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How sugar levels can be high, even when you haven’t eaten anything

If your sugar levels are HIGH – logic says, the solution is just simply to STOP EATING.

This is a philosophy I see many type 2 diabetics adopt,  particularly when the usual things to keep sugar levels in check, fail.

Does it work ?

Not as much as one would think.

The source of the sugar

You see, the reason sugar levels are high is not because you just ate a carb loaded snack per se.

It’s a little more nuanced than that.

Let’s start with what happens when you’re not eating….

The sugar supply when you’re starving

You still need fuel.   Supporting our giant sized “heads” is HARD WORK. The idea is your body reaches into the cookie jars, jars with an s, to keep “everyone” happy.

Of course, “everyone” is NOT equal.

The boss, i.e. the brain gets first dibs on fuel and the brain is a power user of sugar.

The sugar cookie jar

The jar that is particularly important, when it comes to blood sugar levels, is the liver.

Now the liver is the chief cook and bottle washer of the body, but his number one priority is to feed the brain.  So when sugar supplies drop, he makes a plan.

A big part of THE PLAN involves synthesizing sugar from other things.

This manufacturing process is called gluconeogenesis and when it happens in the liver, it is referred to as hepatic gluconeogenesis.

The liver is pretty adept at this job.

A laundry list of things can be turned into sugar, including certain amino acids, lactate and glycerol.

Hepatic gluconeogenesis is the default mode

Hepatic gluconeogenesis is a bit like breathing –  if it is NOT HAPPENING, it’s tickets !

So………………… Mother Nature in her wisdom has set things up, in such a way, as to keep the liver pumping out sugar, day and night.

UNLESS you’re eating…..

Stopping sugar production

When you eat, the food you eat, makes fuel available for “EVERYONE”.

Now exactly which fuels are found in the food, depends on the food type, but if the food contains carbohydrate, you’re getting sugar.

Some foods supply TRUCK loads of the stuff,  other foods it’s a trickle.

The point is………….. the liver’s sugar supplies are no longer needed.

On paper at least,  the liver should be able to stand down from sugar making duties and switch his attention to other things.  Among them  fuel storage.

In the insulin resistant …………….. the liver doesn’t get the memo.

Sugar production continues in full swing

And this is the problem.

body sugar + food sugar =  lots of sugar

Too much for insulin to handle, especially in light of the fact, that key players are deliberately ignoring insulin’s pleas to take sugar deliveries.  Eish !

So why did the liver not get the memo ?

Blame insulin resistance

The short answer is insulin resistance.

The long answer – the fat cells forgot to send the memo.

Because they were busy IGNORING insulin, they didn’t let asprosin know, her services were no longer needed.

This is what a group of researchers, based at Baylor College of Medicine have uncovered.

Asprosin the white lady

Asprosin is a “new” hormone, it was first described in 2016.

Her existence only came to light when researchers began studying a genetic condition, known as neonatal progeroid syndrome.

Folks with this condition, don’t make asprosin.

And this impacts their glucose metabolism.

In a good way……………sort of.

Asprosin keeps home fires burning

The team found, asprosin is one of the hormones, that tells the liver to produce sugar.

It turns out, asprosin is one of a multitude of adipokines i.e. chemicals produced by fat cells.

And in those blessed with “lots of fat”,  asprosin levels are elevated, since fat cells going about their business, pump the stuff out.

This in and of itself………………… is not a problem.

Asprosin doesn’t get time off

The problem comes when the fat cells become bolshie and fail to respond to insulin.

This means………… sugar doesn’t get taken up by the fat cells.

Now in the big picture of things, fat cells are actually not considered big sugar consumers.  After all……they’re fat cells.  What they do or don’t do with THE FAT, is considerably more important.  But, it turns out, the wee amounts of glucose being delivered to the fat cells, are important for asprosin.

They give asprosin permission to take some time off.

Which temporarily….stops hepatic gluconeogenesis.  And this stops postprandial sugar spikes.

Giving asprosin time off

The team confirmed the benefits of giving asprosin time off.

They used a special monoclonal antibody, designed to interfere with asprosin’s ability to do her job, in  mice suffering from metabolic troubles, it HELPED………….

It stabilized  glucose and it lowered insulin.

Graph showing glucose and insulin levels, in mice with diet induced obesity, following treatment with anti-asprosin antibody. Copyright 2016 Elsevier Inc.

So what does it mean for you ?

Anti-asprosin therapies

Maybe.   But this will take years to make a reality.

In the mean time, this research confirms the battle is not just a battle against sugar, but a battle against insulin / insulin resistance.

Give your asprosin a little R & R, by reining in insulin.

Further reading

Want to discover more ways to create BETTER BODY CHEMISTRY ?