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? Eat less and eat more? Is the most common rule of keeping in good health, and there is another saying called? Eating too much hurts your brain? .

Is this statement scientific and reliable? The author found a passage in the process of verification.

? Long-term satiety will lead to the increase of fibroblast growth factor in the brain, which will lead to arteriosclerosis. At this time, the oxygen and nutrition provided to the brain will be reduced, which will cause brain tissue atrophy and functional degradation. ?

This passage is often used as? Eating too much hurts your brain? Evidence is widely cited, even though it lacks literature sources and research topics. But is this really the case?

Science needs not only correct conclusions, but also rigorous argumentation process. We might as well analyze this argument.

This passage contains three meanings:

1, long-term satiety will lead to fibroblast growth factor (which is mentioned in the report? Fibroblast growth factor? ) huge growth;

2. Fibroblast growth factor can cause the proliferation of capillary endothelial cells and adipocytes, leading to vascular sclerosis;

3. Angiosclerosis leads to brain tissue atrophy and functional degradation.

First, let's learn about fibroblast growth factor.

Fibroblast growth factor (FGF) is a kind of polypeptide with extensive biological activity, which can be divided into many subtypes according to its physical and chemical characteristics (isoelectric point). In 1974, the researcher (Gospodarowiez) isolated a peptide from bovine pituitary gland and named it fibroblast growth factor. Subsequently, it was confirmed that basic fibroblast growth factor mainly exists in vascular-rich tissues, such as brain, pituitary, hypothalamus, retina, adrenal gland, placenta and ovary. Basic fibroblast growth factor can also be extracted from various tumor tissue homogenates. Acidic fibroblast growth factor exists only in brain, hypothalamus and retina. 1

Studies have shown that fibroblast growth factor is synthesized by endothelial cells, combined and stored in basement membrane. Vascular endothelial cells are both synthetic cells of fibroblast growth factor and effector cells. The proliferation, differentiation, morphological and functional changes of endothelial cells are closely related to fibroblast growth factor.

Its biological activities can be divided into two types: (1) mitogenic activity, which can promote the division and proliferation of tissues and cells, including embryonic development, morphogenesis, angiogenesis and tissue damage repair; (2) Non-mitogenic activity, including vasodilation, myocardial protection, ischemic protection and neuroprotection. This makes it a research hotspot in vascular regeneration, ulcer healing, wound repair and even cancer. 2

Let's examine the above three meanings one by one.

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First, long-term satiety can lead to the increase of fibroblast growth factor? That's right.

Early studies have shown that fibroblast growth factor does increase after satiety. The latest research shows that FGF2 1 (a fibroblast growth factor) seems to be involved in the regulation of body fat. The researchers found that FGF2 1 can inhibit the production of glucose in mouse liver, promote the production of glycogen and reduce glucagon. However, in the rodent obesity model, FGF2 1 increased significantly and was not affected by exogenous FGF2 1. This suggests that obesity may be a state of resistance to FGF2 1.

The expression of FGF2 1 gene is regulated by hunger and eating signals, that is to say, human FGF2 1 is increased under hunger and satiety. The increase of serum FGF2 1 level occurred in obese adults and children, suggesting that it is related to the body obesity index. The normal reference range has changed in different studies, for example, the average value of 50 healthy people is 468 pg/ml, while the average value of a community group is 225 pg/ml. It was also found that the level of FGF2 1 in healthy people only increased after fasting for 7 days. four

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Second, fibroblast growth factor can cause the proliferation of capillary endothelial cells and adipocytes, leading to arteriosclerosis? In doubt.

About what? Can satiety cause the growth of fibroblasts and lead to brain damage? It was first reported in the first issue of Introduction to Japanese Medicine (1989 0 1) that "Overeating can promote cerebral arteriosclerosis". This paper quotes the research of Professor Omura Yu of Kyushu University in Japan, saying that this peptide can especially proliferate endothelial cells such as smooth muscle and capillaries that make up blood vessels. Therefore, Professor Omura said? After eating too much, this peptide is secreted in large quantities in the brain, and the cells that form blood vessels proliferate, leading to cerebral arteriosclerosis? .

However, the search for Professor Omura Yu's paper "Physiological Function of Acidic Sporozoites" did not find a description directly related to this.

Because basic fibroblast growth factor can promote the division of vascular smooth muscle cells (SMCs), researchers believe that this factor may be related to the development of atherosclerosis, but its specific role is questionable.

Most scholars support arteriosclerosis? Endothelial injury response theory? It is believed that various main risk factors, such as age, hypertension and smoking, will eventually damage the intima of arteries, and the formation of sclerosing lesions is the result of inflammatory-fibroproliferative reaction of arteries to endothelial and intima damage. Fibroblast growth factor plays an active role in arteriosclerosis when endothelial injury occurs.

