Mimicry Maxima

Edit: Found this old post collecting dust in my archives so I thought I would publish it despite being written 2 years ago since I haven’t updated this website for awhile.

The Great Ape Trust of Iowa are finding that primates have a more flexible audio repertoire than previously believed. On the other side of the world, Japan found a way to show that Bengal finches get excited over grammatical syntax. Yet neither of these have caused as much a stir in me as the Lyre Bird.

Sometimes the things you see on the Flintsones are not so far away from the truth!

My Bloody Evolution

Interesting article on the evolution of blood types – in primates and why the differences between populations.

Read more here.

Off With Their Genes!

The New Scientist title says it all: Black Queen tells microbes to be lazy. The idea is that keystone microbes would do the ‘dirty work’ while other microbes shed their genes in order to conserve energy.

Read more here.

The Spongebob Among-us

Mr. Squarepants has much to celebrate about after the latest fungal discovery from Malaysia was named after him. I love how scientists immortalise random things in their so-called ‘scientific’ nomenclature.  😉

Read more here.

When Success Becomes Your Worst Enemy

Clinical trials of therapies are becoming increasingly difficult to conduct due to patients’ contentment with current therapies. A solution for this is to employ the impoverished in developing nations who would not have access to expensive drugs otherwise. The other solution is better compensation for patients in developed countries. Are either of these solutions sufficient to push drug discovery to new heights?

Read more here.

Pierced Tongue in the Name of Science

Dr. Maysam Ghovanloo, assistant professor of electrical and computer engineering at the Georgia Institute of Technology, has created a wheelchair system which uses the tongue to steer it. So far, the only way to attach the sensor to the tongue is by piercing it. Clinical trials are being held at the Northwestern University School of Medicine.

Read more here.

The Mitochondriac

“…the cells were not actually dying during this period of time without oxygen..they weren’t happy…but they weren’t dead so it was clear that death was being accelerated by reperfusion [of oxygen].”

Your killer or your saviour may lie within you.

This 6 min section of a documentary speaks more about a ‘centre for death’ within your cells:

Bin The Insulin

(Image: http://www.sciencemagnews.com)

‘Is it time to bin the insulin?’ was the catchy title in a New Scientist article released a couple of weeks ago, suggesting that glucagon could be the alternative treatment to insulin for Type I Diabetic patients who have to inject themselves with insulin regularly to compensate for a deficiency which could kill them.

A paradigm shift is always exciting but to be honest I was pretty puzzled when I read the above statement considering conventional science indicates that glucagon releases the sugar stores in our liver when we’re hungry to normalise blood sugar levels. “How does that work?”, I mused. This week’s article is an easy explanation based the paper itself and some additional research.

Some background on Type I Diabetics:

Their body destroys the cells which make insulin in the pancreas (beta cells) hence the cells which make glucagon (alpha cells) fill up the space left i.e. they have more alpha cells than healthy people.

As a result, these patients have a quadraple whammy for elevated blood glucose levels:

1. Extra alpha cells = extra glucagon = hyperglycemia due to gluconeogenesis and lipolysis
2. Exra glucagon = inhibit uptake of glucose by the liver
3. No beta cells = no insulin = hyperglycemia
4. No insulin = extra glucagon since insulin usually keeps glucagon production in check

You could call it hyperglycemia with a vengeance!

So how does more glucagon help the problem? Actually it’s the opposite. What Roger Unger and his team have done is they first got rid of the glucagon receptors (Gcgr) by producing Gcgr knockout mice. The result of this is that the body doesn’t respond to glucagon hence no gluconeogenesis and no conversion of glycogen to glucose. The researchers then simulated Type I Diabetes by destroying the mice beta cells and while normal mice with no insulin exhibited hyperglycemia, the knockout mice without insulin showed normal blood glucose levels even after eating!

This was unexpected and the question is, how do the knockout mice cope with the extra glucose from eating without any insulin to squirrel it away; and where does it go? To be honest the researchers are still investigating this but they posed 2 theories:

1. They found that glucagon-like peptide 1 (GLP-1) levels were dramatically elevated in the knockout mice with diabetes (but not in normal mice with diabetes) and these act to increase muscle glucose uptake i.e. the body compensates with something else.
2. The knockout mouse livers acts the same way when both hormones are absent as when they are present because livers are already poised to uptake glucose passively (particularly when they have never encountered the effects of glucagon ). This is based on the assumption that insulin acts mostly to counteract the glucagon produced when we’re hungry before a meal.

These two situations don’t normally occur in Type I Diabetic patients since they have elevated glucagon so inhibiting glucagon function may work to normalise their blood glucose instead of using insulin to do the same.

Have a read of the paper here and the commentary published at the same time. I know most people don’t have access so please leave a comment or ask any questions and I’ll be happy to reply.