Blame It On Your Hypothalamus

Blame It On Your Hypothalamus

  This post described how insulin resistance affects the body and how it can effect appetite and weight gain.  Many people are overweight when diagnosed and it’s a popular misconception that overweight causes diabetes.  The real fact is that weight gain is a symptom of diabetes as well as constant hunger in many cases.  The more resistant your body is the more insulin you produce.  The excess insulin in your system not used in a short time is stored as fat.  You might be eating the same amount you always did, but gaining weight rapidly or not be able to lose weight.

I ran across this chart and thought I’d share it. Sometimes it’s easier to understand with a picture. I’ve included a “blurb” from the study which I translated into “regular people” language. The source is also included, but you have to be a member or pay to see the whole text.

Here’s the chart

Impaired insulin secretion results in decreased insulin levels and decreased signaling in the hypothalamus, (sort of the “brain control center”) leading to increased food intake and weight gain, decreased inhibition of hepatic glucose production (your liver doesn’t get the signal to stop putting glucose into your system), reduced efficiency of glucose uptake in muscle,(your muscles can’t absorb and use the glucose) and increased lipolysis in the adipocyte,(increase fat (lipolysis) stored in your fat cells (adipocyte) resulting in increased plasma NEFA(non-esterfied fatty acids) levels(fat transporters that are carried to the liver). The increase in body weight and NEFAs contribute to insulin resistance, and the increased NEFAs also suppress the -cell’s adaptive response to insulin resistance. The increased glucose levels together with the elevated NEFA levels can synergize to further adversely affect -cell health and insulin action, often referred to as ‘glucolipotoxicity’ (a whole bunch of glucose).

So in Lizzy Language what this means is:

Defects in insulin secretion such as slow first-phase insulin production (when you first start to eat no insulin is produced immediately) leads to the hypothalamus gland in your brain not getting the signal that food is coming in, thereby your “hunger signal” stays on longer and your “full signal” doesn’t trip over as it should. This leads to weight gain because you stay hungrier longer.

Your liver stays in “liver gone wild” mode pumping glucose into your system because it doesn’t receive the signal that your glucose is already high and keeps dumping more into your system(Hepatic Glucose Production).

Your muscles can’t absorb and use the glucose properly.

Increased fat is stored in the fat cells because of the extra glucose in your system that can’t be utilized properly.

The increased fat also results in increased fat in the blood which is carried to the liver (explains diabetic fatty liver)

And all of this in turn can cause weight gain, high cholesterol levels, and more insulin resistance. In other words it’s a vicious cycle.  Losing weight if often indicated to reduce insulin resistance but insulin resistance itself causes weight gain!!!!!!

Here’s some more info. about the hypothalamus which includes:

The hypothalamus controls body weight and appetite, but it is not entirely clear how. Sensory inputs, including taste, smell, and gut distension, all tell the hypothalamus if we are hungry, full, or smelling a steak. Yet it is mysterious how we are able to vary our eating habits day to day and yet maintain about the same weight (sometimes despite all efforts to the contrary!) . The “set-point” theory is an old one in diet science, but until recently the mechanics of maintaining that set point were unknown.

It appears that there is an endocrine component to the appetite system. Recent studies in mice have shown that the fat cells of normal overfed mice will release a protein called leptin (or OB, after the gene name), which reduces appetite and perks up metabolism. Leptin is presumably acting on the hypothalamus. Underfed mice, on the other hand, produce little or no leptin, and they experience an increase in appetite and a decrease in metabolism. In both of these mice, the result is a return to normal weight. But what would happen if a mouse (or human) had a defective OB gene? Weight gain would never trigger fat cells to release leptin, the hypothalamus would never slow the appetite or increase metabolism, and the mouse would slowly but surely become obese (how the gene got its name).

Source:  click here

Here’s more information on NEFA’s: click here

So you’re not only fighting the weight gain from your body producing too much insulin but unable to properly utilize it, your brain is telling you you’re starving and eat, eat, eat!

The good news is that you can reduce the effects, first by getting and keeping lower numbers.  The a low-carb diet very often quiets the food-monster, and increased physical activity also helps reduce resistance.

Lizzy

Knowledge is Power

© LO 11/1/10