Amanda Page

Professor Amanda Page

Senior Research Fellow

Adelaide Medical School

Faculty of Health and Medical Sciences

Eligible to supervise Masters and PhD - email supervisor to discuss availability.


Professor Amanda Page has established herself as a leading authority on vagal innervation of the gut, and how this relates to major disease states including obesity and gastro-oesophageal reflux disease. This has involved pioneering studies on the phenotypic specialisation of vagal sensory endings and a classification of gastrointestinal sensory nerves that has been adopted world-wide. One of her major findings, that GABAB receptor agonists inhibit peripheral gastro-oesophageal vagal afferent endings, prompted 2 full scale drug development programs and the production of 5 patents. Investigation of the effects of different nutritional states (for example: food restriction and excess) on these afferents has resulted in major contributions in the understanding of gastric satiety signalling.

OVERARCHING RESEARCH VISION: To improve understanding of the physiology and pathophysiology of gastrointestinal vagal afferent sensory signalling with the ultimate aim to provide new pharmacological targets or dietary therapeutic approaches for the treatment of diseases such as obesity and functional dyspepsia.

To date the Vagal Afferent Research Group has made significant contributions towards this vision, transforming the research field. This includes:

  • pioneering studies on the phenotypic specialisation of vagal afferent endings
  • elucidation of the role of G-protein coupled receptors in vagal afferent regulation of lower oesophageal sphincter function; validating them as novel targets to treat gastro-oesophageal reflux disease.
  • Elucidation of the role of mechanosensitive ion channels in visceral sensory transduction with correlation to functional outcomes.
    More recent research focusses on the role of gastric vagal afferent signalling in the regulation of food intake with seminal observations that vagal afferent signals:
  • are dampened in high fat diet (HFD)-induced obesity and remain compromised after return to a normal diet.
  • are dampened in HFD-induced obesity due to disruption in transient receptor potential, vanilloid 1 (TRPV1) channel signalling.
  • exhibit circadian rhythmicity to finely tune food intake to energy demand; a property that is lost in HFD-induced obesity but maintained by time-restricted feeding.
  • are regulated by gastrointestinal appetite hormones in a nutritional status dependent manner. Notably, leptin effects on gastric vagal afferents switch from ‘anorexigenic’ in lean mice to ‘orexigenic’ in HFD mice.
  • are exaggerated in chronic stress conditions reflective of enhanced gastrointestinal luminal sensitivity in functional dyspepsia.

The Vagal Afferent Research Group intends to build on these strong research foundations to expand understanding on how individual subtypes of gastrointestinal afferent contribute to motor and sensory function of the gut, as it applies to food intake and appetite regulation. In addition, the group plans to establish how this system adapts to normal physiological conditions, such as pregnancy, and also how this is altered in disease, such as obesity and functional dyspepsia.   

The overall aims of the Vagal Afferent Research Groups research program for the next 5 years are to establish the:

  1. subtype specificity of gastrointestinal vagal afferents in motor and sensory function.
  2. plasticity of gastrointestinal vagal afferents in ‘normal’ physiological conditions, such as pregnancy.
  3. molecular mechanisms responsible for the modulatory effect of hormones/peptides (e.g. leptin) on gastrointestinal vagal afferent function and the changes that occur in high fat diet-induced obesity.
  4. molecular mechanisms responsible for gastrointestinal vagal afferent responses to mechanical and chemical stimuli and the changes that occur to induce:
    • hyposensitivity in high fat diet-induced obesity.
    • hypersensitivity under chronic stress conditions.

CLINICAL SIGNIFICANCE: The prevalence of obesity has more than doubled in the last 30 years and it is estimated that, by 2025, ~70% of the Australian population will be overweight or obese. According to the Australian Bureau of Statistics there were 1,043 deaths in 2009 (median age 61.1yrs) for which obesity was an underlying or associated cause of death. The total annual cost of obesity in 2008 was estimated at ~$58 billion. Consequently, there is increased impetus to improve knowledge of the human biology of obesity and the biological mechanisms that drive the condition.

