The Evaluation of Two Response Thresholds to Continuous Ketone Monitoring Information Minimising Ketosis in People With Type 1 Diabetes Treated With Dapagliflozin

Sodium glucose cotransporter 2 (SGLT2) inhibitors are a type of medicine that help the kidneys get rid of extra sugar in the blood through urine. In people with type 2 diabetes (T2D), these medications help lower blood sugar levels, help people lose weight and improve heart and kidney health.
SGLT2 inhibitors are mainly used in T2D, however some studies show they might also help people with type 1 diabetes (T1D). The same health benefits observed in people with T2D the investigators anticipate may help those with T1D. Currently, there is a safety concern that people with T1D using these medicines can raise the risk of diabetic ketoacidosis (DKA). DKA occurs when the body doesn't have enough insulin (a hormone made in the pancreas that helps your body use sugar (glucose) for energy), it starts to break down fats as a source of energy. This breakdown of fats produces ketones. Very high levels of ketones in the blood can make the blood acidic (toxic) and lead to DKA. If not treated in time, this can make the person living with T1D very ill and can be life-threatening. Because of this risk, health agencies like the FDA in the U.S., and the TGA in Australia have not approved use of SGLT2 inhibitors for people with T1D.
Still, some experts believe SGLT2 inhibitors may safely be used alongside insulin in T1D if DKA risk is carefully managed. This might be possible with early detection and treatment of rising ketone levels. One approach is using continuous ketone monitors, which track ketone levels in real time and can alert users early. People would also need proper education on what to do if ketone levels start rising.
To date, there's no official agreement on the exact ketone level that should trigger action. Some suggest action when ketone levels reach 1.0 or 1.5 mmol/L. A lower limit like 1.0 mmol/L may be safer, but it could also lead to too many alarms and extra stress, or unnecessary eating to bring ketones down.
Therefore, the aim of this study is to assess if initiating responses to elevated ketone levels at a threshold of 1.0 mmol/L, compared to a threshold of 1.5 mmol/L, will reduce the risk of DKA in people with T1D using Dapagliflozin.
The investigators will recruit 115 adults with T1D and provide Dapagliflozin (SGLT2 inhibitor) and continuous glucose and ketone monitoring (DGK) devices. Participants will be randomly assigned to two groups. Group 1 will wear a DGK with alarms set at ketone level of 1.0 mmol/L and receive education about taking action when ketone levels are ≥1.0 mmol/L. Group 2 will wear a DGK with alarms set at ketone level of 1.5 mmol/L and receive education about taking action when ketone levels are ≥1.5 mmol/L. Participants will be assessed for time spent with critically high ketone levels, incidence of DKA, glucose and person reported outcomes.
Findings from this study will provide real life data and clinical evidence to help guide safe use of SGLT2 inhibitors in people with T1D by informing protocols for monitoring and managing associated DKA risks.

开始日期2026-02-01

申办/合作机构

St. Vincent's Hospital Melbourne Pty Ltd.

[+4]

NCT06925529

/ Not yet recruitingN/AIIT

Protecting Neurovascular Function In lOng-term Breast caNcer Survivors With ExercisE tRaining - The PIONEER Study

Study Rationale:
Breast cancer survivors are more likely to develop cardiovascular disease (CVD) or neurocognitive disease than age-matched counterparts without a history of cancer diagnosis. Some anti-cancer treatments cause damage to the cells of heart and the walls of blood vessels, which may exacerbate neurovascular dysfunction and cancer-related cognitive impairment (symptoms such as 'chemo-brain'), as well as accelerating the onset of neurocognitive disease. Therefore, effective policies and therapeutic strategies are needed to minimize neurovascular dysfunction and neurocognitive disease in at-risk populations like breast cancer survivors.
Regular exercise training is effective in slowing or preventing the development of CVD. Furthermore, higher fitness levels are associated with lower dementia risk in older adults, which may be due to better neurovascular function. However, whether exercise training incorporated into a Cardio-Oncology Rehabilitation and Exercise (CORE) programme can improve neurovascular function in breast cancer survivors is currently unknown. Therefore, the primary aim of this study will be to determine the effect of a CORE programme on neurovascular function in long-term breast cancer survivors.
Study Description:
This study will be a randomised controlled trial to investigate the effect of a CORE programme on neurovascular function in long-term breast cancer survivors.
Participants will complete a series of baseline assessments, including lifestyle questionnaires, a cognitive function assessment, dual-energy x-ray absorptiometry (DXA), a cardiopulmonary exercise test (CPET), ultrasound assessments of arterial stiffness and vascular function, and brain magnetic resonance imaging (MRI). Furthermore, participants will wear a blood pressure monitor at home for 24 hours, and a physical activity monitor for seven days.
Following completion of baseline assessments, participants will be randomised to either the CORE program or a 'usual care' group. The CORE program will include a 6-month exercise training program supervised by an Exercise Physiologist at the Baker Heart and Diabetes Institute. The usual care group will carry on with healthcare from their usual healthcare provider(s) for 6 months.
Participants will then complete two follow-up study visits following completion of the 6-month intervention period, with identical procedures to the baseline study visits.
Study Duration:
This study involves two baseline study visits in month 1, followed by two study visits in month 7. Participants randomised to the CORE program will be asked to attend the Baker Heart and Diabetes Institute on a weekly basis for supervised exercise training sessions. However, the supervised exercise training sessions will be provided by a mix of in-person, video-conferencing and tele-health modes depending on each participants availability and needs.

