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Welcome

Welcome to the website for the Diabetes Research Centre (DRC): a collaboration between The Walter and Eliza Hall Institute of Medical Research (WEHI) and The Royal Melbourne Hospital (RMH). Researchers at the DRC aim to develop a prevention or cure for diabetes through the research studies and clinical trials that you can read about within this website. 

Please click on the tabs above to read about diabetes, our current or completed trials, published findings, and who to contact for more information on any of these topics. See below for an update on the recent happenings within the Diabetes Research Centre. 

Latest News

September 2010

  • INIT II has reached another milestone - 50 participants have now been randomised to treatment.

August 2010

  • INIT II has a page on facebook. Click the like button below to support and promote the trial.
  • Prof Len Harrison and Dr John Wentworth's discovery that links type 2 diabetes to inflammation in fat tissues has made headlines. Watch the 7 news story by clicking the link below.

July 2010

  • The INIT II Trial was on 7 news recently. If you missed the segment, watch it here:
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    Video courtesy of Channel 7


  • July 11-17 was National Diabetes Week. Research Nurse, Candice, attended a number of Diabetes Week Events. Here she is in the foyer of Royal Melbourne Hospital.

  • Photo courtesy of Czesia Markiewic, WEHI

  • Research from the DRC has been published in the latest issue of Diabetes. To view the article abstract, click here.

June 2010

  • Research from the DRC has been published in the latest issue of Diabetes Care. To view the article abstract, click here.

May 2010

  • There are now 45 participants in the Type 1 Diabetes Prevention Trial (INIT II) leaving 57 to be recruited. Visit Stop Diabetes today to register or find out more.
  • INIT II is going to Germany!

April 2010

  • We have a new website!! Use the tabs at the top to navigate your way around the site and let us know what you think.

March 2010

  • The Type 1 Diabetes Prevention Trial (INIT II) is now on Facebook. Click here to join our group.
  • We have a new webmaster, Rhiannon Jones, who has taken on the position of Administrative Officer for the Autoimmunity and Transplantation Division at WEHI.

What Is Diabetes?

Overview

Diabetes, a life-long condition that can affect both children and adults, occurs when the hormone, insulin, is not present, or is unable to function as normal. Without insulin, glucose is unable to enter the cells to provide fuel for cellular function and this causes the 'high blood sugar' that we use to diagnose diabetes. Over time, high blood sugar can lead to complications such as heart disease and blindness. 

There are a number of types of diabetes, which differ in how they are diagnosed and treated. The DRC is primarily focused on the prevention of type 1 diabetes, commonly known as 'juvenile' or 'insulin dependent' diabetes. However, our interests are expanding as we are continue to learn how the different types of diabetes are related.

Visit the Clinical Trials and Publications links above to find out more about what we are doing or click on one of the headings below to learn more about the different types of diabetes.

Type 1 Diabetes

In consultation with Professor Len Harrison, biomedical animators, Etsuko Uno and Drew Berry, have put together a short film showing regular insulin production and how it's destroyed in type 1 diabetes. Click on the picture to see the animation or read below to find out more.

animation

What is type 1 diabetes?

Type 1 diabetes is one of the most common chronic diseases beginning in childhood and is becoming more common, with 100,000 Australians now depending on insulin injections every day to stay alive.

Type 1 diabetes occurs when the insulin-producing beta cells of the pancreas are damaged or destroyed. Without insulin, the body’s cells are unable to absorb glucose, which is an important fuel for cellular function. Insulin must then be given regularly by injection to control the blood glucose levels, however they are never perfectly normal. This sets the stage for longer- term complications involving blood vessels and nerves, leading to cardiovascular disease, blindness, kidney failure and other problems.   

Due to their high blood-glucose levels, people with undiagnosed diabetes are often constantly thirsty, dehydrated and urinate frequently. Significant weightloss and even coma may occur just prior to diagnosis.

The diagnosis of type 1 diabetes signals a dramatic upheaval in the life of the child and the family.  The child requires insulin injections, sometimes up to four a day, to survive. In addition, skin prick tests, to measure the level of sugar (glucose) in the blood, must be performed several times a day to calculate the volume of insulin to inject.  In young children, the responsibility for keeping the child well can place a terrible on burden on the family, day after day.  

How does type 1 diabetes occur?

In type 1 diabetes, the insulin-producing beta cells are destroyed because the body’s immune system mistakenly attacks them as if they are foreign. Children and young adults who develop type 1 diabetes have a genetic susceptibility, but factors in the environment such as infections are also necessary to trigger the misdirected immune response.  

