Tuesday Feature Episode 29: Alexander Ryan

Life Science Archive

From science on the screen, to science in the labs – this week’s Tuesday Feature looks at Alexander Ryan. He’s a new post doctoral researcher in the Faculty, so read about his research into his congenital hyperinsulinism.

Please explain your research for the general public in ten sentences or less.

At the moment I’m looking at congenital hyperinsulism which is when the pancreas secretes too much insulin. It affects roughly 1:50000 new-borns and its potentially really awful because the high levels of insulin leads to low levels of glucose which can have major problems with development, especially in the brain. The children usually go onto die because they don’t develop properly. My research is looking at trying to stop the insulin secretion and to prevent the hypoglycaemia (the low levels of glucose) and therefore help the children.

How can this benefit the person reading this blog?

Obviously with it effecting…

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“Sir, it’s only wafer thin”

Why do we eat dessert?

You know, when you’ve already munched your way through a bowl of nachos, a burrito, maybe a quesadilla or a couple of tacos, you’ve gorged on salsa, guacamole and sour cream, and someone pops up with a churro*. Are you going to say no? Of course not!

I assume, I mean I don’t know you, but I bet you like a pudding!

There’s an obesity epidemic at the moment, with over 600 million people affected. With it there’s increased risk for Type 2 Diabetes, cancer, cardiovascular problems, basically a hefty slice of doom pie.

The other week I got to see Dr Giles Yeo give a talk, titled “Are YOUR genes to blame when your jeans don’t fit?”. As a geneticist he studies the effect on obesity, so, if you recognise the name it’s because he’s to blame for giving fat people excuses. In not-lies Dr Yeo studies the reasons why certain people eat more, and others exercise more. Obesity is hereditary in the same way as height, so obviously your genetics play a massive role.

Dr Yeo began talking about leptin; a protein hormone, the deficiency of which makes everyone’s favourite critter, big fat rodents. (I even included a picture of leptin-deficient rat in a 1st year essay explaining the benefits of Genetic Modification. Of course I received a comment explaining that the leptin-deficient rats were a natural mutation, but still big fat animals!) In a similar way there are also leptin-deficient people, and yes, they manifest in the same way. The lack of leptin leads to increased fat gain, hyperinsulinaemia, hyperphagia, hypogonadotrophism and a dysfunction immune system. That basically means you’re left with infertile, obese people who can’t distinguish edible foods. Luckily, these people can be treated with leptin, and the results are amazing. So, can everyone just eat leptin and be thin?

Well, no, and that’s a bit of a stupid question really.

The thing is leptin only works as a treatment when there is a problem in the first place. Leptin binds to a receptor in the brain, which tells you that you’re full. The people without leptin never get this signal, so their brains tell them that they are hungry, starving in fact. This is why they eat anything they can get their hands on. Their bodies think they are struggling for nutrients so it doesn’t waste time with things like babies (hence the infertility) and the immune system (what’s the point wasting energy combating disease when you’re going to starve to death anyway?).

Obviously this leptin-deficiency is an extreme example, but what if there were similar proteins and receptors? What if less drastic mutations meant you felt full slightly less often, or slower than is appropriate? Well there is.

Dr Yeo talked about a couple of receptors which maintain appetite and food intake, the melanocortin 4 receptor , and Tropomysin receptor kinase B. Now they sound complicated so we’ll called them Mark and Trevor, ok?

1% of those with a BMI over 30 have a mutation in Mark, making it the most common mutation linked to obesity. If Mark isn’t working then food intake is increased. Trevor acts as a receptor for a protein called BDNF (let’s go with Brian). Brian reduced food intake, and if he’s not knocking about this tends to lead to obesity and Type 2 Diabetes.

Interestingly, there are subtle mutations in Mark and Brian which effect how well they work. Basically the lazier Mark and Brian, the more food you eat, and the more weight you gain. The awesome thing is that these mutations may only result in someone eating slightly more, but it happens for every meal. If you consistently eat 50 calories more than someone else, and if this happens every time you eat, you will begin to put on weight.**

(Also I have a bit of soft spot for Brian, as it was one of the first myokines (something your muscle spits out) that I thought might affect β cells. It doesn’t seem to, but still it was one of my very first pet projects. So, yeah, me and Brian are total bebus.)

And these aren’t even the only causes. Genome-wide association studies have discovered 75 genes which correlate with obesity. It’s important to recognise that correlation does not equal causation, and these need further study, but still the potential is huge. Each of these could have multiple mutations and activities, acting somewhat independently of each other.

This is amazing, you understand that right? There could be millions of combinations dictating how much food you want, how frequently you eat and how quickly you feel full. And this isn’t even including genes which effect exercise and fat storage!

I should point out that this doesn’t fully determine your weight. As Dr Yeo said “your genes are like a hand of poker”, it all depends on how you play them. “You can win with a bad hand, and you can definitely lose with a good hand.” The risk of obesity increases with certain genes, but sensible meal management and regular exercise can overcome them. Unless of course you’re one of those people who are exercise-resistant. I’ll cover that later though…

So, why do we eat dessert?

Dr Yeo wrapped up his talk with a nice little theory. Think about the past, imagine you’ve just chased down a gazelle. (Yes, in this story you are some sort of super human.) You’ve munched his little face until you’re full, and content. But say you’ve wasted 1,000 calories chasing down dinner, and what if tomorrow’s gazelle is made of kryptonite, sapping your ability to run, leap and gobble that jerk? Well the simple answer is you eat more food. This happens all the time in nature really. Animals will consume far more food than is appropriate to make sure they’ve had enough calories for when times are hard. However, as I’m sure your annoying friend has told you, meat is not really calorie-dense. You know what is though? Cheesecake, brownies and brownie cheesecake. By “making room” for sweet things, your body is still able to ingest the calorie-rich treats, regardless of how much antelope you’ve eaten.

Today’s quote is from Monty Python.

* Replace with whatever you want, I don’t know you. Sauerkraut, currywurst and kirschtorte? Fish, chips, mushy peas and a 99? Charcuterie, gnocchi, cacciatore and gelato? I’m hungry now…

**I don’t care what you say; “interestingly” and “awesome” are the correct words.