skeletal muscle, fat and liver that we believe contribute to the pathogenesis of tissue insulin resistance. This reduced anabolic response to insulin will impact on tissue mass/function thus contributing to increased frailty, reduced life quality and increased healthcare costs. Our work indicates that drugs countering age-induced changes in EC receptor function will not only ameliorate loss in peripheral tissue insulin sensitivity but promote loss of adiposity. Our research will also address whether age-related changes in EC receptor expression and the associated metabolic sequalae can be mitigated by implementing a physical activity program. Such work will be appeal to other academics with an interest in ageing research and those in the pharmaceutical sector with research programmes targeting the EC system. Ultimately, the work will be of particular benefit to the elderly in terms of counteracting age-related changes in tissue mass/function, thereby improving health/quality of life and reducing overall healthcare costs. The discoveries, materials and expertise will be made available to other academics and interested commercial beneficiaries through publications, meetings and Material Transfer Agreements, which may benefit the UK economic competitiveness in biopharmaceutical products. Appointed staff will benefit from institutional initiatives promoting career development and training in public engagement.

What will be done to ensure that they benefit from this research?
Both lead and non-lead institutions are fully committed to maximizing their research impact. This commitment was recognised by the BBSRC by way of the 2011 BBSRC Excellence with Impact Award to the College of Life Sciences (CLS). Impact was also a key measure in REF2014, and CLS was recently rated best in biological sciences of any UK University. The applicants have established networks for communicating their research and its benefits via public engagement/outreach activities (e.g. via hosting public visits, Café Science) as well as professional bodies that they are members of (e.g. Diabetes UK and Royal Society of Edinburgh) who interact directly with the public. The impact of our research is publicised on our respective College websites or, where appropriate, through press releases from our Publicity Offices or engagement with our Technology Transfer Offices in matters concerning Intellectual Property Rights and commercial development.

Publications

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Lipina C (2016) Is REDD1 a Metabolic Éminence Grise? in Trends in endocrinology and metabolism: TEM

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Lipina C (2017) Lipid modulation of skeletal muscle mass and function. in Journal of cachexia, sarcopenia and muscle

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Lipina C (2019) GPR55 deficiency is associated with increased adiposity and impaired insulin signaling in peripheral metabolic tissues. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology

 
Description There is considerable interest in the clinical potential of a class of compounds, termed cannabinoids, for the treatment of obesity and diabetes. Cannabinoids were originally identified in the cannabis sativa plant but the mammalian body also produces cannabinoid-like molecules, termed endocannabinoids, which exert their effects by "locking onto" specific binding molecules, known as cannabinoid (CB1 and CB2) receptors, present in the membrane of cells. Two well characterised endocannabinoids are anandamide (AEA) and 2-arachidonoylglycerol (2-AG), which serve as activators for the CB1 and CB2 cannabinoid receptors, respectively. The focus of this project has been to understand how the action of AEA and 2-AG at these receptors impacts upon cellular responses that may be of relevance in the development or prevention of metabolic dysfunction as seen in tissues, for example, in diabetes and during the course of aging.

A key observation over the past year has been our finding that AEA and 2-AG can promote anti-inflammatory effects in muscle cells. Chronic low grade inflammation is a feature of obesity and a risk factor implicated in the pathogenesis of insulin resistance. Previous studies from the Hundal lab have shown that sustained exposure of muscle cells to saturated fatty acids, such as palmitate, as commonly seen during obesity induces signalling events promoting a heightened pro-inflammatory state (characterised by increased expression of genes encoding proinflammatory cytokines, e.g. IL-6, CINC-1 and COX-2). Strikingly, we have discovered that coincubation of muscle cells with palmitate and AEA or 2-AG helps to antagonise the proinflammatory drive initiated by palmitate as evidenced by a reduction in proinflammatory gene expression. Moreover, our studies have shown that the ability of 2-AG to protect against palmitate induced inflammation is blocked by molecules which inhibit CB2 activity, whilst being unaffected by molecules which block CB1 function. Notably, the anti-inflammatory action of 2-AG coincides with its ability to prevent palmitate-induced insulin resistance, an effect which is also blocked by CB2 inhibition. We are currently exploring the mechanisms by which 2-AG acts to promote its anti-inflammatory and insulin-sensitising response in muscle cells through the CB2 receptor.

