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The model includes metabolic overload (mitochondria), endoplasmic reticulum (ER) stress and deposition of harmful amyloid fibrils.
Our team investigate the molecular mechanisms by which glucolipotoxicity, and the subsequent metabolic stress, alters the function of both skeletal muscle and beta cells of pancreas in type 2 diabetes.
Topic 3 : Strategies to restore homeostasis of mitochondria and ER Our goal is to identify new targets for improving the functioning of both mitochondria and ER, as well as their interactions, in order to imcrease muscle insulin sensitivity and insulin secretion by pancreatic beta cells. Nutrition is of utmost importance for individuals with diabetes because it is food that we eat that effects the changes in insulin that the pancreas may or may not produce in response.
In type II diabetes the goal is usually weight loss and weight management because of the insulin resistance (how the body can use the insulin effectively) and that requires a balanced nutrition plan to make sure not only the foods the person is eating is appropriate for their blood sugar, but also reducing the amount of fat and overall calorie intake because of the reduced load the body will then have to deal with. Using the Canada’s Food Guide is the first step because most individuals over consume and consume foods inefficiently, the Canada’s Food Guide has portion sizes, food ideas that one may have no considered before, and the amount from each food  group one should get. Additionally, if you know you have type II diabetes, it’s really important to contact a dietitian, specifically one that specializes in diabetes care. Nutrition at this stage is probably the most important aspect of intervention because these individuals will have to take insulin for the rest of their lives and will require knowledge about how their blood sugars are affected by the foods they eat and how to prevent complications associated with extremely high or low blood sugars. Overnutrition and increased lipid supply induce enzymes of -oxidation, such as carnitine palmitoyltransferase-1 (CPT1), resulting in increased acetyl CoA levels, allosteric activation of pyruvate carboxylase (PC) and constitutive upregulation of pyruvate cycling.


We are working on pharmaceutical approach to restore these alterations by improving the two organelles. We study the involvement of an altered interaction between the two organelles in the development of muscle insulin resistance and in alterations of insulin secretion by pancreatic beta cells.
Iorn oxide nanoparticules labelling enables later in vitro cell isolation for metabolic stress assessment at the sub-cellular level. Research has shown that a small decrease in body weight can have large improvements in body blood sugar regulation which is why treating diabetes type II with weight loss and addressing it fast are important for later complications. This is due to pancreas cells being genetically defective or, as it is becoming more pronounced later in life, can be attributed to insulin resistance that is emphasized by unhealthy lifestyle options as well environmental agents. This leads to basal insulin hypersecretion and loss of the glucose-stimulated increment in pyruvate cycling flux, thereby blunting glucose-stimulated insulin secretion. We carry both gene-candidate approaches (eg overexpression and invalidation of specific protein of MAM) and large-scale approaches (differential analysis of MAM proteins by proteomic approaches) in both rodent models of type 2 diabetes and cellular models exposed to glucolipotoxicity.
In mice, we have shown in-vivo by MRI the modulation of inflammation under treatment with the renin-angiotensin inhibitor Irbesartan. If you cannot go to a dietitian or specialist for any reason, below are two sites you can visit by clicking on them.


The increased demand for insulin biosynthesis increases demand (workload) in the ER, gradually leading to ER stress and increased protein misfolding.
In the same animal model, we also evaluate the modulation by physical activity of oxydative stress and inflammation. They have resources that you could use as well as a way to contact other health care professionals related to diabetes management. ER stress is initially relieved by the unfolded protein response (UPR), mediated by the transcription factor XBP1, but over time, the UPR becomes less effective and the deleterious effects of ER stress lead to cell death, mediated by IRE1. Finally, insulin hypersecretion is accompanied by amylin secretion, which in humans can form amyloid fibrils that accumulate at the surface of -cells to induce dysfunction and apoptotic death.




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