Diabetes Research WA is pleased to announce the winner of our 2025 grant as Dr Kimberley Wang from the University of Western Australia. Her project, entitled “Impact of intrauterine growth restriction on skeletal muscle glucose metabolism – link to increase risk of diabetes?” aims to determine the effects of intrauterine growth restriction (IUGR) on fibre type, abundance of myogenesis, glucose and insulin signalling molecules and glycogen storage in the skeletal muscle, and whether it occurs in a sex-dependent manner.
The work could lead to more effective therapies for the prevention and treatment of diabetes and other metabolic diseases.
The Research Team
The project is led by Dr Kimberley Wang from The University of Western Australia and supported by co-investigators Dr Erin Lloyd (The University of Western Australia), Professor Robyn Murphy (La Trobe University).
Developmental origins of metabolic diseases
Epidemiological and experimental studies have demonstrated that IUGR and low birth weight increase the risk for metabolic disease in later life, including insulin resistance and type 2 diabetes. In 2021, 6.6% of babies were classified as low birth weight in Western Australia. A meta-analysis reported that low birth weight individuals experienced a 45% higher risk of type 2 diabetes compared with healthy birth weight individuals, with females having a greater risk than males. The underlying mechanism(s) however remains unknown.
Unique mouse model to investigate the association between IUGR and type 2 diabetes
Dr Wang has established a mid-gestation maternal hypoxia-induced IUGR mouse model whereby the hypoxic exposure for this mouse model was limited to the period of myogenesis, which is the formation of skeletal muscular tissue process. This specific exposure period allows us to assess what will happen to the metabolic health when skeletal muscle development is disrupted.
Our overarching hypothesis is that adaptations that occur within skeletal muscle in response to IUGR include changes to fibre type, protein abundance involved in myogenesis, glucose and insulin metabolism, and glycogen storage in adulthood, and these changes will subsequently increase the risk of metabolic disease. Outcomes will contribute to discovery knowledge by revealing potential mechanistic explanations for the development of metabolic syndrome in IUGR individuals.