But will the increase of fibroblast growth factor directly lead to endothelial damage? In other words, can fibroblast growth factor be an independent cause of arteriosclerosis?

Some researchers (Lindn et al.) confirmed that basic fibroblast growth factor (bFGF) was used all over the body after arterial intima injury, and smooth muscle cells divided more and intima thickened. However, when the intima of artery was not damaged, smooth muscle cells did not respond when basic fibroblast growth factor was used. They pointed out that the arterial wall can synthesize basic fibroblast growth factor, which is an effective mitogen of smooth muscle cells, and any factor that leads to the release of endogenous basic fibroblast growth factor can stimulate the proliferation of smooth muscle cells and lead to intimal damage.

Other researchers believe that basic fibroblast growth factor has positive significance in repairing endothelial injury. In cerebral ischemia injury, the increase of basic fibroblast growth factor expression is positively correlated with the increase of the number of cerebral capillaries. After treatment with basic fibroblast growth factor, the content of cholesterol in arterial wall in atherosclerotic brain decreased and atherosclerotic plaques decreased, suggesting that basic fibroblast growth factor may have the effect of protecting intima of artery and delaying atherosclerosis.

The experimental results of rats showed that after feeding with high-fat diet for 6 weeks, the blood lipid of rats increased and the antioxidant capacity of brain tissue decreased, indicating that atherosclerosis caused by hyperlipidemia aggravated brain tissue damage. After treatment with basic fibroblast growth factor, the blood lipid level decreased and the antioxidant capacity increased, suggesting that basic fibroblast growth factor may delay or prevent the occurrence and development of cerebral arteriosclerosis by regulating blood lipid, thus alleviating brain tissue damage. five

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Third, vascular sclerosis leads to brain tissue atrophy and functional degradation? That's true.

Cerebral atherosclerosis often invades the internal carotid artery, basilar artery and vertebral artery. The place where the internal carotid artery enters the brain is a prone area, and the lesions are mostly concentrated in the bifurcation of blood vessels. Atherosclerotic plaque causes vascular stenosis, insufficient cerebral blood supply or local thrombosis or plaque rupture, and debris falling off causes cerebrovascular accidents such as cerebral embolism; When long-term chronic cerebral ischemia causes brain atrophy, it can develop into vascular dementia.

The research and application of fibroblast growth factor mainly focus on nerve repair, otolaryngology repair, bone repair, wound healing and tissue repair, wound healing and organ repair after hemorrhoid and fistula surgery. Fibroblast growth factor after DNA recombination is also used as the raw material of advanced cosmetics, which plays an anti-aging and beauty role mainly by improving microcirculation and restoring elasticity. At present, it is generally believed that it is safe to use growth factors to promote the repair of body surface wounds. After more than 3,000 large-sample and multi-center controlled clinical applications at home and abroad, there are no reports of body surface or visceral complications caused by growth factors, among which basic fibroblast growth factor has been used to treat patients with body surface trauma for several years. eight

At present, most people think that fibroblast growth factor can promote vascular sclerosis after vascular endothelial injury; But at the same time, fibroblast growth factor has positive significance in repairing vascular endothelial injury.

conclusion

The latest research shows that in humans and rodents, obesity is indeed related to the damage of the brain area responsible for weight control. Long-term high fructose diet will not only lead to hypertension, diabetes and hyperlipidemia, but also directly cause changes in insulin metabolism and brain damage. seven

However, whether the increase of fibroblast growth factor will cause endothelial damage or even arteriosclerosis has not been found.

Therefore, long-term satiety and the increase of fibroblast factors caused by brain injury cannot be equated. For the media, authenticity should be the first principle, and the original source should be indicated in the report or the research topic should be mentioned.

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References:

1, Zhang changmo, Zhang, Wu, biological function and application of fibroblast growth factor [J]? China Journal of Repair and Reconstruction Surgery, 1997,11(5): 272-272;

2. Tan Yaqing, Liu, Research progress of human acidic fibroblast growth factor [J], Biotechnology Bulletin, 20 13, 5: 22-27;

3. Kazuo Sasaki, Yuji Omura, Li, et al. Physiological function of acid spore-forming factor [J]. Technical research report of Institute of Information and Communication, MBE, Me

4. Lu Pan, Research Progress of Fibroblast Growth Factor 2 1 in Type 2 Diabetes and Obesity [J], Modern Medicine and Health, 2014,30 (1);

5. Zhu Junde, Wang Guixue, Yu Yan, et al. Effects of basic fibroblast growth factor on the parietal cortex and middle cerebral artery in atherosclerotic model rats [J]. Journal of Shandong University (Medical Edition), 2012,50 (11);

6. Thaler J P, Yi C X, Schur E A, et al., Relationship between obesity and hypothalamic injury in rodents and humans [J], Journal of Clinical Investigation, 20 12,122 (1):153-/kloc-0.

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Author: Zhao Yanchang