Functional dyspepsia is a disease in which luminal sensitivity to gastric distension and small intestinal lipid is abnormally enhanced leading to gastrointestinal symptoms including nausea, bloating and early satiety(1). Functional dyspepsia affects about 20% of the population, significantly impairing quality of life. There is limited research in this area, even in humans, and important questions, relating to the mechanisms driving abnormally heightened perception, have not been addressed.

Over- or under-nutrition during pregnancy can create significant health risks for the mother and her developing fetus. Studies indicate that under- or over-nutrition in pregnancy can result in a ‘programming’ effect during the vulnerable fetal developmental periods(2). The result is a predisposition to chronic conditions in adulthood, such as type 2 diabetes mellitus, renal(3) and cardiovascular disease(4). It also increases offspring susceptibility to obesity(2). Despite the detrimental effects of over- and under-nutrition, on offspring health, there is limited knowledge on the role of the gastrointestinal tract in food intake and nutrient absorption during pregnancy.

BACKGROUND: In animals, the acquisition of nutrients in order to maintain life requires the intake of food. As a consequence, evolution has developed a sophisticated and well integrated multilevel system to finely control energy intake. Although great advances have been made in our basic understanding of this system the finer complexities remain a mystery. We know the gut-brain axis plays an important role in the: 1) regulation of gastrointestinal motility and secretions to optimise absorption of nutrients, and 2) regulation of appetite to control meal size. However, there is inadequate knowledge of the mechanisms involved in initiating these signals, the plasticity of these mechanisms under normal physiological conditions (i.e. pregnancy) and whether changes in these mechanisms are associated with diseases such as obesity or functional dyspepsia. In the periphery, vagal afferent sensory nerves innervating the gut are ideally positioned to respond to both the volume and type of food consumed. They can be activated by mechanical stimulation, from the physical presence of food in the gut, or chemical stimulation, by gastrointestinal peptides released in response to specific nutrients. In addition, the gastrointestinal peptides and circulating hormones can modulate the response of vagal afferents to both mechanical and chemical stimuli(5). Therefore, vagal afferents display a remarkable degree of adaptability in response to daily variations in food intake and nutritional status. However, extension of this adaptability to normal physiological states, including during high energy demand, such as in pregnancy, is unknown. In addition, disruption of this system can have significant health implications. Understanding the mechanisms that drive exaggerated or dampened vagal afferent signalling will lead to new diet regimes and/or pharmacotherapies for treatment of diseases such as obesity and functional dyspepsia.

METHODOLOGY: Consistent with the Vagal Afferent Research Groups research to date, a multidisciplinary approach is utilised combining molecular (e.g. quantitative RT-PCR, Western blot, laser capture microdissection), appetite hormone measurements, electrophysiology, imaging (e.g. immunohistochemistry), functional (e.g. gastric emptying, metabolic monitoring) and behavioural (e.g. open field, elevated maze, forced swim & sucrose preference tests) studies with mouse models (e.g. HFD-induced obesity, chronic unpredictable stress, genetically modified strains, pregnancy) and human tissue.

SPECIFIC PROJECTS AVAILABLE:

The projects below provide information on the research areas available for Higher Degree by Research students. These projects can be split into smaller components to accommodate 3rd year Research Placements and Honours students.

