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Publications of the Week

Beta-Cell Specific Insr Deletion Promotes Insulin Hypersecretion and Improves Glucose Tolerance Prior to Global Insulin Resistance

By February 28, 2022No Comments

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This week we profile a recent publication in Nature Communications from the lab of Dr. James Johnson (pictured)
at the Diabetes Research Group, Life Sciences Institute, and Department of Cellular and Physiological Sciences.

Can you provide a brief overview of your lab’s current research focus?

Our lab doesn’t really have a ‘focus’. Instead there is a plethora of projects on a variety of topics related to insulin, metabolism, diabetes, obesity, and cancer, to name just a few, each driven by one of the outstanding students, fellows or staff in the group.

What is the significance of the findings in this publication?

We are excited about this publication for a few reasons. First, it helps explain the causal connection between insulin resistance and insulin hyper-secretion, two critical features of obesity and early type 2 diabetes. A team led by a former fellow, Dr. Søs Skovsø, determined that the loss of insulin signalling through the insulin receptor (i.e. insulin resistance) specifically in the insulin-secreting pancreatic beta-cells resulted in insulin hyper-secretion when stimulated by glucose. This means that insulin normally has a negative feedback effect on the beta-cells that release it in response to sugar. Secondly, Søs organized an extremely rigorous study that I believe is a benchmark for how to do physiological research in an era where people are concerned about reproducibility. We examined the effects of beta-cell specific insulin receptor detection in both female and male mice (with differing results), in the context of 3 difference diets, and at multiple ages – resulting in comprehensive picture of this important area of biology.

What are the next steps for this research?

In the big picture, this research helps us understand the earliest stages of type 2 diabetes, which will hopefully give us insight into the design of better prevention and treatment approaches. Here, we think that nutrition may hold the key and we are working with the Institute of Personalized Therapeutic Nutrition to design future trials in this area.

We also hope that other research groups are inspired by our results and conduct follow-up studies to answer some of the questions that are remaining from our work.

If you’d like to mention your funding sources, please list them.

This work was supported by CIHR and Diabetes Canada.


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