Beware of hypoxic fat cells, they spread cancer!

As I wrote elsewhere, when I add the transcription factor HIF-1α to the search, activator of (pseudo)hypoxia, activator of metabolism without the use of oxygen, something interesting always appears in the results. So this time it's quite the bomb. Fat cells spread cancer by spreading the message of lack of oxygen.

The study does not say it directly, but if we consider that the activation of the transcription factor HIF-1α is behind the hypertrophy of fat cells, i.e. their constant enlargement to enormous dimensions, then it is not surprising that these cells spread many problematic signals around the body. One such little-known signal is small extracellular vesicles called exosomes.

Extracellular vesicles containing regulatory signals sent by fat cells.

I have already shown several times here that the activation of (pseudo)hypoxia, i.e. the transcription factor HIF-1α in adipose tissue, is at the beginning of subsequent changes in the entire organism. Studies in mice show that if HIF-1α activation can be prevented, then these changes will not occur, the fat cells will remain healthy, the liver will remain healthy, the metabolic disorders associated with a high-fat diet will be eliminated. I also showed that the adipose tissue is naturally protected from this change by the fact that the presence of saturated and monounsaturated fats naturally prevents the activation of pseudohypoxia in fat cells. These cells are supposed to burn fat or die, not ferment glucose. But modern polyunsaturated fats, high in omega-6 without short or medium-chain fats, as well as other poisons, can activate HIF-1α in adipose tissue. And that's the beginning of big problems, as we'll see, even cancer.

I found a study that shows that the presence of extracellular vesicles emitted by adipose tissue promotes the growth of tumors and the rate of metastases in tumors in the breast tissue. The authors investigated this phenomenon in two cultures of tumor tissue as well as in mice.

The addition of extracellular vesicles sent by fat cells can activate the HIF-1α factor in the target tissue, i.e. pseudohypoxia.


Targeted suppression of the factor HIF-1α (shHIF-1α) cancels this effect (VEGF vessel formation, Invasion Assay - invasion activity)

So beware of a lack of oxygen in fat tissue! It is precisely the poor blood supply of adipose tissue, narrowed vessels and low flow that can be responsible for the problems of modern civilization. We already know that the vasodilating function of blood vessels with the help of arginine and the enzyme eNOS declines with increasing age. I have recently found that there are other vasodilation mechanisms controlled by hydrogen peroxide and nitrite, but also by the short fatty acids acetate, propionate and butyrate. These are formed not only by our intestinal bacteria, but, for example, acetate is created by our liver from alcohol or from fats by activating omega oxidation or fasting, it can also be taken in the diet as vinegar, and butyrate is of course part of butter, i.e. milk fat. There are other ways to achieve a better blood and oxygen supply to the tissues, including proper breathing.


Previous 

Next


References:

Adipocyte-derived extracellular vesicles promote breast cancer cell malignancy through HIF-1α activity

Microbial short chain fatty acid metabolites lower blood pressure via endothelial G protein-coupled receptor 41


Comments

Post a Comment

Popular posts from this blog

How to make fructose in the liver, but you better not do it!

Image
In one of my previous posts , I looked at the work of Richard Johnson, who claims that we have something like a fat switch in our body. While it is turned off, the body works normally and burns fat. If you inadvertently turn it on, you will store more fat and burn less. We also learned from him that the easiest way to turn it on is to quickly flood the liver with sugars dissolved in water, ie with the help of sweet drinks. If we start to look in more detail at what process we will actually start, we will find this interesting enzymatic pathway (production line), which resides in liver cells and other organs that have glucose intake independent of insulin levels. This enzymatic pathway can convert glucose, generally considered a good and harmless sugar, into fructose, which according to research is considered to be one of the causes of metabolic problems such as obesity, diabetes, heart attack, etc. It is called the polyol pathway . Quotation from Wikipedia (you can skip it, if you wan
Read more

Are carbohydrates toxic?

Image
In an older post, I focused on what to eat , what is probably harmful to us and, above all, in what quantity. I used the information here from Paul Jaminet's book  Perfect Health Diet . In the section on carbohydrates, it states that the recommended maximum amount of carbohydrates is 150 g (600 kcal). Why? What happens in the body when the daily intake of carbohydrates is higher? So let's investigate. First, let's look at this image from a study examining changes in metabolism in humans with varying amounts of carbohydrates and fat consumed , which I've added a little. The picture shows the dependence of DNL on energy intake, CH=carbohydrates, P=proteins, fat intake does not affect this process. Empty bars show continuous process, full bars when eating. What do we see here? The process of de-novo lipogenesis (DNL), i.e. the formation of fats from glucose, is a natural protection against high carbohydrate intake. The total amount of fat thus produced in the liver or adip
Read more

Can Vinegar Be the Solution to Alzheimer's and Senile Dementia?

Image
Vinegar or acetate is a very interesting substance, a food supplement. If you would like to know more and in detail about it and its metabolism in the body, read this two-part article . It is devoted to acetate only and has two parts, a total of 49 densely annotated pages in two columns. All this about a molecule that contains only two carbons. Incredible. It apparently affects all processes in the body. Acetate acts not only by activating AMPK during its conversion to acetyl-CoA, but also directly on the FFAR2 receptor, thus, for example, it supports vasodilation, i.e. better blood and oxygen supply to tissues. First, let's review the basic mechanism by which acetate in the body acts against obesity. It is the result of the processes associated with the activation of acetate in the cell, i.e. the connection with the CoA molecule to form acetyl-CoA. This reaction consumes energy (ATP) and creates a signal of shortage, activates the enzyme AMPK, which limits the ACC enzyme by phosp
Read more