  1. Establish the subtype specificity of gastrointestinal vagal afferents in motor and sensory function.

Background: The Vagal Afferent Research Groups research on gastric vagal afferent satiety signalling in health and obesity has contributed to a paradigm shift in understanding of gut-brain signalling. For example, we have established that there are distinct subpopulations of gastric vagal afferent, namely mucosal and tension sensitive vagal afferents. However, the exact physiological role of these afferent subtypes has not been fully elucidated. For instance, there is no direct evidence for the role of gastric mucosal receptors in motility or appetite regulation. Aim: Establish the contribution of specific subtypes of gastric vagal afferent to gut function and appetite regulation. New technology is now available to determine this aim including a transgenic mouse carrying the Cre recombinase gene driven by tartrate-resistant acid phosphatase (TRAP) promotor that will express Cre only in neurons that express the transcriptional factor Fos after a stimulus. Therefore, mucosal stimuli will restrict Cre in mucosal vagal afferent neurons. Further, injection of a Cre dependent virus to stimulate/inhibit this population of vagal afferent neurons will enable determination of function. Outcomes and Significance: This research will increase fundamental knowledge of gastric vagal afferent function and identify specific subtypes of gastric vagal afferent to target for the treatment of diseases such as obesity and functional dyspepsia.

2. Establish plasticity of gastrointestinal vagal afferents in ‘normal’ physiological conditions, such as pregnancy.

Background: During pregnancy the supply of energy must be sufficient to ensure adequate growth and development of the fetus with the degree of maternal nutrition having substantial implications for fetal development and subsequent postnatal health. For example, nutrient restriction during pregnancy can have adverse metabolic consequences in the adult offspring(6, 7) with increased cardiovascular and type 2 diabetes risk(8, 9).   To meet the energy demands of the growing fetus a state of positive energy balance is developed through adaptation of homeostatic processes including the regulation of food intake(10-12). It is known that there are gross anatomical changes in the gastrointestinal tract, predominantly the small intestine, that increase the surface area and thus increase the absorptive capacity of the gut. However, the mechanisms by which the gut senses and responds to food intake involves the interplay of multiple complex pathways that, among other processes, regulate appetite and modulate absorption of nutrients. Fundamental knowledge on the plasticity of these processes during pregnancy is lacking. We propose that gastrointestinal satiety signalling is dampened during pregnancy to permit the intake of food at a time of high energy demand. Further, we hypothesise that nutrient transporter molecule expression is increased and contributes to increased nutrient absorption during pregnancy. Objectives: (i) Characterise gastrointestinal vagal afferent satiety signalling during pregnancy; and (ii) Characterise the contribution of gastrointestinal nutrient transporter molecules in nutrient absorption during pregnancy. Outcome: This project will substantially increase understanding of the plasticity of gastrointestinal vagal afferent signalling, appetite regulation and nutrient absorption during pregnancy. Significance: This work will significantly increase knowledge of the adaptive mechanisms within the GI tract necessary to meet the energy demands of the growing fetus. Further, the findings will direct future research investigating strategies to combat over- or under-nutrition of the developing fetus.

3. Establish the molecular mechanisms responsible for the modulatory effect of hormones/peptides (e.g. leptin) on gastrointestinal vagal afferent function and the changes that occur in high fat diet-induced obesity.

Background: Appetite hormones, such as leptin and ghrelin, modulate gastric vagal afferent satiety signals in a nutritional status dependent mannere.g.(13-16). Notably, leptin effects on gastric vagal afferents switch from ‘anorexigenic’ in lean mice to ‘orexigenic’ in HFD mice(14). Consistent with these results, it has been reported that targeted vagal afferent leptin receptor knockout increases weight gain in lean (chow-fed) mice but paradoxically decreases weight gain of mice fed a HFD compared to wildtype controls on equivalent diets(17). Unravelling the mechanisms that drive this switch will have significant implications for the development of new targets for the treatment of obesity and will be a primary focus of this project.  Outcomes: This project will substantially increase our understanding of the mechanism of leptin-induced modulation of  gastric vagal afferent satiety signals and establish why there is a switch in the effect of leptin on gastric vagal afferents from ‘anorexigenic’ in lean mice to ‘orexigenic’ in HFD-induced obese mice. Significance: Establishing the mechanism that underlies this switch in effect of leptin is central to the development of peripheral obesity pharmacotherapies.

4. Establish the molecular mechanisms responsible for gastrointestinal vagal afferent responses to mechanical and chemical stimuli and the changes that occur to induce: a) hyposensitivity in high fat diet-induced obesity and b) hypersensitivity under chronic stress conditions.

a) The underlying mechanisms responsible for TRPV1 signalling and its disruption in HFD-induced obesity.

