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Clinical Trials Research Article

The Scientific Community has Found the "Chief Culprit" of Obesity Caused by "Eating too Much"

2019.09.17

For many "fat people", the more they eat, the more they want to eat, and they can hardly control themselves. Through the case study of obesity caused by eating, scientists found that obesity is related to the brain, intestine and fat, they affect each other and work together, letting people eat more and become more fat. Let's take a look at the "chief culprit" of obesity that the scientific community has found through various studies over the years.

Conclusion 1: High-fat diet suppresses signals from brain nerve

Scientists have long believed that the lateral hypothalamic area (LHA) plays an important role in regulating food intake. Scientists from the Department of Psychiatry at the University of North Carolina at Chapel Hill and cooperators from America, Sweden and Britain found that the vesicular glutamate transporter 2 (VGlu 2) expressing neurons in LHA plays a role in suppressing food intake. They found that when mice eat a high-fat diet, their VGlu 2-expressing neurons will be inhibited and could not send a strong signal to stop eating, leading to overeating and ultimately obesity.

Conclusion 2: High-fat diet destroys intestinal enzyme activity

TOPSANTE, a French health journal, cited the research findings and stated that the gut will produce an enzyme called "NAPE-PDL" normally when people eat, which sends a satiety signal to the brain, activates the anorexic neurons in the hypothalamus and tells the body to stop eating. However, if the high-fat foods are continuously ingested, the activity of the enzyme "NAPE-PDL" will decrease, which will prevent the communication between your gut and your brain, affecting the appetite control. As a result, a greasy diet will deactivate the enzymes that control appetite in the gut, making it harder for people to stop eating.

Conclusion 3: High-fat diet causes fat to send the wrong signals to the brain

The body's white fat produces a hormone called "leptin". Scientists once believed that "leptin" could help people lose weight by affecting the cranial nerves and peripheral metabolism.

But scientists from the University of Texas have found a reversal of the effect of "leptin": in some cases, "leptin" will fail to make people thinner, on the contrary, it will lead to obesity. After giving "leptin" to obese mice with a high-fat diet, the researchers found that the mice became fatter instead of losing weight. Their weight, fat, glucose tolerance and insulin sensitivity were also decreased; reducing of the "leptin" level can restore the "leptin" sensitivity of mice, making them thin.

The researchers believed that there is a balance between "leptin" level and "leptin resistance". When people are obese, they have high "leptin" level and "leptin resistance" at the same time, and the "leptin" will not make them thin, but make them gain moer weight; when the "leptin" decreases to the appropriate level, the "leptin resistance" will disappear and the sensitivity will be recovered, and the expected effect of reducing food intake could be achieved; however, when "leptin" level fall again, food intake will increase again and the weight will increase accordingly.

Conclusion 4: High-fat diet causes "leptin resistance"

A new study, led by the Baylor College of Medicine in the United States, confirmed the mechanism by which high-fat foods can disrupt the gut and send out appetite-suppressing signals to the brain by combining with previous factors that contribute to obesity. Gastric inhibitory peptide (GIP) is one of the most important metabolic hormones in the intestinal tract, which can affect the energy management of the body.

Experiments showed that when the animals eat a balanced diet, the level of gastric inhibitory peptide (GIP) will not increase, and "leptin" can normally send signals to the brain, making the brain have satiety and commanding it to stop eating. However, when animals eat a high-fat diet and become obese, the level of blood gastric inhibitory peptide (GIP) will increase. Gastric inhibitory peptide (GIP) flows into the hypothalamus, causing "leptin resistance". At this time, the animals don't have satiety, thus they will continue to eat, causing the further weight gain. When the interaction between gastric inhibitory peptide (GIP) and hypothalamus of obese mice is blocked, the effect of "leptin" can be restored, causing the loss of appetite and weight .

In short, various studies have found that high-fat diet is the "chief culprit" of obesity caused by "eating too much". Therefore, if you want to lose weight scientifically, you must eat a reasonable diet and reject high-fat foods.

References:

[1]The author is unknown. Why Does the Greasy Diet Make People Want to Eat More and More? [J]. Food Industry, 2019, 40 (6): 315.

[2] Alnory A,Gad H,Hegazy G,etal. The association of vaspinrs2236242 and leptinrs7799039 polymorphism with metabolic syndrome in Egyptian women. Turk J Med Sci,2016,46:1335-1340.

[3] www.yidianzixun.com.html.

[4]New discovery explains how fatty food disrupts appetite control, causing obesity.