Until the 1970s, we knew very little about how type 1 diabetes occurred. Most of what we know about this disease has been discovered in just the last three decades.  In the 1970s, researchers in Sydney discovered that women who contracted German measles (rubella) during pregnancy gave birth to children with a high risk of getting type 1 diabetes. Vaccination against rubella has put a stop to this, but there are obviously other important environmental factors, because the incidence of the disease is not decreasing.   

Recently, researchers at the DRC discovered an important link with another virus called rotavirus.  Rotavirus infection, the commonest cause of diarrhoea in infants, was found to be associated with the onset of immune attack against the beta cells.  The same researchers in Melbourne have also: identified genes that predispose to type 1 diabetes; identified chemicals from immune cells that kill the beta cells; developed tests that identify children likely to get type 1 diabetes; and are now conducting trials to prevent type 1 diabetes.  

Can type 1 diabetes be prevented?

By understanding how the immune system kills the beta cells that make insulin, the researchers at the DRC have been able to prevent diabetes in a mouse model of the human disease. This milestone has lead to a vaccine that has already undergone a successful pilot trial in children and adolescents who were at high risk for the disease.

A large trial of this vaccine is currently underway to determine if the vaccine will stop children at risk from becoming diabetic. Those at risk first need to be identified and their chance of getting diabetes within a specified timeframe needs to be estimated.  This is done by a simple blood test. However, for every 100 eligible candidates screened, no more than three are likely to be eligible for the prevention trial. Many thousands of children and adolescents will therefore have to be screened and this massive logistical exercise falls outside the scope of available research funding.  

Melbourne researchers are in a leading position to take up the challenge to prevent type 1 diabetes and if the trial proves successful, the benefits to children and families would be inestimable.

Type 2 Diabetes

Type 2 diabetes is much more common than type 1 diabetes and affects about 10% of Australian adults, but the frequency is increasing dramatically throughout the country. 

Whilst people with type 1 diabetes have insufficient insulin production, those with type 2 diabetes are still able to produce insulin, but their body is unable to use it to help enable glucose to enter cells. This ‘insulin resistance’ develops very slowly, so at the time of diagnosis, individuals with type 2 diabetes may have had the disease for several years and often will not feel unwell. However, over a period of many years, type 2 diabetes can cause significant health problems.  

As in type 1 diabetes, uncontrolled type 2 diabetes can lead to damage of the eyes, kidneys and feet. Individuals with type 2 diabetes also carry a much greater risk of heart disease and stroke.

Physical inactivity and obesity are two major causes of insulin resistance that explain much of the increased incidence of type 2 diabetes in Australia. Accordingly, physical exercise and a change in diet are important treatments for all people with type 2 diabetes. Another effective treatment is ‘lapband’ surgery, which leads to sustained weight loss and dramatically improves type 2 diabetes. 

Other treatments available in Australia include medications that improve insulin action (eg. metformin, pioglitazone, rosiglitazone), increase insulin production (eg. gliclazide, glimeperide, glibenclamide) or decrease glucose absorption from food (acarbose). Although most people with type 2 diabetes do not require insulin injections at the time of diagnosis, after several years, the body may lose the ability to produce insulin thus resulting in the need for insulin injections. 

The prevalence of type 2 diabetes and the high personal and financial costs of treatment and complications make this disease a national health priority. Prevention strategies that increase opportunities for exercise and healthy eating are being implemented in several communities and the causes of insulin resistance are being investigated in the hope this will lead to improved treatments for type 2 diabetes.   

Latent Autoimmune Diabetes of Adulthood (LADA)

Many doctors find it difficult to diagnose type 1 or type 2 diabetes in some individuals, due in part to the fact that both types may occur in the one individual.

In type 1 diabetes, the immune system reacts against the insulin-producing beta cells in the pancreas, which eventually results in a lack of insulin. In type 2 diabetes insulin production is sufficient but the body has developed insulin resistance. Extremes of each case will give rise to either type 1 or type 2 diabetes, however a combination of both processes could also lead to diabetes. This condition is known as latent autoimmune diabetes in adults (LADA).

LADA

It has become evident that there are many people who have both type 1 and 2 diabetes processes. The largest study to show this was the United Kingdom Prospective Diabetes Study published in 1997. They identified that 1 in 10 adults (aged 25 – 65) with presumed type 2 diabetes had glutamic acid decarboxylase antibody (GAD Ab), a highly specific marker of autoimmune destruction of the beta cells, ie. evidence of a type 1 diabetes process. Many other studies have identified a similar number of people, approximately 1 in 10 adults, who have GAD Ab and are presumed to have type 2 diabetes. It is important to diagnose individuals with LADA because adults with insulin resistance and GAD Ab have a high probability of requiring insulin injections within 6 years of diagnosis and have significant insulin deficiency, so may be at risk of future ketoacidosis  

Because our understanding of LADA is relatively recent, there are few, if any, websites devoted to this particular subgroup of diabetes. Sites that may be of use to you include:

Diabetes Australia (Victoria) - this site contains research and clinical news on type 1 and type 2 diabetes with diet and lifestyle tips and is the home of one of the major Australian diabetes support groups.