Background: TRPV1 has been implicated in obesity and we have established that dampened gastric vagal afferent satiety signalling in HFD-induced obesity is due to a disruption in TRPV1 signalling(18). Endocannabinoids (ECs: e.g. anandamide (AEA)), which are endogenous ligands for TRPV1, have peripheral effects on appetite regulation(19). To date such effects have been considered mediated by the cannabinoid receptor 1 (CB1) with overactivity of this system increasing food intake. However, there is cross-talk between CB1 and TRPV1. We propose that dampened satiety signalling in HFD-induced obesity is due to inhibition of TRPV1 channels as a consequence of overactivity of CB1 receptors in gastric vagal afferents. Objectives: (i) Characterise the gastric vagal afferents expressing TRPV1, CB1 or both; (ii) Determine the interaction between TRPV1, ECs and CB1 on gastric vagal afferent mechanosensitivity and gastric vagal afferent neurone excitability in lean and HFD-induced obese mice; (iii) Measure levels of endocannabinoids in the stomach in lean and HFD-induced obese mice; and (iv) Establish the physiological significance of TRPV1 in gastric vagal afferent satiety signalling in lean and HFD-induced obese mice. Outcome: This project will substantially increase understanding of the interactions between the EC system and TRPV1 in the control of gastric vagal afferent satiety signalling. It will also increase understanding of how these interactions are altered in obesity to dampen gastric vagal afferent satiety signalling and perpetuate the problem of obesity. Significance: This work will identify much-needed new targets for the treatment of obesity.

b) Mechanisms that drive GI vagal afferent hypersensitivity under chronic stress conditions.

Background: Functional dyspepsia is characterised by hypersensitivity to gastrointestinal stimuli relating to a meal(1) and is associated with symptoms including early satiety, fullness, bloating, nausea and epigastric pain. Psychological disorders (e.g. anxiety and depressive disorders) often precede or exacerbate functional dyspepsia symptoms(20, 21). We have preliminary data demonstrating chronic unpredictable stress induces hypersensitivity of gastric vagal afferents. The symptoms of functional dyspepsia are associated with both the stomach and duodenum. Using the chronic stress model along with the gastrointestinal vagal afferent preparations we aim to unravel the mechanisms responsible for vagal afferent hypersensitivity, in both the stomach and small intestine. In patients with IBS, which is predominantly a functional disorder of the lower gastrointestinal tract, the response to capsaicin (TRPV1 ligand) is potentiated compared to healthy volunteers(22). TRPV1 receptors are involved in vagal afferent signalling(18) and therefore gastric vagal afferent hypersensitivity observed in chronic stress conditions could be due to heightened TRPV1 mediated signalling and, as above, alterations in the interaction between TRPV1, CB1 and endocannabinoids. Stress-induced hypersensitivity may also be mediated through inflammation since the enhanced capsaicin response, in IBS patients, is mimicked by pre-incubation with the mast cell mediator histamine and is dependent on histamine 1 receptor (H1R) activation(22). Objective: (i) Characterise the gastrointestinal vagal afferents expressing TRPV1, CB1 and H1R; and (ii) Determine the relationship between TRPV1 and histamine (from mast cells, gastrointestinal mucosa or microbiome) in chronic stress induced hypersensitivity. Outcome: The proposed research will significantly advance understanding of the mechanisms involved in chronic stress-induced vagal afferent hypersensitivity.  Significance: This research will provide new pharmacological targets or diet regimes for the treatment of functional dyspepsia patients with psychological stress-associated symptoms.

REFERENCES

1.         Feinle-Bisset C. Upper gastrointestinal sensitivity to meal-related signals in adult humans - relevance to appetite regulation and gut symptoms in health, obesity and functional dyspepsia. Physiol Behav. 2016 Aug 01;162:69-82. DOI: 10.1016/j.physbeh.2016.03.021.

