Can we have our cake and eat it?

As a population we are getting fatter. With our extra portion of cake -and there are daily offerings in the Avacta Life Sciences office!- we can then expect to suffer a panoply of health conditions from heart disease and cancer to type 2 diabetes.

Type 2 diabetes is a condition in which the insulin secreting cells of the pancreas, the ?-cells, do not produce enough insulin to function properly, or the body doesn’t react properly to the insulin produced leading to high blood sugar levels. This in turn can cause nerve damage, retinopathies and kidney disease. It is the most common type of diabetes in the Western world and closely linked to the rise in obesity, an increase in unhealthy diets and a lack of exercise. Unfortunately due to our poor lifestyle and an aging population the prevalence of type 2 diabetes is on the rise.
Although the exact mechanism behind the failure of ?-cells in type 2 diabetes remains a matter of debate, inflammatory pathways have been implicated and IL-1? has been shown to play a role in this. In recent years IL-1? has emerged as a master cytokine regulating pancreatic islet chemokine production and causing impaired insulin production and ?-cell death. Despite the generally disappointing results seen in trials of IL-1 therapy for type 1 diabetes, a number of IL-1 antagonist based therapies are now reaching phase III clinical trials for diabetes and the associated cardiovascular complications. However, such monoclonal antibody based therapies are expensive to produce. A vaccine would ultimately prove more cost-effective and convenient for the patient.
A recent study (link is external) offers new hope for a vaccine against type 2 diabetes. Based on the injection of a mutant form of IL-1? chemically cross-linked to virus-like particles of the bacteriophage Q?, the preclinical characterisation of this vaccine showed good tolerability and induced long-lasting but reversible IL-1?-neutralising antibody titres. This resulted in improved glucose tolerance and enhanced insulin secretion in the diabetic mouse model under study, suggesting that this may prove an additional safe and effective treatment for type 2 diabetes.
The authors also note that targeting other inflammation markers in this manner to induce neutralising antibodies to additional cytokines, such as TNF-?, may increase the response and improve the therapeutic effect for diabetic patients. However, this must be offset against the increased risk of infection in the patient, demonstrating the delicate dance we must always perform in translating our understanding of biological systems into new therapies.
Whilst these results look promising, they do only reflect pre-clinical trials and further studies are essential to understand the function and toxicity of such therapies in higher mammals and man. Nonetheless it may soon be possible to have our cake and eat it, guilt-free.