The International Diabetes Institute - this site contains a wealth of information about type 1 diabetes, including current research, living with diabetes, diet and clinical information.

The American Diabetes Association - this is an overseas website, which focuses on living with diabetes, with information on weight loss and diet, sections for parents, children and doctors, and even recipes.

You could also read a brief article on LADA written by Dr Spiros Fourlanos and Assoc. Prof Peter Colman at the Diabetes Research Centre (article reproduced here with the kind permission of Diabetes Australia and the Diabetes Management Journal) or you could visit the clinical trials tab, above, to learn more about our recently-completed trial of intranasal insulin in LADA.

Gestational Diabetes

Gestational diabetes, as its name suggests, is a form of diabetes that develops during pregnancy.  It usually appears in the last trimester of pregnancy, and disappears shortly after birth, although it frequently recurs in later pregnancies and may indicate an increased risk of type 2 diabetes later in life.  

Like type 2 diabetes, gestational diabetes is characterised by insulin resistance,  where the body is creating enough insulin to remain healthy, but it is unable to be used effectively. During pregnancy, production of the hormones estradiol, cortisol, and human placental lactogen (HPL), is increased. This makes the mother’s cells more resistant to insulin to ensure that the fetus gets enough glucose to continue growing and developing. The mother’s body compensates for this by creating more insulin, and by using stores of fat to create energy for her own consumption.  In about 5% of pregnancies, however, the mother’s body can’t create enough insulin to keep up with the rising hormone levels, and gestational diabetes results.  

Gestational diabetes is usually treated quite aggressively, with diet and exercise plans, but also frequently with insulin injections.  Specialist obstetric endocrinologists, diabetes educators and nutritionists will work with expectant mothers to keep blood sugar as close to normal as possible.  This is because gestational diabetes poses health risks to both mother and baby, which can be greatly reduced with good prenatal care. At present, this Centre is not conducting research into Gestational Diabetes.  

Where can I find out more about Gestational Diabetes?

Australia Diabetes In Pregnancy Society - this is a scientific society dedicated to advancing clinical and scientific knowledge of diabetes in pregnancy. It is also involved in the development of health policy regarding diabetes in pregnancy at the National and State levels. A good starting point for finding out about current research and best practice in your area.

Diabetes Australia (Victoria) - this site will tell you everything you need to know about both Gestational Diabetes, and pre-existing diabetes in pregnancy. It also contains contains clinical and research news and recipes, and is the home of one of the major Australian diabetes support groups.

The American Diabetes Association (ADA) Gestational Diabetes Resource Guide - this page contains a lot of useful information on gestational diabetes, how it is treated and why it needs to be treated carefully. Check out the rest of this site, as it has great information on living with diabetes, with information on diet, and even recipes.

Ongoing Clinical Trials

Type 1 Diabetes Prevention Trial (INIT II)

The aim of the INIT II trial is to determine if exposure of the immune system to intranasal insulin, will stop the immune reaction and further loss of beta cells. This could prevent diabetes and the need for insulin injections. The intranasal insulin acts only on the mucus membranes and is not absorbed into the body and therefore does not affect blood glucose and will not cause hypoglycaemia.  

The INIT II trial is now recruiting in Australia and New Zealand and will soon be making its way to Germany.

Click here to visit the INIT II website to find out more. 

Click here to read more about INIT II.

TrialNet Natural History Study

The aim of the TrialNet Natural History Study is to study the development of type 1 diabetes in individuals, in the hope that better understanding may help to prevent diabetes or develop a cure. 

Click here to read more about the TrialNet Natural History Study.   

TrialNet Oral Insulin Study

The aim of the TrialNet Oral Insulin Study is to determine if capsules of insulin, taken by mouth will help delay or prevent the onset of type 1 diabetes in individuals at risk of developing the disease.

Click here to read more about the TrialNet Oral Insulin Study.

Lap-band surgery versus lifestyle in type 2 diabetes

It has been shown that type 2 diabetes improves dramatically when obese people lose around 20 kg and following the weight loss, most have normal blood sugar levels despite stopping medication. A recent study in people who were obese showed huge improvements for those with diabetes who had lap-band surgery. The aim of this study is to determine if lap-banding is more effective than lifestyle approaches for overweight individuals who are newly diagnosed with type 2 diabetes. 

Click here to read more about the Lap-band study.