2.         Ross MG, Desai M. Developmental programming of offspring obesity, adipogenesis, and appetite. Clin Obstet Gynecol. 2013 Sep;56(3):529-36. DOI: 10.1097/GRF.0b013e318299c39d.

3.         Bacchetta J, Harambat J, Dubourg L, Guy B, Liutkus A, Canterino I, et al. Both extrauterine and intrauterine growth restriction impair renal function in children born very preterm. Kidney Int. 2009 Aug;76(4):445-52. DOI: 10.1038/ki.2009.201.

4.         Salam RA, Das JK, Bhutta ZA. Impact of intrauterine growth restriction on long-term health. Curr Opin Clin Nutr Metab Care. 2014 May;17(3):249-54. DOI: 10.1097/MCO.0000000000000051.

5.         Kentish SJ, Page AJ. Plasticity of gastro-intestinal vagal afferent endings. Physiol Behav. 2014 Sep;136:170-8. DOI: 10.1016/j.physbeh.2014.03.012.

6.         Locke AE, Kahali B, Berndt SI, Justice AE, Pers TH, Day FR, et al. Genetic studies of body mass index yield new insights for obesity biology. Nature. 2015 Feb 12;518(7538):197-206. DOI: 10.1038/nature14177.

7.         Hales CN, Barker DJ. Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologia. 1992 Jul;35(7):595-601.

8.         Fall CH, Osmond C, Barker DJ, Clark PM, Hales CN, Stirling Y, et al. Fetal and infant growth and cardiovascular risk factors in women. BMJ. 1995 Feb 18;310(6977):428-32.

9.         Hales CN, Barker DJ, Clark PM, Cox LJ, Fall C, Osmond C, et al. Fetal and infant growth and impaired glucose tolerance at age 64. BMJ. 1991 Oct 26;303(6809):1019-22.

10.       Ladyman SR, Carter KM, Grattan DR. Energy homeostasis and running wheel activity during pregnancy in the mouse. Physiol Behav. 2018 Oct 1;194:83-94. DOI: 10.1016/j.physbeh.2018.05.002.

11.       Ladyman SR, Grattan DR. Region-specific reduction in leptin-induced phosphorylation of signal transducer and activator of transcription-3 (STAT3) in the rat hypothalamus is associated with leptin resistance during pregnancy. Endocrinology. 2004 Aug;145(8):3704-11. DOI: 10.1210/en.2004-0338.

12.       Ladyman SR, Fieldwick DM, Grattan DR. Suppression of leptin-induced hypothalamic JAK/STAT signalling and feeding response during pregnancy in the mouse. Reproduction. 2012 July 1, 2012;144(1):83-90. DOI: 10.1530/rep-12-0112.

13.       Kentish S, Li H, Philp LK, O’Donnell TA, Isaacs NJ, Young RL, et al. Diet-induced adaptation of vagal afferent function. J Physiol. 2012;590(1):209-21. DOI: 10.1113/jphysiol.2011.222158.

14.       Kentish SJ, O'Donnell TA, Isaacs NJ, Young RL, Li H, Harrington AM, et al. Gastric vagal afferent modulation by leptin is influenced by food intake status. J Physiol. 2013 April 1, 2013;591(7):1921-34. DOI: 10.1113/jphysiol.2012.247577.

15.       Kentish SJ, Ratcliff K, Li H, Wittert GA, Page AJ. High fat diet induced changes in gastric vagal afferent response to adiponectin. Physiol Behav. 2015 Dec 1;152(Pt B):354-62. DOI: 10.1016/j.physbeh.2015.06.016.

16.       Kentish SJ, Li H, Frisby CL, Page AJ. Nesfatin-1 modulates murine gastric vagal afferent mechanosensitivity in a nutritional state dependent manner. Peptides. 2017 Mar;89:35-41. DOI: 10.1016/j.peptides.2017.01.005.

