Another Reason Why Diabetes Causes Obesity?

A study described in today's edition of Science Daily may point to yet another reason, besides the raging hunger caused by high post-meal blood sugar surges, that obesity is not the cause of diabetes but is caused by the blood sugar abnormalities which characterize the early stages of blood sugar dysfunction.

Here's the report: Researchers Shed Light On Fat Burning

It's a rodent study, which means that we can't be sure that the finding will hold up when applied to humans. But what the researchers discovered has the feel of basic physiology--the kind of thing that may apply across species.

What they found was this: "... during the process of burning fat — called lipolysis — fat cells use sensory nerves to feed information to the brain."

Furthermore, Science News reports,

they found that the brain uses part of the nervous system used to regulate body functions, called the sympathetic nervous system, to in turn communicate back to the cells to initiate, continue or stop the fat burning depending upon the information the brain receives from the fat.

"The brain can trigger lipid burning by fat cells and through these sensory nerves, the fat cell can give the brain feedback," Bartness explained. "This is a really important concept in biology, as it can regulate the process of lipolysis much like how a thermostat regulates temperature in your house, using input from the air and output to a furnace or heating unit.

Why did this set off alarm bells when I read it? Because small fiber sensory nerves are the very first nerves to be damaged by high blood sugars--blood sugars in the so-called "prediabetic" range. You can read about the research studies that documented this finding HERE.

So if it is true that the thermostat that regulates how much fat we burn and how much we store depends on tiny nerve cells that reach into our fat, destruction of those tiny nerve cells early on in the deteriorative process could go a long way towards explaining why people who are experiencing "prediabetic" blood sugars--including those who do not go on to develop full-fledged diabetes--get fat.

That this may be true is suggested by another finding about the function of tiny nerve cells in an unexpected context: one that did test out in human beings. Dr. Kevin Tracey's work has established that the inflammatory response mounted by the immune system is regulated by the brain in response to signals it receives from the vagus nerve.

The vagus nerve it the major nerve pathway of the autonomic nervous system and as it branches out, it looks very much like an upside down tree that extends throughout our bodies until it terminates in tiny nerve fibers that reach all our cells.

If these nerve endings are crippled by neuropathy, the body does not sense invasion properly and may not mount an effective counterattack against infection. This may have a lot to do with why people who have developed neuropathy are so prone to getting infections that won't heal.

This new research points to yet another way that the nerves and brain may communicate to regulate the vital functions that sustain life.

We'll have to keep alert to learn if there is more followup to this research. Unfortunately, breakthroughs in basic science such as this one don't get the press that trivial news about the latest overhyped drugs receive.

Meanwhile, this is yet another factor that should motivate people with prediabetes to rein in their post-meal blood sugars. We know without the slightest doubt that blood sugars that rise over 140 mg/dl for more than an hour or so damage small nerve fibers. This has been confirmed by several independent studies. Keeping your blood sugar under 140 mg/dl as much as possible also appears, based on anecdotal evidence, to slowly reverse neuropathy over a period of several years.

To learn how to lower your blood sugar, visit this page:

How to Get Your Blood Sugar Under Control