开始日期2025-11-03

申办/合作机构

Baker Heart & Diabetes Institute

NCT06894875

/ RecruitingN/A

Examining the Safety and Tolerability of Lentil Protein Hydrolysate in Healthy Males and Females Whilst Exploring the Effects of a Dose Range on Blood Pressure Control and Vascular Function and Exercise Performance

Examining the safety and tolerability of Lentil Protein Hydrolysate in healthy males and females whilst exploring the effects of a dose range on blood pressure control and vascular function and exercise performance

开始日期2025-06-24

申办/合作机构

Nuritas Ltd.

[+2]

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项与 Baker Heart & Diabetes Institute 相关的文献（医药）

2026-12-31·Gut Microbes

Gut bacteria presence in the brain is increased after ischemic stroke in mice

Article

作者: Jama, Hamdi A. ; Kemp-Harper, Barbara K. ; Muralitharan, Rikeish R. ; Peh, Alex ; Wong, Connie H.Y. ; Nakai, Michael ; Barker, Charlotte M.O. ; Zheng, Tenghao ; Wilson, Jenny L. ; Rupasinghe, Samoda ; Marques, Francine Z. ; Dinakis, Evany ; Broughton, Brad R.S. ; Modarresi, Mahnaz

Systemic infections are a common cause of complications and death after stroke. These infections can occur due to the breakdown of the gut epithelial barrier and the translocation of bacteria from the gut to peripheral systemic tissues. However, it remains unclear whether gut bacteria also translocate to the brain and contribute to stroke-induced neuronal damage. In this study, we observed a significant number of peptidoglycan- and lipopolysaccharide-positive bacteria in the ischemic hemisphere of mice subjected to either photothrombotic (PT) stroke or middle cerebral artery occlusion (MCAO). In contrast, no bacteria were observed in the ischemic brains of germ-free mice following MCAO. Absolute quantification via PCR also revealed increased bacteria in the ischemic hemisphere and blood of PT mice. Bacterial translocation to the brain is associated with the breakdown of the gut-epithelial and blood-brain barriers. Although inhibition of sympathetic tone reduces gut-epithelial barrier permeability, the bacterial load in the brain and functional deficits poststroke, it does not affect cerebral apoptosis, neuroinflammation or infarct volume. Collectively, these findings indicate that activation of the sympathetic nervous system after stroke promotes the migration of gut-derived bacteria into the ischemic brain, and this process worsens motor function in mice.

2026-12-01·Journal of Sport and Health Science

Influence of diet-induced obesity and voluntary exercise training on cardiac lipids and mitochondrial function in mice

Article

作者: Egan, Casey L ; Ritchie, Rebecca H ; Velagic, Anida ; Meikle, Peter J ; Terry, Lauren V ; Tham, Yow Keat ; Tegegne, Surafel ; De Blasio, Miles J ; Mellett, Natalie A ; Parker, Alex M ; Febbraio, Mark A ; Fuller, Oliver K ; Deo, Minh ; Perera, Nimna

BACKGROUND:

Obesity is a risk factor for developing cardiometabolic disease. Exercise training is pivotal in the treatment of obesity and is associated with reduced cardiovascular mortality. This study examined the effect of high-fat feeding on cardiac morphology and mitochondrial function, alongside the mitigating effects of voluntary exercise training.

METHODS:

Six-week-old male C57Bl/6 J mice commenced a high fat diet (HFD) or chow diet and were randomized to receive locked (sedentary) or unlocked (voluntary exercise training (VET)) running wheels at 10 weeks of age. Mice were monitored until 30 weeks of age and euthanized for collection of tissues. Magnetic resonance imaging was performed to assess body composition, and echocardiography was performed to assess cardiac function.