17.       de Lartigue G, Ronveaux CC, Raybould HE. Deletion of leptin signaling in vagal afferent neurons results in hyperphagia and obesity. Mol Metab. 2014 Sep;3(6):595-607. DOI: 10.1016/j.molmet.2014.06.003.

18.       Kentish SJ, Frisby CL, Kritas S, Li H, Hatzinikolas G, O'Donnell TA, et al. TRPV1 Channels and Gastric Vagal Afferent Signalling in Lean and High Fat Diet Induced Obese Mice. PLoS One. 2015;10(8):e0135892. DOI: 10.1371/journal.pone.0135892.

19.       Sharkey KA, Pittman QJ. Central and peripheral signaling mechanisms involved in endocannabinoid regulation of feeding: a perspective on the munchies. Sci STKE. 2005 Mar 29;2005(277):pe15. DOI: 10.1126/stke.2772005pe15.

20.       Wouters MM, Boeckxstaens GE. Is there a causal link between psychological disorders and functional gastrointestinal disorders? Expert Rev Gastroenterol Hepatol. 2016;10(1):5-8. DOI: 10.1586/17474124.2016.1109446.

21.       Aro P, Talley NJ, Johansson SE, Agreus L, Ronkainen J. Anxiety Is Linked to New-Onset Dyspepsia in the Swedish Population: A 10-Year Follow-up Study. Gastroenterology. 2015 May;148(5):928-37. DOI: 10.1053/j.gastro.2015.01.039.

22.       Balemans D, Alpizar YA, Nasser Y, Valdez-Morales EE, Moonen A, Cirillo C, et al. Evidence for Histamine-Mediated Sensitization of TRPV1 Signaling in Sensory Neurons in Mice and IBS Patients. Gastroenterology. 2014;146(5):S220-S1.

 

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  • Appointments

    Date Position Institution name
    2016 Professor University of Adelaide
    2010 - 2016 Associate Professor University of Adelaide
    1995 - 2009 Research Officer (Funded by AstraZeneca Pharmaceuticals and NHMRC) Royal Adelaide Hospital
    1993 - 1995 Research Fellow (Medical Research Council grant) University College London
    1989 - 1993 MRC Postgraduate Scholar (Medical Research Council grant) University College London
  • Education

    Date Institution name Country Title
    1994 University College London United Kingdom Doctor of Philosophy (PhD)
    1989 University of Liverpool United Kingdom B.Sc. Class II (I) Hons Pharmacology
  • Research Interests

Research Support

I have obtained over $3.5 million in competitive research funding since 2011.  In the last 10 years I have held 5 NHMRC grants, one ARC Discovery Project, an ARC LIEF grant, and a Diabetes Australia grant all as CIA.

Research Support

I have obtained over $2.5 million in competitive research funding since 2011, including funding from the NHMRC, ARC and Diabetes Australia. In the last 10 years I have held 4 NHMRC grants, one ARC Discovery Project, an ARC LIEF grant, and a Diabetes Australia grant all as CIA.

Category 1 funding

2019-2022 NHMRC Project Grant (APP1159744)

Chief Investigators: AJ Page (CIA); G Wittert.

Title: TRiPing oVer appetite regulation in the stomach.

$985,724.80

2018 Diabetes Australia General Grant (DART)

Chief Investigators: AJ Page (CIA); G Wittert.

Title: TRiPing oVer diabetes.

$59,521

2015 ARC LIEF grant (LE150100037)

Chief Investigators: AJ Page (CIA); SM Brierley; TN Dear; PA Hughes; D Keating; S Koblar; J Lucinio; S Nicholls; C Proud; Q Schwarz; S Wesselingh, M-L Wong; R Young.

Title: Laser capture microdissection facility.

$170,000

2014 – 16 ARC Discovery project (DP140102203)

Chief Investigators: AJ Page (CIA); G Wittert; TN Dear

Title: Plasticity of gastrointestinal vagal afferents.

