I write about science and postdoc life; mostly diabetes and complaining.
Check out my latest post here. I was interviewed on my work my the communications team here at Manchester, so it’s a bit different from my usual stuff.
Check out my regular pieces on Science Sunday and Postdoc Problems discussing my life in lab and attempts to get a “real job”. I’ve previously blogged my entire PhD thesis writing experience if you fancy some tips, or like reading swear words…
I’m currently a postdoctoral research associate at The University of Manchester. Here’s a little CV-type thing, which may not be the most interesting thing, but you should probably feel sorry for me, as I have to live this nonsense. I’ve spared you a lot of horrible science; partially to protect you, but selfishly as I need to publish it first.
I completed my Undergrad in Biochemistry at The University of Manchester, and received my Physiology PhD from there in 2013. I was sponsored by Diabetes UK, and my project was to investigate PtdIns(4,5)P2 in the onset of insulin resistance in skeletal muscle and adipose tissue.
You know how cells have a membrane around the outside? And that that membrane is made up of things called lipids (basically fats)? One of these lipids is called phosphatidylinsoitol (4,5)-bisphosphate, or PtdIns(4,5)P2, or PIP2 if you want to be slightly inaccurate… So, normally muscle and fat cells take up more sugar (I mostly call it glucose) after insulin stimulation. However in “insulin resistance” this doesn’t happen. If you recognise the term insulin resistance, that’s because it’s a major precursor to Type 2 Diabetes.
Well with that all in mind, my project was to look at that fat PIP2, and the possible role it can have in the progression of insulin resistance. As well as looking at the folks which control PIP2, and how insulin resistance can affect them.
I then moved to University of California San Diego for my first postdoctoral position. As a grown up researcher, vaguely in charge of what I want to do, I had a few projects, but my main one was looking at the effect muscle can have on pancreatic beta cells, and insulin secretion.
So, you know how before I mentioned insulin resistance? Well when that happens glucose levels don’t go down, as they glucose doesn’t move into fat and muscle. Then the pancreas secretes more insulin in an attempt to make the glucose move into the muscle and fat. However, the pancreas can’t keep that up, and eventually cells stop trying and die.
It turns out muscle cells secrete (spit out) a whole bunch of stuff, called myokines. It’s not really surprising, but it’s only recently been properly proven. In insulin resistance and Type 2 Diabetes the secretion changes, and a bunch of nasty things come out.
Some of you detectives may have realised what my project involved. Sticking those little jerks on beta cells and seeing what happened? Yep, that was basically it. I collected all of those nasty myokines, put them on beta cells and measured the effects on function.
And that leads to me to where I am now, back at The University of Manchester, looking at congenital hyperinsulinism, or CHI if that’s simpler. I’ve been describing it as “the opposite of diabetes”, which makes it seem like I’ve bailed on Type 2 Diabetes, but it is linked I promise.
In CHI the pancreas makes too much insulin, which causes too much glucose to move into the muscle and fat cells. As Lucozade is keen to point out glucose is important, especially for the brain. Unfortunately, CHI starts at birth, and the messed up insulin/glucose levels can have effects on the development of the child.
So there you have it, I basically save babies for a living.