Vitamin D and Autoimmune Adult-Onset Diabetes

Vitamin D is a steroid hormone with anti-inflammatory properties. People with lower levels of vitamin D may be more susceptible to inflammatory diseases such as type 1 diabetes. The aim of this study is to determine whether vitamin D repletion will slow the progression of adult-onset autoimmune diabetes, possibly obviating the need for insulin injections.  

*** This study is no longer recruiting ***

Click here to read more about the Vitamin D study.
Type 1 Diabetes Genetics Consortium

The Type 1 Diabetes Genetics Consortium is a group of collaborating diabetes researchers from around the world who are collecting samples and information from families with type 1 diabetes, to determine how differences in the genes that are inherited from parents contribute to the risk of developing type 1 diabetes. Research into these genes, may lead to the prevention of diabetes in the future.  

*** This study is no longer recruiting ***

Click here to read more about the Type 1 Diabetes Genetics Consortium.

Completed Clinical Trials

LADA Trial (INIT III)

INIT III was a clinical trial involving an immune therapy in the form of insulin given as a nasal spray to determine whether it can delay or prevent the need for insulin injections in individuals with latent autoimmune diabetes in adults (LADA).    

TrialNet MMTT-GST Research Study

When clinical research is conducted in people with type 1 diabetes, it is important to know how much insulin is still being produced by the pancreas. Currently, two tests, a Mixed Meal Tolerance Test (MMTT) and a Glucagon Stimulation Test (GST) have been used to measure insulin production. The aim of this study was to compare these two tests to find out which is a better measure of insulin secretion, and which test people tolerate better in order to help develop a standardised method of testing for insulin production in pre-clinical and clinical type 1 diabetes. A test of this kind would be invaluable for planning both intervention and prevention studies in type 1 diabetes and for measuring their outcomes. 

Click here to see the results of this study.

Australian BabyDiab Study

Type 1 diabetes is known to run in families, so if a child's mother, father, brother or sister have insulin dependent diabetes, their risk of developing diabetes is increased. The aim of this study was to identify those at increased risk for type 1 diabetes and observe them over time. It may also aid in the recruitment and assessment of those who might qualify for future diabetes prevention trials.    

INIT I

We had previously shown that regulatory T cells that prevent diabetes can be induced by administering insulin to the naso-respiratory tract of diabetes-prone mice. From this result, we conducted a trial of intranasal insulin in 38 humans (median age 10.8 years) at risk for type 1 diabetes to determine the effect of intranasal insulin on immune and metabolic markers and to ensure that this potentially immunoprotective strategy was safe. The intranasal insulin trial (INIT) was randomized, placebo-controlled and double-masked, with a crossover at six months. A separate cohort of 13 subjects (median age 13.0 years), was followed to symptomatic diabetes over 1.0-7.7 years up to the time the trial commenced.

Publications From The Diabetes Research Centre

2009-2010

Wentworth JM, Naselli G, Brown WA, Doyle L, Phipson B, Smyth GK, Wabitsch M, O'Brien PE, Harrison LC (2010). Pro-inflammatory CD11c+CD206+ adipose tissue macrophages are associated with insulin resistance in human obesity. Diabetes 59:1648-1656

Jenkins AJ, Krishnamurthy B, Best JD, Cameron FJ, Colman PG, Farish S, Hamblin PS, O'Connel MA, Rodda C, Rowley K, Teede H, O'Neal DN (2010). Evaluation of an Algorithm to Guide Patients with Type I Diabetes Treated with Continuous Subcutaneous Insulin Infusion (CSII) on How to Respond to Real-Time Continuous Glucose Levels- A Randomised Control Trial. Diabetes Care 33:1242-1248

Honeyman MC, Stone NL, Falk BA, Nepom G, Harrison LC (2010). Evidence for molecular mimicry between Human T Cell epitopes in rotavirus and pancreatic islet autoantigens. J Immunol 184:2204-2210

View abstracts from 2010

Bergin SM, Brand CA, Colman PG, Campbell DA (2009). An evaluation of community-based resources for management of diabetes-related foot disorders in an Australian population. Aust Health Rev 33:671-678. 

Bergin SM, Brand CA, Colman PG, Campbell DA (2009). A questionnaire for determining prevalence of diabetes related foot disease (Q-DFD): construction and validation. J Foot Ankle Res 2:34.

Chan AC, Serwecinska L, Cochrane A, Harrison LC, Godfrey DI, Berzins SP (2009). Immune characterization of an individual with an exceptionally high natural killer T cell frequency and her immediate family. Clin Exp Immunol 156:238-245.