$551,000

2013 NHMRC Equipment grant

Chief Investigators: AJ Page (CIA); GA Wittert; LK Heilbronn; SM Brierley; BT Baune; T Little; N Thompson; RLYoung; J Bowen

Title: Metabolic monitoring equipment.

$94,864

2013 - NHMRC Project Grant (APP1046289)

Chief Investigators: AJ Page (CIA); G Wittert; D Kennaway

Title: Circadian control of peripheral gastric satiety signals.

$676,987

2012 - 14 NHMRC Project Grant (APP1023972)

Chief Investigators: AJ Page (CIA); LA Blackshaw; G Wittert; SM Brierley

Title: Role of adipokines in gastric satiety signalling.

$603,375

2009 - 11 NHMRC Project Grant (APP565186)

Chief Investigators: AJ Page (CIA); LA Blackshaw; G Wittert

Title: Interactions of gastric hormones with vagal afferent pathways and the role of this system in obesity.

$529,500

 

Industry funding

 

2014 – 15 Ironwood Pharmaceuticals Amanda Page Curriculum Vitae June 2016

Chief Investigators: AJ Page (CIA); SJ Kentish

$157,397

2014 – 15 Ironwood Pharmaceuticals

Chief Investigators: AJ Page (CIA); SJ Kentish

$65,380

2013 – 14 Ironwood Pharmaceuticals

Chief Investigators: AJ Page (CIA); SM Brierley

$206,624

 

Internal University of Adelaide funding

2017: Beacon Fellowship

Chief Investigator: AJ Page

$184,000

2018: Beacon Fellowship

Chief Investigator: AJ Page

$184,000

2018: Equipment grant for Anaerobic chamber and sample mixer.

Chief Investigator F: AJ Page

$43,195

2018: Equipment grant for EchoMRI

Chief Investigator A: AJ Page

$105,360

2018: Equipment grant to upgrade Ussing chambers

Chief Investigator A: AJ Page

$11,930.54

2018: Seed funding

Chief Investigator A: AJ Page

$10,000

2017: Development grant

Chief Investigator A: AJ Page

$30,000

2017: Equipment grant for Ussing Chambers

Chief Investigator C: AJ Page

$41,600

2012: Equipment grant for 7500 FAST Real Time PCR System

Chief Investigators: AJ Page (CIA); R Young; SM Brierley

$77,000

2012: Equipment grant for Nanodrop (Spectrophotometer)

Chief Investigators: AJ Page (CIA); R Young; SM Brierley; C Feinle-Bisset

$9,800

 
Teaching, Supervision, Mentoring:

To date 5 PhD and 11 Honours students have successfully completed their degrees under my supervision. I currently supervise 10 PhD, 1MPhil and 1 Honours student. Notably I was principal supervisor of Dr Kentish who completed his PhD with Dean’s commendation. I also co-supervised Dr Hughes who is now supported by an NHMRC Australian Biomedical Fellowship. As a member of the NHMRC Centre of Research Excellence: Translating Nutritional Science to Good Health and the School of Medicine Research Committee I have a continuing role in recruiting and mentoring young scientists, with input into the courses being offered within the School and also direct input into individual research directions, funding applications and overall career development. As the senior member within the Centre for Nutrition and Gastrointestinal Diseases I also mentors 5 early/mid-career research fellows. Although my appointment is a research position, I am actively involved in undergraduate teaching and curriculum development:

HEALTH 3000A&B Course coordinator level III BHlthSci (Adv). 
PATHOL 2200 1 lecture on gastrointestinal diseases, 2 tutorials, assignment and marking of ~20 essays.
ANAT SC 3104 2 lectures on appetite and obesity & supervise a small group research project.
HEALTH 2000 2 Practical sessions.
PHYSIOL 3001&3000 Supervise small group research project.

