Fat cells play key role in development of type 2 diabetes

Jul 06, 2010

Cellular changes in fat tissue -- not the immune system -- lead to the "hyperinflammation" characteristic of obesity-related glucose intolerance and type 2 diabetes, according to new research from the University of Cincinnati (UC).

Cancer and cell biology experts say this new discovery about the cellular mechanisms behind may provide a different target for drugs to treat as well as insights into how aggressive cancers form.

The study, led by Jorge Moscat, PhD, is reported in the July 7, 2010, issue of the scientific journal .

For this study, Moscat and his UC collaborator Maria Diaz-Meco, PhD, looked at the role of a specific gene known as protein kinase C (PKC)-zeta, which has been implicated as a key cellular contributor to malignant tumor growth. Using a preclinical animal model, they found that PKC-zeta had a dual role in the molecular signaling that leads to inflammation, switching from acting as a regulator of inflammation to a proinflammation agent in different circumstances.

"This finding is quite novel because current drug development efforts target immune cells (macrophages, T-cells) to eliminate this hyperinflammation. Our research suggests obesity-related glucose intolerance has nothing to do with the immune system. It may be more effective to target adipocytes ()," explains Moscat, principal investigator of the study and chair of UC's cancer and cell biology department.

In normal cells, explains Moscat, PKC-zeta regulates the balance between cellular inflammatory responses to maintain glucose control. During obesity-induced inflammation, however, the function of PKC-zeta changes and the molecule begins to promote inflammation by causing adipocytes to secrete a substance (IL-6) that travels in large quantities to the liver to cause .

"We believe a similar mechanism of action is at play in malignant . Now we are trying to understand how PKC-zeta regulates IL6 to better determine how we can manipulate the protein to help prevent diabetes and cancer," he adds.

Moscat and his team are working with investigators at UC's Drug Discovery Center to screen compounds that will inhibit PKC-zeta to be used in further research.

Explore further: Gamers helping in Ebola research

Provided by University of Cincinnati Academic Health Center

5 /5 (1 vote)
add to favorites email to friend print save as pdf

Related Stories

Enzyme Crucial to Insulin Resistance Found in Brain

Sep 14, 2009

An enzyme known to cause insulin resistance in muscle is also located in the brain and has a similar function there, a research team that includes a University of Cincinnati scientist has found.

Inflammation in body fat is not only pernicious

Mar 25, 2010

It has been a common opinion that inflammation in adipose tissue may cause insulin resistance, and thereby type 2 diabetes. However, recent research from the Swedish medical university Karolinska Institutet, published in ...

Recommended for you

Gamers helping in Ebola research

17 hours ago

Months before the recent Ebola outbreak erupted in Western Africa, killing more than a thousand people, scientists at the University of Washington's Institute for Protein Design were looking for a way to stop the deadly virus.

Carcinogenic role of a protein in liver decoded

19 hours ago

The human protein EGFR controls cell growth. It has mutated in case of many cancer cells or exists in excessive numbers. For this reason it serves as a point of attack for target-oriented therapies. A study ...

A new way to diagnose malaria, using magnetic fields

Aug 31, 2014

Over the past several decades, malaria diagnosis has changed very little. After taking a blood sample from a patient, a technician smears the blood across a glass slide, stains it with a special dye, and ...

User comments : 0