Couper JJ, Beresford S, Hirte C, Baghurst PA, Pollard A, Tait BD, Harrison LC, Colman PG (2009). Weight gain in early life predicts risk of islet autoimmunity in children with a first-degree relative with type 1 diabetes. Diabetes Care. 32:94-99.

Graco M, Berlowitz DJ, Fourlanos S, Sundram S (2009). Depression is greater in non-English speaking hospital outpatients with type 2 diabetes. Diabetes Res Clin Pract 83:e51-e53.

Honeyman MC, Harrison LC (2009). Congenital rubella, diabetes and HLA. Diabetologia 52:371-372.

Honeyman MC, Harrison LC (2009). Alternative and additional mechanisms to the hygiene hypothesis. In: Progress in Inflammation Research: The Hygiene Hypothesis and Darwinian Medicine (Rook GAW, Ed) Birkhauser, Basel, 279-298.

Mannering SI, Pang SH, Williamson NA, Naselli G, Reynolds EC, O'Brien-Simpson NM, Purcell AW, Harrison LC (2009). The A-chain of insulin is a hot-spot for CD4+ T cell epitopes in human type 1 diabetes. Clin Exp Immunol 156:226-231.

O'Connell MA, Donath S, O'Neal DN, Colman PG, Ambler GR, Jones TW, Davis EA, Cameron FJ (2009). Glycaemic impact of patient-led use of sensor-guided pump therapy in type 1 diabetes: a randomised controlled trial. Diabetologia 52:1250-1257.

Rajamani K, Colman PG, Li LP, Best JD, Voysey M, D'Emden MC, Laakso M, Baker JR, Keech AC; FIELD study investigators (2009). Effect of fenofibrate on amputation events in people with type 2 diabetes mellitus (FIELD study): a prespecified analysis of a randomised controlled trial. Lancet. 373:1780-1788.

Wentworth JM, Fourlanos S, Harrison L (2009). Reappraising the stereotypes of diabetes in the modern diabetogenic environment. Nat Rev Endocrinol. 5:483-489.

View Abstracts from 2009

2007-2008

Fourlanos S, Harrison LC, Colman PG (2008). The accelerator hypothesis and increasing incidence of type 1 diabetes. Curr Opin Endocrinol Diabetes Obes. 15:321-325.

Fourlanos S, Varney MD, Tait BD, Morahan G, Honeyman MC, Colman PG, Harrison LC (2008). The rising incidence of type 1 diabetes is accounted for by cases with lower-risk human leukocyte antigen genotypes. Diabetes Care. 31:1546-1549.

Harrison LC, Honeyman MC, Morahan G, Wentworth JM, Elkassaby S, Colman PG, Fourlanos S (2008). Type 1 diabetes: lessons for other autoimmune diseases? J Autoimmun. 31:306-310.

Harrison LC (2008). Vaccination against self to prevent autoimmune disease: the type 1 diabetes model. Immunol Cell Biol. 86:139-145.

Wentworth JM, Gao N, Sumithran KP, Maartens NF, Kaye AH, Colman PG, Ebeling PR (2008). Prospective evaluation of a protocol for reduced glucocorticoid replacement in transsphenoidal pituitary adenomectomy: prophylactic glucocorticoid replacement is seldom necessary. Clin Endocrinol (Oxf) 68:29-35.

View abstracts from 2008

Barker JM, McFann K, Harrison LC, Fourlanos S, Krischer J, Cuthbertson D, Chase HP, Eisenbarth GS; DPT-1 Study Group (2007). Pre-type 1 diabetes dysmetabolism: maximal sensitivity achieved with both oral and intravenous glucose tolerance testing. J Pediatr. 150:31-36.

Goodall I, Colman PG, Schneider HG, McLean M, Barker G (2007). Desirable performance standards for HbA(1c) analysis - precision, accuracy and standardisation: consensus statement of the Australasian Association of Clinical Biochemists (AACB), the Australian Diabetes Society (ADS), the Royal College of Pathologists of Australasia (RCPA), Endocrine Society of Australia (ESA), and the Australian Diabetes Educators Association (ADEA). Clin Chem Lab Med 45:1083-1097.

Honeyman MC, Elkassaby S, Harrison LC (2007). Seasonal changes in preprandial glucose, A1C, and blood pressure in diabetic patients: response to Liang. Diabetes Care 30:e118.

Keech AC, Mitchell P, Summanen PA, O'Day J, Davis TM, Moffitt MS, Taskinen MR, Simes RJ, Tse D, Williamson E, Merrifield A, Laatikainen LT, d'Emden MC, Crimet DC, O'Connell RL, Colman PG; FIELD study investigators (2007). Effect of fenofibrate on the need for laser treatment for diabetic retinopathy (FIELD study): a randomised controlled trial. Lancet 370:1687-1697.