RESULTS:

Compared with chow-fed animals, the HFD increased body weight and adiposity and decreased cardiolipins (CL) in the heart, which are required for maintaining adequate mitochondrial respiration. Importantly, VET reversed these effects and induced physiological cardiac hypertrophy. Cardiac mitochondrial respiratory chain analysis revealed decreased complexes II and IV activity following high fat feeding, while VET enhanced complex I activity, emphasizing the cardioprotective effect of exercise training in obesity.

CONCLUSION:

This study uncovers mechanisms by which obesity and exercise impact cardiac mitochondrial health and suggests the mitochondria is a therapeutic target in obesity-related cardiovascular diseases.

2026-06-01·JOURNAL OF CRITICAL CARE

Sex differences in venoarterial extracorporeal membrane oxygenation utilisation and clinical outcomes in Australia

Article

作者: Taylor, Andrew J ; Lankaputhra, Malanka ; Kaye, David M ; Burrell, Aidan ; Orosz, Judit ; Stub, Dion ; Pellegrino, Vincent ; Batchelor, Riley J ; Hodgson, Carol L ; Coull, Julia ; Lefkovits, Jeffrey ; Antsey, James

BACKGROUND:

Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is increasingly utilised in critically ill patients with severe cardiac failure and cardiac arrest, yet sex-specific differences in presentation, utilisation, and clinical outcomes are not well understood.

METHODS:

The EXCEL registry is a binational registry capturing data on patients requiring ECMO in Australia and New Zealand. Data were collected on adult patients supported with VA-ECMO in Australia from February 2019 to December 2024. Patients were stratified by sex to assess differences in demographics, clinical characteristics, ECMO indications, complications, and outcomes. Multivariable logistic regression analyses conditional on several baseline covariates assessed associations between sex, in-hospital mortality, and major bleeding.

RESULTS:

Among 1443 patients undergoing VA-ECMO, 32.7% female and 67.3% were male. Females were younger, had lower APACHE IV scores, and more commonly required ECMO for myocarditis, pulmonary embolism, and advanced pulmonary hypertension. Conversely, males predominantly presented with acute myocardial infarction and more frequently had cardiac arrest with a shockable rhythm. Unadjusted in-hospital mortality was comparable between sexes; however, following adjustment, female sex independently predicted higher in-hospital mortality (OR 1.41, 95% CI 1.07-1.87; p = 0.015) and major bleeding (OR 1.40, 95% CI 1.03-1.91; p = 0.033).

CONCLUSION:

Female patients represent one third of the VA-ECMO population and are a distinct cohort to male patients. Despite younger age and fewer traditional risk factors, female sex is associated with increased adjusted risk of in-hospital mortality and bleeding in VA-ECMO patients. These findings should be interpreted as an adjusted association that is contingent on the completeness of covariate adjustment.

项与 Baker Heart & Diabetes Institute 相关的新闻（医药）

2025-10-24

·implicitbioscience.com

MEDIA | Breakthrough data featured in The Australian

Our pioneering work in cardioimmunology has captured national attention, with The Australian today reporting on the publication of our foundational cardiology data in the Journal of the American College of Cardiology (JACC), one of the world’s most influential cardiology journals. The peer-reviewed paper, “CD14 blockade modulates macrophage-mediated immunological injury in a translational model of reperfused ST-elevation myocardial infarction”, co-authored by Dr Daniel Donner of the Baker Heart and Diabetes Institute and an international team of collaborators, represents a significant scientific validation of our strategy to target CD14 in the acute setting of ST-elevation myocardial infarction (STEMI). Click to read the article.

AHA会议

2024-02-20

·NS Medical Devices

Monash University-led consortium gets $33m grant for artificial heart development

