PhD Defence Michael Maris | Leuven Diabetes Lab

October 28, 2010

We warmly congratulate Michael Maris on the successful defense of the PhD thesis entitled “Molecular mechanisms of beta cell dysfunction and beta cell death in models of type 2 diabetes.” The work was carried out under the guidance of Chantal Mathieu (promoter), Lut Overbergh (co-promoter), and Miriam Cnop (co-promoter, Campus Hospitalo-Universitaire d'Anderlecht, Brussels, Belgium). The examination committee was chaired by Jan Ceuppens (Experimental Immunology, KU Leuven, Leuven, Belgium), with Myriam Baes (Laboratory of Cell Metabolism, KU Leuven, Leuven, Belgium) serving as secretary, and further included Frank Wuytack (Laboratory of Physiology, KU Leuven, Leuven, Belgium), Geert Carmeliet (Clinical and Experimental Endocrinology, KU Leuven, Leuven, Belgium), Guy Rutter (Imperial College London, London, UK), and Jean-Christophe Jonas (Pôle d'Endocrinologie, Diabète et Nutrition, UCL, Louvain-la-Neuve, Belgium). This research provided important insights into the cellular and molecular processes leading to beta-cell failure in type 2 diabetes, advancing our understanding of disease progression and potential therapeutic targets. We celebrate this achievement and wish Dr. Maris continued success in the next stage of a promising scientific career.‍

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PhD Research Summary - Dr. Maris

Type 2 diabetes develops when pancreatic beta cells fail to produce enough insulin to counteract insulin resistance in muscle, liver, and fat. Glucolipotoxicity, caused by high levels of sugar and fat, damages beta-cell function, in part through endoplasmic reticulum (ER) stress.

In this thesis, proteomic analyses of INS-1E beta cells exposed to glucose and fatty acids identified novel molecular pathways involved in glucolipotoxicity, offering potential new drug targets.

In a second approach, the role of the ER stress–induced protein CHOP was studied. While CHOP deletion did not affect beta-cell death, it caused obesity and liver fat accumulation but protected insulin sensitivity by reducing inflammation in the liver and fat.

These findings highlight ER stress and CHOP as central players in beta-cell dysfunction, inflammation, and insulin resistance, and point to CHOP as a potential therapeutic target in type 2 diabetes.

More information can be found via the link.

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