In addition to its anti-inflammatory action in muscle cells, we have recently discovered that co-application of the endocannabinoid 2-AG protects against palmitate induced mitochondrial dysfunction in muscle cells by alleviating the reduction in the energy producing capacity of mitochondria following prolonged exposure to the fatty acid. Intriguingly, we have found that exposure to palmitate promotes fragmentation of mitochondria coinciding with their damage and impaired function, whereas co-application of 2-AG prevents this palmitate-induced fragmentation from taking place, thereby leaving mitochondria to remain in a more elongated (or fused) healthy state. Importantly, our work has shown that the ability of 2-AG to protect against palmitate induced insulin resistance and mitochondrial dysfunction is blocked by CB2 inhibiting molecules, thereby supporting a role for this receptor in mediating the protective actions of 2-AG in muscle cells. Furthermore, we have also uncovered a potential role for an enzyme called protein kinase A (PKA) in mediating the protective actions of 2-AG upon mitochondrial health and energy producing capacity in muscle cells, and are currently exploring the link between CB2 and PKA in promoting the beneficial actions of 2-AG.

It is noteworthy that in addition to protecting against palmitate-induced mitochondrial dysfunction, recently we have also discovered that 2-AG can alleviate reductions in mitochondrial energy capacity following chemically induced cellular stress. More specifically, we induced cellular stress using a chemical compound called tunicamycin that disrupts protein folding (and hence protein function) in a compartment of cells known as the endoplasmic reticulum (ER) which plays a crucial role in determining protein quality control. We have found that promoting ER cellular stress induced by tunicamycin causes a marked reduction in the energy producing capacity of mitochondria in muscle cells which, crucially, can be prevented by co-application of 2-AG. Our on-going studies currently involve assessing how 2-AG is able to mitigate stress induced mitochondrial dysfunction in muscle cells.

In addition, we have also discovered that exposing muscle cells to 2-AG is able supress the production of damaging oxygen containing molecules known as reactive oxygen species (ROS) which damage cells and impair their function. More specifically, we have been able to demonstrate that the presence of 2-AG can alleviate chemically induced production of ROS in cultured skeletal muscle cells. Therefore, these initial findings uncover a potential role for 2-AG in the modulation of ROS levels which we are currently investigating the implications of with respect to muscle cell function. Allied to this, recently we have also uncovered a potential role for a protein known as Nrf2 in mediating the protective action of 2-AG against palmitate induced mitochondrial dysfunction. Specifically, Nrf2 is a protein involved in activating genes which encode for proteins with an antioxidant function - that is proteins which act to 'mop-up' ROS molecules thereby alleviating their damaging effects in cells. In muscle cells, we have found that applying molecules which inhibit Nrf2 activity can prevent protection by 2-AG against palmitate-induced reductions in the levels of key proteins required for mitochondrial health and function (e.g. PGC-1alpha and SDHA). Assessing how crucial Nrf2 is in mediating the protective actions of 2-AG in muscle cells is a key focus of on-going work in our research group.

In addition to work performed using cultured muscle cells, we have also performed studies in aged mice challenged with an exercise regime allowing us to explore the effects of physical activity upon the levels of CB1 and CB2 in skeletal muscle. Using this approach, we have been able to show that voluntary exercise increases levels of a gene product molecule known as messenger RNA (mRNA) specifically encoding for the production of CB2 receptor protein in skeletal muscle tissue of aged mice. It is also noteworthy that we have observed a reduction in CB2 mRNA abundance in skeletal muscle in aged versus young adult mice, concomitant with reduced insulin sensitivity and higher body fat mass in older mice. Notably, the observed increase in the expression of muscle CB2 mRNA following exercise coincided with significant improvements in insulin sensitivity (determined by measuring whole body glucose disposal and tissue insulin signalling) as well as reduced body fat content. Moreover, exercise in aged mice was also found to increase levels of proteins that are important for energy production in mitochondria (MTCO1, UQCRC2, ATP5A) in fat tissue, reflective of increased fat burning capacity.
Exploitation Route We believe that the findings of this work will be useful for developing future treatments for type 2 diabetes and obesity, as well as related metabolic diseases such as cardiovascular disease. Moreover, our discoveries will also provide a basis for better understanding the development of metabolic impairments including insulin resistance and mitochondrial dysfunction in response to ageing and diet-induced obesity.
Sectors Education,Healthcare,Pharmaceuticals and Medical Biotechnology

URL https://www.harihundal.com/endocannabinoid-system
 
Description C5aR, a novel immunomodulator of metabolic signalling and energy metabolism in skeletal muscle
Amount £274,686 (GBP)
Funding ID 18/0005875 
Organisation Diabetes UK 
Sector Charity/Non Profit
Country United Kingdom
Start 02/2019 
End 01/2022
 
Description Delineating the roles of GPR55 in cellular metabolism and energy homeostasis
Amount £411,233 (GBP)
Funding ID BB/S00033X/1 
Organisation Biotechnology and Biological Sciences Research Council (BBSRC) 
Sector Public
Country United Kingdom
Start 01/2019 
End 12/2021
 
Description Lipid-induced insulin resistance and metabolic dysfunction: the role of caveolins and cavins
Amount £93,500 (GBP)
Funding ID 15/0005350 
Organisation Diabetes UK 
Sector Charity/Non Profit
Country United Kingdom
Start 10/2016 
End 09/2019
 