 

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  • Current Higher Degree by Research Supervision (University of Adelaide)

    Date Role Research Topic Program Degree Type Student Load Student Name
    2019 Principal Supervisor Fibretype Specific Molecular Mechanisms Driving Gastric Vagal Afferent Satiety Signalling Doctor of Philosophy Doctorate Full Time Ms Yoko Brigitte Wang
    2019 Co-Supervisor Gut mechanisms linking artificial sweeteners to impaired glycaemic control Doctor of Philosophy Doctorate Full Time Miss Denise Kreuch
    2018 Co-Supervisor Evolution of Metabolic Control in Mammals Doctor of Philosophy Doctorate Full Time Miss Natasha Paige Bradley
    2017 Principal Supervisor TRPV1 and Endocannabinoids in Gastric Vagal Afferents Doctor of Philosophy Doctorate Full Time Mr Stewart Christie
    2017 Co-Supervisor Impact of Time-Restricted Feeding on Glucose Metab and Health in Type 11 Diabetes Doctor of Philosophy Doctorate Full Time Mr Prashant Regmi
    2017 Co-Supervisor Association between Nutrition and Depression Doctor of Philosophy Doctorate Full Time Mr Prem Raj Shakya
    2017 Principal Supervisor Altered Dietary Intake in Mice and the Prolonged Effects on Glucose Tolerance Doctor of Philosophy Doctorate Full Time Miss Rebecca Jane O'Rielly
    2017 Co-Supervisor Impact of prolonged fasting and shiftwork in Autophagy and Telomere and risk of Type 2 Diabetes Doctor of Philosophy Doctorate Full Time Mr Rajesh Chaudhary
    2017 Co-Supervisor Novel Immunomodulatory Treatments for Patients with Autonomic Dysfuntion Doctor of Philosophy Doctorate Full Time Ms Rachel Mary Wells
    2017 Co-Supervisor Investigating The Metabolic Health Benefits of Low Glycemic Index Grains Doctor of Philosophy Doctorate Full Time Mr See Meng Lim
    2016 Principal Supervisor Effect of Nutrients on Gastric Secretion of Leptin and Ghrelin in Health and Obesity Doctor of Philosophy Doctorate Full Time Miss Maria Nunez
  • Past Higher Degree by Research Supervision (University of Adelaide)

    Date Role Research Topic Program Degree Type Student Load Student Name
    2014 - 2018 Co-Supervisor Dietary Intervention and Tissue Remodelling Doctor of Philosophy Doctorate Full Time Dr Bo Liu
    2010 - 2011 Principal Supervisor Modulation of Mechanosensitive Gastro-Oesophageal Vagal Afferents by Novel Targets Doctor of Philosophy Doctorate Full Time Mr James Slattery
    2010 - 2013 Principal Supervisor Obesity Induced Dysfunction of Gastric Vagal Afferent Signalling Doctor of Philosophy Doctorate Full Time Mr Stephen James Kentish
    2009 - 2014 Principal Supervisor Modulation of neuropeptide W on gastric vagal afferents Doctor of Philosophy Doctorate Full Time Dr Hui Li
    2004 - 2008 Co-Supervisor Localisation and Function of Mechanosensory Ion Channels in Colonic Sensory Neurons Doctor of Philosophy Doctorate Full Time Mr Patrick Hughes
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  • Committee Memberships

    Date Role Committee Institution Country
    2016 - ongoing Member Faculty of Health and Medical Science Research Committee
    2016 - ongoing Member SAHMRI Research Executive SAHMRI
    2016 - ongoing Member SAHMRI Appointment Committee
    2016 - ongoing Member School of Medicine Executive Team
    2016 - ongoing Chair Adelaide Medical School Research Committee University of Adelaide
    2015 - ongoing Member SAHMRI Nutrition and Metabolism Executive Committee
    2014 - ongoing Member SAHMRI Bioscience Pillar Committee SAHMRI
    2013 - ongoing Member SAHMRI Bioscience Pillar Committee
  • Position: Senior Research Fellow
  • Phone: 81284840
  • Email: amanda.page@adelaide.edu.au
  • Campus: North Terrace West
  • Building: SAHMRI, floor 7
  • Org Unit: Medical Specialties

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