Comprising five universities, three clinical partners and an Australian-grown firm, the consortium intends to develop three next-generation implantable cardiac technologies, that are collectively referred as the Total Artificial Heart Australian government awards A$50m grant to develop artificial heart technology. (Credit: Monash University) A transdisciplinary consortium led by Monash University has secured an A$50m ($32.7m) grant from the Australian government to advance its artificial heart technology. The consortium, which is called Artificial Heart Frontiers Program, is based at the Monash Alfred Baker Centre for Cardiovascular Research at the Alfred Hospital in Melbourne. Its goal is to come up with longer-term solutions for every form of debilitating heart failure. The Artificial Heart Frontiers Program comprises five universities, three clinical partners and an Australian-grown firm. The intention of the partners is to develop three next-generation implantable cardiac technologies, that are collectively referred as the Total Artificial Heart. Apart from Monash University, the other universities in the consortium are the University of Sydney, the University of New South Wales, the Griffith University, and the University of Queensland. Clinical partners include the Alfred Hospital, Baker Heart & Diabetes Institute, and St Vincent’s Health Australia while the industrial partner is medical device company BiVACOR. The Medical Research Future Fund (MRFF) grant awarded by the Australian government will help develop and commercialise the three key devices for treating the most prevailing types of heart failure. According to Monash University, the devices include a Mini-Pump which is a wholly new miniature device for patients who have no other options for treating their heart failure symptoms. The second product is a new type of left ventricle assist device (LVAD) that is implanted right beside a natural heart to help it pump. The other device in the suite is BiVACOR’s Total Artificial Heart (TAH). It is intended to fully replace a natural heart. Monash University said that all three devices can respond to the physical needs of the body like a normal heart. These products are said to offer heart failure patients a first-of-its-kind treatment that encourages physical activity. Monash University vice-chancellor and president Sharon Pickering said: “The Artificial Heart Frontiers Program underlines Monash’s commitment to purpose-driven research and innovation to deliver tangible and significant outcomes. “An MRFF grant of this scale recognises the strength of Monash’s world-leading cardiac and engineering research, and our commitment to working with partners in research, industry, government and the community to address global challenges.” The funding will also support clinical trials to start early within the programme. The Total Artificial Heart device is anticipated to hit the market as early as 2025, with the LVAD and Mini-Pump to follow in 2029 and 2031, respectively. The advanced artificial heart project by the year 2036 is anticipated to boost local manufacturing and research while creating over 2,000 jobs. It will also support the Australian healthcare system and grant early access to clinical trials and life-saving technologies for Australians. Australian Minister for Health and Aged Care Mark Butler said: “As well as the obvious health benefits, this is an incredible story of Australian ingenuity and sovereign manufacturing, with collaboration across universities, clinical hospitals and industry to develop the world’s most advanced artificial heart.”

AHA会议

2023-11-24

·implicitbioscience.com

New Precision Nuclear Medicine Tool to be Used with Implicit’s Heart Drug

Summary: New imaging technology allows clinicians to see immune cells that cause many heart diseases. Implicit’s antibody reprograms these immune cells and prevents damage, restoring heart function. This new technology will accelerate development of Implicit’s atibuclimab and pioneer a new era of precision cardiac medicine. The development of new treatments in cardiology has been very difficult because of the heterogeneity of the patient population and the resulting variation in response to treatment. Very recent scientific advances in immunology and precision medicine now allow targeted approaches to identify groups of patients who can be predicted to benefit from a particular treatment based on their specific immune profile, thus increasing the probability of clinical success required for drug approval. New research from the Center for Cardiovascular Research and the Cardiovascular Precision Medicine Research Initiative at Washington University in St Louis positions Implicit Bioscience’s monoclonal antibody atibuclimab (IC14) at the forefront if this transformative field of cardioimmunology. This work builds on initial breakthrough discoveries by our collaborators at the Baker Heart and Diabetes Institute in Melbourne, Australia. This research shows that a particular type of immune cell called a CCR2+ macrophage is causally linked to chronic disease progression following heart attacks. Macrophages lacking the CCR2 receptor are responsible for cardiac tissue repair after injury but are aggressively displaced by invading CCR2+ cells early in the disease. Using nuclear medicine, our collaborators in St Louis have created a tag for the CCR2 receptor that permits them to visualize these cells in patients using a PET/CT scanner. “This new precision medicine tool will allow us to see the cells that cause the disease, select the patients most likely to respond to our drug and track the effect of atibuclimab on those cells in those patients”, said Implicit Bioscience CEO, Garry Redlich. Anti-inflammatory drugs like corticosteroids that suppress the overall immune response cannot discriminate between the “bad” inflammatory immune cells that cause disease and the “good” reparative immune cells, and drugs that target just a single immune pathway are unable to retune the whole immune response. In a new paper currently being prepared for publication, the Implicit Bioscience team shows that blocking atibuclimab’s target in these serious cardiology diseases profoundly and selectively rewires the genome of immune cells that cause these diseases. Everything downstream of these genes is thus deflected away from inflammation, fibrosis, scarring, muscle failure and electrical disturbance and back towards the normal repair and recovery functions that result in a regular heartbeat and efficient pumping of blood. “Having a monoclonal antibody with this extraordinary capability is remarkable enough,” said Mr. Redlich. “But also having access to a technology that will allow our clinicians to both select patients most likely to benefit and to monitor the drug’s effectiveness could lead to a major transformation in how patients with inflammatory heart diseases are treated.” Lavine, K.J. and Liu, Y. Visualizing inflammatory monocytes and macrophages in the human heart. Nature Cardiovascular Research, September 2023. Lavine, K.J., et al. CCR2 imaging in human ST-segment elevation myocardial infarction. Nature Cardiovascular Research, September 2023. – ENDS –

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