Schneider HG, Goodall I, Colman PG, McLean M, Barker G; Australian Working Party for HbA1c standardization (2007). New haemoglobin A1c: the way it is reported is about to change... Intern Med J 37:213-215.

Wentworth JM, Harrison LC (2007). Does insulin resistance need resistin? J Clin Endocrinol Metab 92:2036-2037.

View abstracts from 2007

2005-2006

Fourlanos S, Perry C, Stein MS, Stankovich J, Harrison LC, Colman PG (2006). A clinical screening tool identifies autoimmune diabetes in adults. Diabetes Care. 29:970-975.

Locke NR, Stankovic S, Funda DP, Harrison LC (2006). TCR gamma delta intraepithelial lymphocytes are required for self-tolerance. J Immunol 176:6553-6559.

Narendran P, Neale AM, Lee BH, Ngui K, Steptoe RJ, Morahan G, Madsen O, Dromey JA, Jensen KP, Harrison LC (2006). Proinsulin is encoded by an RNA splice variant in human blood myeloid cells. Proc Natl Acad Sci USA 103:16430-16435.

Wraight PR, Lawrence SM, Campbell DA, Colman PG (2006). Retrospective data for diabetic foot complications: only the tip of the iceberg? Intern Med J 36:197-199.

View abstracts from 2006

Fourlanos S, Harrison LC (2005). Insulin resistance in children and adolescents with type 1 diabetes mellitus: relation to obesity. Pediatr Diabetes 6:3-4.

Fourlanos S, Dotta F, Greenbaum CJ, Palmer JP, Rolandsson O, Colman PG, Harrison LC (2005). Latent autoimmune diabetes in adults (LADA) should be less latent. Diabetologia 48:2206-2212.

Harrison LC (2005). The prospect of vaccination to prevent type 1 diabetes. Hum Vaccin 1:143-50.

Lee P, Nicoll AJ, McDonough M, Colman PG (2005). Substance abuse in young patients with type 1 diabetes: easily neglected in complex medical management. Intern Med J 35:359-361.

Mannering SI, Harrison LC, Williamson NA, Morris JS, Thearle DJ, Jensen KP, Kay TW, Rossjohn J, Falk BA, Nepom GT, Purcell AW (2005). The insulin A-chain epitope recognized by human T cells is posttranslationally modified.  J Exp Med 202:1191-1197.

Narendran P, Estella E, Fourlanos S (2005). Immunology of type 1 diabetes. QJM 98:547-556.

Wraight PR, Lawrence SM, Campbell DA, Colman PG (2005). Creation of a multidisciplinary, evidence based, clinical guideline for the assessment, investigation and management of acute diabetes related foot complications. Diabet Med. 22:127-136.

View abstracts from 2005

2000-2004

Fourlanos S, Narendran P, Byrnes GB Colman PG Harrison LC (2004). Insulin resistance is a risk factor for progression to type 1 diabetes. Diabetologia 47:1661-1667.

Harrison LC, Honeyman MC, Steele C, Stone NL, Sarugeri E, Bonifacio E, Couper JJ, Colman PG (2004). Pancreatic beta-cell function and immune responses to insulin following administration of intranasal insulin to humans at-risk for type 1 diabetes. Diabetes Care 27:2348-2355.

Harrison LC, Fourlanos S, Every A, Honeyman MC, Steptoe RJ, Martinez NR, Jensen KP, Funda DP, Mannering SI, Colman PG, Narendran P (2004). Prevention of type 1 diabetes. In: International Textbook of Diabetes Mellitus (Ferranini E, Zimmet P, De fronzo R and Keen H, Eds). John Wiley & Sons, Chichester, UK. 3rd Ed, 115, pp1879-1898.

Hussein Z, Wentworth JM, Nankervis AJ, Proietto J, Colman PG (2004). Effectiveness and side effects of thiazolidinediones for type 2 diabetes: real-life experience from a tertiary hospital. Med J Aust 181:536-539.

Lawrence SM, Wraight PR, Campbell DA, Colman PG (2004). Assessment and management of inpatients with acute diabetes-related foot complications: room for improvement. Intern Med J 34:229-233.

Mannering SI, Morris JS, Stone NL, Jensen KP, VAN Endert PM, Harrison LC (2004). CD4+ T cell proliferation in response to GAD and proinsulin in healthy, pre-diabetic, and diabetic donors. Ann N Y Acad Sci 1037:16-21.

View abstracts from 2004

Fourlanos S Colman PG, Harrison LC (2003). Late-onset autoimmune diabetes in relatives of people with type 1 diabetes. Ann NY Acad Sci 1005:370-373.

