UNC study helps clarify link between high-fat diet and type 2 diabetes. (sat. fat n.g.)

New research from the University of North Carolina at Chapel Hill School of Medicine adds clarity to the connection. The study published on-line April 10th in the journal Nature Immunology finds that saturated fatty acids but not the unsaturated type can activate immune cells to produce an inflammatory protein, called interleukin-1beta.

CHAPEL HILL, N.C. – A diet high in saturated fat is a key contributor to type 2 diabetes, a major health threat worldwide. Several decades ago scientists noticed that people with type 2 diabetes have overly active immune responses, leaving their bodies rife with inflammatory chemicals.

In addition, people who acquire the disease are typically obese and are resistant to insulin, the hormone that removes sugar from the blood and stores it as energy.

For years no one has known exactly how the three characteristics are related. But a handful of studies suggest that they are inextricably linked.

New research from the University of North Carolina at Chapel Hill School of Medicine adds clarity to the connection. The study published online April 10 in the journal Nature Immunology finds that saturated fatty acids but not the unsaturated type can activate immune cells to produce an inflammatory protein, called interleukin-1beta.

I’m not sure if this research is “reinventing the wheel”, or just poorly described in this article.

To start with, it has long been known that there are clusters of cells in the white fat, called MAST cells (also known as mastocytes and labrocytes). They are clusters of cells of several types of tissues and contains many granules rich in histamine and heparin, which when irritated, they release into the body as part of the immune response.

A typical person with a normal amount of body fat has a given amount of these MAST cells. But when a person gains weight, not only do they develop a *proportional* amount of MAST cell bodies, but they get *more* than a proportional number.

And this is where the problem lays. Because MAST cells, when they get irritated, tend to stay irritated, and producing histamines and heparin, which, oddly enough, encourages the development of more white fat cells.

Because starvation has been a problem for people for tens of thousands of years, our bodies have adapted to try and gain weight, and to keep extra weight, to survive seasons when there wasn’t enough food. So tricking the body into losing weight isn’t easy.

When we first try to lose weight, we have about a two week period in there before we start losing fat, which starts first in the liver. But when the liver begins to burn fat, it reacts by becoming more efficient and lowering our metabolic rate so we don’t burn fat as quickly.

In any event, going to their research, they have discovered that if you have a lot of MAST cells, which implies a lot of extra fat, and you consume more saturated fats, it tends to irritate your MAST cells to start producing histamines and heparin.

This, in turn, can interfere with our insulin sensitivity.

But this is not the whole story. As has been clearly shown in recent years, if you *just* consume meat and fats, not carbohydrates, people tend to lose weight, often a lot of weight. This is because protein and fats work in a complementary fashion with carbohydrates.

So by themselves, saturated fats may not be wholly responsible for irritating MAST cells.

Physiological insulin resistance is when there’s a lot of saturated fat floating around. The muscles and other tissue which are capable of using fat as a source of energy become insulin resistant in order to spare glucose for the brain, which can’t use fat.

The reason is that when your glycogen stores run out, the brain has to run on glucose produced by the liver, and the muscles and most other tissue can run on fat, so they spare the glucose for the brain.

The same thing will happen if you eat a high fat and high carb meal, but the carb absorption is somewhat slowed by the fat, so it’s not that bad.

Pathological insulin resistance is what tested by a glucose tolerance test, and the fasting glucose.

The GTT is basically feeding 75g or so of sugar/carbs (no fat) and then measuring blood glucose. If it’s high, this means that your body is insulin resistant despite the lack of fat in your bloodstream.

Similar for the fasting glucose. After fasting overnight, you’re probably done digesting the food, so it will measure the glucose level needed to feed your body.

A high triglyceride level is also related to insulin resistance ...

Does that make sense ?

I’m not sure if this research is “reinventing the wheel”, or just poorly described in this article.

A poor description in a press release is nothing new. IMHO, they figured out a cell signaling pathway for inflammation and insulin resistance. Does it apply to all saturated fatty acids? Maybe we'll find out soon enough. Check the dates it was received and accepted. It wasn't very long between those dates.

Fatty acid–induced NLRP3-ASC inflammasome activation interferes with insulin signaling

Combined immunology and diabetes lists, FReepmail me if you want on or off either list.

They are correct. I have had significant success with an extremely low carb diet. In fact, to have success I have to go to around 20 grams per DAY...a “lifestyle” that has proven nearly unsustainable. Right now I’m looking into the Insulin Resistance Diet, which utilizes the food combining method: if you eat carbs, balance it with protein and such. My family doc and obgyn both recommended Atkins or a modified version of such for me. Nice to have 2 docs who take the time to listen and research on my behalf!

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