Description Nutrient-induced mitochondrial dysfunction and its reciprocal control by inflammatory signalling: implications for skeletal muscle insulin action.
Amount £203,494 (GBP)
Funding ID 16/0005484 
Organisation Diabetes UK 
Sector Charity/Non Profit
Country United Kingdom
Start 06/2017 
End 05/2020
 
Description Assessing effects of rimonabant on whole body energy expenditure 
Organisation University of Aberdeen
Country United Kingdom 
Sector Academic/University 
PI Contribution Our team has been able to provide some of the basic research tools (drugs/antibodies etc) to investigate how modulation of the cannabinoid system affects in vivo metabolism in mice using techniques that are up and running in the partners laboratory.
Collaborator Contribution The partner has been able to provide a whole host of skills that enable measurement of whole body composition and in vivo energy expenditure that have allowed us to vlaidate some of our cell based findings in whole animals
Impact One manuscript was recently published that includes data generated from this collaborative effort (Lipina et al, Aging Cell, 15: 325-35, 2016 (PMID 267557949). We still have data from this joint collaborative investigation that is being prepared for a further publication that specifically examines the role of exercise in ageing animals on cannabinoid receptor expression and its association with insulin sensitivity.
Start Year 2012
 
Description GPR55 its role as a modulator of insulin action and metabolism 
Organisation Robert Gordon University
Country United Kingdom 
Sector Academic/University 
PI Contribution We have partnered with investigators at RGU to provide our knowledge and expertise on insulin signalling and metabolism
Collaborator Contribution Our collaborators are in possession of a GPR55 mouse knock-out model. Tissues from these mice have been made available to us for analysis of protein expression and tissue signalling experiments
Impact We have very recently published an article on the effects that GPR55 deficiency has upon adiposity and insulin signalling in peripheral metabolic tissues. This work has cemented a three way academic collaboration with researchers at the University of Dundee, University of Aberdeen and Robert Gordons University
Start Year 2015
 
Description Use of a novel human adipocyte cell line for analysis of the role played by CB2 in metabolic signalling 
Organisation University of Ulm
Country Germany 
Sector Academic/University 
PI Contribution We have entered into a collaboration with Professor Dr Martin Wabitsch at Ulm University who has established a human pre-adipocyte cell line from an infant with Simpson-Golabi-Behmel Syndrome (SGBS). The cell strain exhibits a high capacity for adipose differentiation, resulting in mature fat cells which are biochemically and functionally similar to human adipocytes. It is the only available human preadipocyte cell line and consequently represents an invaluable tool for studies assessing human adipocyte biology, lipid metabolism and energy metabolism. Professor Wabitsch has provided the SGBS human adipocyte cell line to us for use in our BBSRC funded project to interrogate the role that the endocannabinoid system may play in adipocyte physiology. We have now established use of SGBS adipocytes in the Hundal lab and have found that these express the CB2 cannabinoid receptor. Intriguingly, activation of this receptor initiates signalling events within cells that result in the activation of a key energy sensing kinase called AMPK, which is known to influence fuel oxidation in mitochondria and also function as an anti-inflammatory signalling molecule. The Hundal lab hosted a summer 2017 intern student from Singapore Polytechnic who was able to show that this AMPK activation by CB2 receptor activation was critically dependent on inducing nitric oxide (NO) production. inhibiting nitric oxide synthase within SGBS cells attenuated the CB2-dependent activation of AMPK. Precisely how CB2 induces NO production and how this mechanistically linked to AMPK is currently unknown, but the subject of on-going studies that will hopefully delineate the nature of these molecular links.
Collaborator Contribution The utility of SGBS cells as a research tool for studies assessing adipocyte signalling and metabolism requires an extensive characterisation of their responses to hormonal and nutritional cues as well as a thorough understanding of how such responses compare to those of freshly isolated human adipocytes. The Wabitsch lab has performed detailed characterisation of the cells they have provided for use in our studies and we have access to data (some unpublished) that is useful in helping us to design and formulate the experiments we are carrying out in these cells.
Impact No outputs to report as yet as studies are still ongoing.
Start Year 2017
 
Description Blairgowrie Primary School, Angus 
Form Of Engagement Activity Participation in an activity, workshop or similar
Part Of Official Scheme? No
Geographic Reach Regional
Primary Audience Schools
Results and Impact In 2015, my Research Division hosted a public engagement activity called "Incredible Immunology" at Dundee Science Centre. This event involved all members of the division engaging with the attending public and discussing, in lay terms, the basis of their research programme and its relevance to public health. The event was extremely well received and based on the feedback that was received the Division decided to host another Incredible Immunology event but to hold it in a regional community school centre so as to widen access to audiences out with the city of Dundee. In May 2017 the Division held a 2 day public engagement activity in the town of Blairgowrie in Angus that targeted primary school children on day 1 and the local town community on day 2. My lab, and others from my Division, utilised intelligent game play and props that members of Division had created to inform the children and local public of our research methods and findings. The two day activity got local press coverage and the feedback suggested that the attending public thought the event both "informative and enjoyable" and one that they would like see repeated in the future.
Year(s) Of Engagement Activity 2017
 