Greenbaum CJ, Harrison LC (2003). Guidelines for intervention trials in subjects with newly-diagnosed type 1 diabetes. Diabetes 52:1059-1065.

von Herrath MG, Harrison LC (2003) Antigen-induced regulatory T cells in autoimmunity. Nature Reviews Immunology 3:223-232.

View abstracts from 2003

Colman PG, McNair PD, Gellert S, Kewming K, Schmidli RS, Steele CE, Harrison LC (2002). Development of autoantibodies to islet antigens is not restricted to early childhood: implications for pre-clinical type 1 diabetes screening. Pediatric Diabetes 3:144-148.

Petrovsky N, Kyvik KO, Bonnevie-Nielsen V, Beck-Nielsen H, Green A, Harrison LC (2002). Evidence from twin studies for acquired cellular immune hyperreactivity in type 1 diabetes. Immunology 106:584-589.

View abstracts from 2002

Hänninen A, Braakhuis A, Heath WR, Harrison LC (2001). Mucosal antigen primes diabetogenic cytotoxic T lymphocytes regardless of dose or delivery route. Diabetes 50:771-775.

Harrison LC (2001) Risk assessment, prediction and prevention of type 1 diabetes. Pediatric Diabetes 2: 71-82.

Solly NR, Honeyman MC, Harrison LC (2001) The mucosal interface between 'self' and 'non-self' determines the impact of environment on autoimmune diabetes. Curr Dir Autoimmun 4:68-90.

View abstracts from 2001

Colman PG, Steele C, Couper JJ, Beresford SJ, Powell T, Kewming K, Pollard A, Gellert S, Tait B, Honeyman M, Harrison LC (2000) Islet autoimmunity in infants with a type 1 diabetes relative is common but usually restricted to one autoantibody. Diabetologia 43:203-209.

Colman PG, McNair P, King J, Caudwell J, Jankulovski C, PG, Tait BD, Honeyman MC, Harrison LC (2000) Screening for preclinical type 1 diabetes in a discrete population with an apparent increased disease incidence. Pediatric Diabetes 1:193-198.

Couper J, Pollard A, Kallincos N, Colman PG, Honeyman MC, Harrison LC, Rischmueller M (2000) Toxic shock syndrome associated with newly-diagnosed type 1 diabetes. J Pediatr Child Health 36:279-282.

Hänninen A, Harrison LC (2000) Gamma delta T cells as mediators of mucosal tolerance: the autoimmune diabetes model. Immunological Rev 173:109-119.

Harrison LC, Hafler D. Novel therapeutic strategies in autoimmune diseases: antigen-specific (2000) Curr Opin Immunol 12:704-711.

Honeyman MC, Coulson BS, Stone NL, Gellert SA, Goldwater PN, Steele CE, Couper JJ, Tait BD, Colman PG, Harrison LC (2000) Association between rotavirus infection and pancreatic islet autoimmunity in children at-risk for type 1 diabetes. Diabetes 49:1319-1324.

Honeyman MC, Coulson BS, Harrison LC (2000) Rotavirus is a candidate cause of pancreatitis leading to type 1 diabetes. N Engl J Med 342:1835-1837.

View abstracts from 2000

1995-1999

Couper JJ, Steele C, Beresford S, Powell T, McCaul K, Pollard A, Gellert S, Jankulovski C, Harrison LC, Colman PG (1999) Lack of association between duration of breast feeding and introduction of cows' milk and development of islet autoimmunity. Diabetes 48:2145-2149.

Harrison LC, Honeyman MC (1999) Cows' milk and type 1 diabetes. The real issue is mucosal immune function. Diabetes 48:1501-1507.

View abstracts from 1999

Couper JJ, Harrison LC, Aldis JE, Colman PG, Honeyman MC, Ferrante A (1998) IgG subclass antibodies to glutamic acid decarboxylase and risk for progression to clinical insulin-dependent diabetes. Human Immunol 59:493-499.

View abstract from 1998

Honeyman MC, Brusic V, Harrison LC (1997) Strategies for identifying and predicting islet autoantigen T-cell epitopes in insulin-dependent diabetes. Ann Med 29:402-404.

Honeyman MC, Stone N, DeAizpurua HJ, Rowley MJ, Harrison LC (1997) High T-cell responses to the glutamic acid decarboxylase (GAD) isoform 67 reflect a hyperimmune state that precedes the onset of insulin-dependent diabetes. J Autoimmunity 10:165-173.

Noorchashm H, Kwok W, Rabinovitch A, Harrison LC (1997) Immunology of type 1 diabetes. Diabetologia 40:B50-B57.

View abstracts from 1997

Harrison LC, Dempsey-Collier M, Kramer DR, Takahashi K (1996) Aerosol insulin induces CD8 gamma-delta T cells that suppress murine insulin-dependent diabetes. J Exp Med 184:2167-2174.

