Community Research and Development Information Service - CORDIS

The role of DPP4 in diet-induced obesity

In the search for the mechanisms behind metabolic diseases such as obesity and type 2 diabetes, attention has turned to the role of DPP4 in body fat.
The role of DPP4 in diet-induced obesity
Fat, or adipose tissue (AT), releases very potent and diverse bioactive factors known as adipokines. The EU-funded ADDIO (Role of adipose DPP4 deletion in diet-induced obesity) project has performed an in-depth characterisation of the factors released from adipocytes.

Interestingly, the researchers have identified one of these factors – dipeptidyl peptidase 4 (DPP4) – as a potential link between obesity and metabolic syndrome. An enzyme that cuts certain hormones resulting in an increase in insulin, DPP4 is also a target compound in therapies against diabetes.

Looking at specially bred AT-specific DPP4 knockout (KO) mice, ADDIO researchers explored the factor's impact in diet-induced obesity. Comparing a normal with a high-fat diet (HFD), they measured and analysed body composition, glucose and insulin tolerance, AT inflammation and hepatic trygliceride content after a period of 24 weeks.

The results showed that AT is an important source of DPP4 in mice. The KO animals showed an increase in body weight and body fat under a HFD but this was not accompanied by increased glucose intolerance.

As the KO mice have smaller adipocytes in line with a positive correlation with amount of DPP4 produced, DPP4 deletion under a HFD regime would be beneficial. This would be the case where an HFD results in adipose tissue remodelling, especially in visceral fat.

Further research is needed to show how exactly DPP4 deletion can be translated into protection against metabolic diseases. This would be of particular relevance in overweight type 2 diabetes patients who are treated with DPP4 inhibitors.

Related information


Diet-induced obesity, metabolic diseases, type 2 diabetes, adipose, ADDIO, DPP4, high-fat diet
Follow us on: RSS Facebook Twitter YouTube Managed by the EU Publications Office Top