Description Dundee Science Centre - Incredible Immunology 
Form Of Engagement Activity Participation in an activity, workshop or similar
Part Of Official Scheme? No
Geographic Reach Regional
Primary Audience Public/other audiences
Results and Impact Members of the Division of Cell Signalling & Immunology (CSI) held a two day event at Dundee Science centre - the first day engaged students from the Tayside region and the second day was a family fun day. Both days were aimed at conveying the relevance of the research being done by members of CSI to the public ranging from infection, immunity and nutritional disorders. Numerous stands with interactive activities were set up to inform how are research matters to the public at large. The event in total had more than 200 visitors and those coming from the schools reported that they found the event to be fun, informative and a great learning experience
Year(s) Of Engagement Activity 2015
URL http://discovery.dundee.ac.uk/portal/en/researchunits/cell-signalling-and-immunology(cf577b0d-98ed-4...
 
Description Edinburgh International Science Festival 
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 I attended and presented in a session called 'Ask a Researcher' at the opening night party of the Edinburgh International Science Festival in March 2018, which was staged at the city's Art Centre. During the course of the evening over 600 members of the public were welcomed to the opening event and were able to participate in numerous hands on activities that had been arranged by the organisers and various vendors/participants. I met a significant number of the visiting public spanning the full age spectrum from young children to individuals in their nineties. Appropriately, I was discussing the importance of nutrition, exercise and healthy living during the human life span and fielded numerous questions during the night in relation to healthy and unhealthy living. I was able to utilise tools that my institution had provided (for measurement of muscle grip strength, skin-fold callipers, blood pressure monitors etc.) that allowed me to engage with the visiting public in a meaningful way that also allowed me to discuss my research and its significance to public health issues such as obesity and diabetes. I believe I had a positive impact on individuals that I met based on a shift in their understanding and request for further information.
Year(s) Of Engagement Activity 2018
URL https://edinburghfestival.list.co.uk/festival/edinburgh-international-science-festival/
 
Description Incredible Immunology 
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 Incredible Immunology is an event focused on helping school pupils and teachers to learn about the human immune system and the research taking place at the University of Dundee School of Life Sciences.

During the event researchers and students from the Division of Cell Signalling and Immunology facilitated interactive activities at 'stands' at Arbroath High for over 120 S1 pupils and science teachers. These stands touched on topics like vaccination, herd immunity, and immune responses.

My research was represented in this program of work by demonstrating the role that components of the endocannabinoid system (CB1, CB2 and GPR55) play in regulating whole body energy metabolism and how this might impact on the function of tissues such as skeletal muscle and cells of the immune system. Feedback from pupils from Arbroath High and public members showed an increased interest in science as a topic and increased familiarity with concepts and vocabulary associated with immunology. The School of Life Sciences has since been invited back to repeat the activity, and the school has also visited us on campus to take part in laboratory activities linked to the curriculum.
Year(s) Of Engagement Activity 2019
 
Description Life Sciences - Open Doors Day 
Form Of Engagement Activity Participation in an open day or visit at my research institution
Part Of Official Scheme? No
Geographic Reach Local
Primary Audience Public/other audiences
Results and Impact This event was held on 7/11/2015 and enables members of the public to look more closely at the outstanding technologies within our research labs that are crucial to our success. The event allows the public to appreciate how biologists, physicists, chemists, clinicians and computing specialists work together to address the most challenging scientific questions and to develop research tools to advance scientific discovery.
We invite the public to tour Dundee's world-class technology research laboratories and discover, through hands on activities, how research science really works.
Year(s) Of Engagement Activity 2015
URL http://www.lifesci.dundee.ac.uk/impact/public-engagement
 
Description Pint of Science 
Form Of Engagement Activity Participation in an activity, workshop or similar
Part Of Official Scheme? No
Geographic Reach Regional
Primary Audience Public/other audiences
Results and Impact Pint of Science has become an annual worldwide science festival that is run by a non-profit organisation that invites science researchers to share what they do and why they do it with the public over three days in May. The event takes place in casual venues such as pubs and cafes where researchers give a talk and the audience have the opportunity to ask them any questions in relation to their research and to chat with them in an informal setting. Professor Hundal was invited to participate in a "Pint of Science" event that was held in Dundee in May 2019 where he gave a 30 minute presentation entitled "The metabolic price of gluttony". The event was held in a local pub and tickets to his talk were sold out on the night.
Year(s) Of Engagement Activity 2019