View abstract from 1996

Tait BD, Harrison LC, Drummond B, Stewart V, Varney M, Honeyman MC (1995) HLA antigens and age at onset of insulin-dependent diabetes. Human Immunol 42:116-122.

View abstract from 1995

Useful Contacts

Where are we?

The Diabetes Research Centre (Melbourne, Australia) is located at the Walter & Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria, and at the neighbouring Burnet Clinical Research Unit on the Royal Melbourne Hospital campus. Mail can be directed care of:

Candice Breen
Burnet Clinical Research Unit
The Royal Melbourne Hospital
Parkville, 3050, VIC
Australia

Tel: 03 9342 7672
Fax: 03 9349 3199
Candice.Breen@mh.org.au
Current Clinical Trials

INIT II

Visit our website to register, or call our Call Centre on 1300 138 712 (it's a local call throughout Australia).

Candice Breen
Research Nurse and INIT II Site Co-Ordinator
Burnet Clinical Research Unit
The Royal Melbourne Hospital
Parkville, 3050, VIC
Australia

Tel: 03 9342 7672
Mob: 0402 593 041
Fax: 03 9349 3199
candice.breen@mh.org.au

Prof. Peter Colman
Professor/Head
Department of Diabetes & Endocrinology
The Royal Melbourne Hospital
Parkville, 3050, VIC
Australia

Tel: 03 9342 7428
Fax: 03 9342 7898
Peter.Colman@mh.org.au

Prof. Len Harrison
Professor/Head, Burnet Clinical Research Unit
Head, Autoimmunity & Transplantation Division
The Walter and Eliza Hall Institute of Medical Research
1G Royal Parade
Parkville, 3050, VIC
Australia

Tel: 03 9345 2460
Fax: 03 9347 0852 (att: Len Harrison)
harrison@wehi.edu.au

 

The TrialNet Natural History Study

Maree Farley
Research Nurse
Burnet Clinical Research Unit
The Royal Melbourne Hospital
Parkville, 3050, VIC
Australia

Tel: 03 9345 7063
Fax: 03 9349 3199
Maree.Farley@mh.org.au

 

The Lap-band versus Lifestyle Study

Julie Playfair
Trial Co-ordinator
Centre for Obesity Research and Education
Monash Medical School Building
The Alfred Hospital
Commercial Road
Melbourne Victoria 3181 Australia

Mob: 0418 390 963
julie.playfair@med.monash.edu.au

 

Prof. Paul O'Brien
Centre for Obesity Research and Education
Monash Medical School Building
The Alfred Hospital
Commercial Road
Melbourne Victoria 3181 Australia
paul.obrien@med.monash.edu.au

 

John Wentworth
Clinical Researcher
The Walter and Eliza Hall Institute of Medical Research
1G Royal Parade
Parkville, 3050, VIC
Australia

Tel: 03 9345 2462
Fax: 03 9347 0852
wentworth@wehi.edu.au

 

The Vitamin D and Autoimmune Diabetes Study

Dr Shirley Elkassaby
Clinical Researcher
The Walter and Eliza Hall Institute of Medical Research
1G Royal Parade
Parkville, 3050, VIC
Australia

Tel: 03 9345 2422
Fax: 03 9347 0852 (att: Shirley Elkassaby)
elkassaby@wehi.edu.au

 

The Type 1 Diabetes Genetics Consortium

Amanda Loth
Research Nurse
Burnet Clinical Research Unit
The Royal Melbourne Hospital
Parkville, 3050, VIC
Australia

Tel: 03 9345 2601
Fax: 03 9345 2318
Amanda.Loth@mh.org.au
Completed Clinical Trials

The INIT III (LADA) Trial

Dr Spiros Fourlanos
Clinical Researcher
Burnet Clinical Research Unit
The Royal Melbourne Hospital
Parkville, 3050, VIC
Australia

Tel: 03 9349 3599
Fax: 03 9349 3199 (att: Spiros Fourlanos)
spiros.fourlanos@mh.org.au

 

The BabyDiab Study

Prof. Peter Colman
Professor/Head
Department of Diabetes & Endocrinology
The Royal Melbourne Hospital
Parkville, 3050, VIC
Australia

Tel: 03 9342 7428
Fax: 03 9342 7898
Peter.Colman@mh.org.au
This website

Rhiannon Jones
Website Manager, Diabetes Research Centre
The Walter and Eliza Hall Institute of Medical Research
1G Royal Parade
Parkville, 3050, VIC
Australia

Tel: 03 9345 2460
Fax: 03 9345 2911
rjones@wehi.edu.au