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Recently, the Le Yingying research group of the Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences published an online publication titled High Fat Diet and High Cholesterol Diet Reduce Hepatic Vitamin D-25-Hydroxylase Expression and Serum 25-Hydroxyvitamin D3 Level through in Molecular Nutrition & Food Research.
Research papers on Elevating Circulating Cholesterol, Glucose, and Insulin Levels
.
The study used a mouse model of diet-induced obesity and metabolic disorders and found that elevated blood cholesterol, glucose, and insulin levels inhibit liver vitamin D metabolism and reduce blood 25(OH)D3 levels
.
Vitamin D is an essential vitamin for the human body.
It plays an important role in the development and maintenance of calcium and phosphorus homeostasis in the body and bone health.
It also has the functions of regulating immune cell function, anti-inflammatory, and antioxidant
.
Vitamin D is catalyzed by vitamin D 25-hydroxylase (mainly CYP2R1) to produce 25(OH)D in the liver, and the latter is catalyzed by 1α-hydroxylase (CYP27B1) in the kidneys to produce 1,25(OH) with biological activity 2D, or catalyzed by 24-hydroxylase (CYP24) to generate 24,25(OH)2D without biological activity
.
25 (OH) D is the major form of vitamin D in the blood, is a biological indicator of vitamin D nutritional status
.
Epidemiological studies have shown that people with obesity and related metabolic diseases (hyperlipidemia, insulin resistance, type 2 diabetes) have insufficient vitamin D (blood 25(OH)D 21-30 ng/ml) or lack (blood 25( OH)D <20 ng/ml), and vitamin D supplementation cannot effectively increase blood 25(OH)D levels
.
The role of vitamin D deficiency in the occurrence and development of obesity and related diseases has received wide attention from researchers, but there are few studies on the mechanism of vitamin D deficiency in these diseases
.
In this study, the researchers first used high-fat, high-cholesterol diet-induced obesity and glucose and lipid metabolism mouse models combined with in vitro experiments to explore the causes and mechanisms of vitamin D deficiency
.
The results showed that compared with mice on a normal diet, the obesity/insulin resistance mice induced by the high-fat diet showed a significant decrease in serum 25(OH)D3 and 1,25(OH)2D3; the liver Cyp2r1 expression was significantly decreased; while the kidney Cyp27b1 and Cyp27b1 and There was no significant change in Cyp24 expression
.
In the process of high-fat diet leading to obesity, the blood levels of cholesterol, triglycerides, fatty acids, glucose and insulin rise successively
.
These changes occurred before the decrease in liver Cyp2r1 expression and the decrease in blood 25(OH)D3 concentration
.
The expression of Cyp2r1 in the liver of obese mice induced by high-fat and high-sugar diet was also significantly lower than that of mice with normal diet
.
High cholesterol diet mice showed a significant increase in blood cholesterol levels and a significant decrease in liver Cyp2r1 expression after 2 days.
These changes all occurred before the blood 25(OH)D3 concentration decreased
.
Further in vitro experiments found that high concentrations of cholesterol, glucose, and insulin alone can inhibit the expression of Cyp2r1 in mouse liver cells, while fatty acids have no significant effect on the expression of Cyp2r1
.
These results suggest that the increase in blood cholesterol, blood sugar, and insulin in obese mice induced by high-fat diet, and the increase in blood cholesterol in mice caused by high-cholesterol diet can all reduce liver Cyp2r1 levels and reduce liver 25(OH)D synthesis.
, Resulting in a decrease in blood 25(OH)D levels
.
The researchers further used high-fat diet-induced obesity and metabolic disorder model mice to observe whether reducing body weight and improving glucose and lipid metabolism disorders by restricting diet can improve vitamin D metabolism.
They found that the food intake of mice was reduced to that of control mice.
Ten weeks later, the weight of the mice was significantly reduced, hypercholesterolemia and hyperglycemia were significantly reduced, and the expression of liver Cyp2r1 and blood 25(OH)D levels were significantly increased
.
In summary, the study used diet-induced obesity and glucose and lipid metabolism animal models, combined with in vitro experiments and diet restriction experiments, and found that blood cholesterol, blood sugar, and insulin increased by inhibiting liver Cyp2r1 expression led to a decrease in blood circulation 25(OH)D ; It is suggested to avoid high-fat and high-cholesterol diet, and treat obesity and glucose and lipid metabolism disorders not only to improve vitamin D metabolism and vitamin D deficiency, but also to enhance vitamin D supplementation by increasing liver Cyp2r1 levels
.
The research was funded by the National Natural Science Foundation of China and the Ministry of Science and Technology
.
High-fat, high-cholesterol diet interferes with vitamin D metabolism and limits the improvement of vitamin D metabolism in obese mice.
Links to papers: https://onlinelibrary.
wiley.
com/doi/10.
1002/mnfr.
202100220 2020 Hot Article Selection 1.
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Unbelievable! Scientists reversed the "permanent" brain damage in animals overnight, and restored the old brain to a young state.
.
.
Research papers on Elevating Circulating Cholesterol, Glucose, and Insulin Levels
.
The study used a mouse model of diet-induced obesity and metabolic disorders and found that elevated blood cholesterol, glucose, and insulin levels inhibit liver vitamin D metabolism and reduce blood 25(OH)D3 levels
.
Vitamin D is an essential vitamin for the human body.
It plays an important role in the development and maintenance of calcium and phosphorus homeostasis in the body and bone health.
It also has the functions of regulating immune cell function, anti-inflammatory, and antioxidant
.
Vitamin D is catalyzed by vitamin D 25-hydroxylase (mainly CYP2R1) to produce 25(OH)D in the liver, and the latter is catalyzed by 1α-hydroxylase (CYP27B1) in the kidneys to produce 1,25(OH) with biological activity 2D, or catalyzed by 24-hydroxylase (CYP24) to generate 24,25(OH)2D without biological activity
.
25 (OH) D is the major form of vitamin D in the blood, is a biological indicator of vitamin D nutritional status
.
Epidemiological studies have shown that people with obesity and related metabolic diseases (hyperlipidemia, insulin resistance, type 2 diabetes) have insufficient vitamin D (blood 25(OH)D 21-30 ng/ml) or lack (blood 25( OH)D <20 ng/ml), and vitamin D supplementation cannot effectively increase blood 25(OH)D levels
.
The role of vitamin D deficiency in the occurrence and development of obesity and related diseases has received wide attention from researchers, but there are few studies on the mechanism of vitamin D deficiency in these diseases
.
In this study, the researchers first used high-fat, high-cholesterol diet-induced obesity and glucose and lipid metabolism mouse models combined with in vitro experiments to explore the causes and mechanisms of vitamin D deficiency
.
The results showed that compared with mice on a normal diet, the obesity/insulin resistance mice induced by the high-fat diet showed a significant decrease in serum 25(OH)D3 and 1,25(OH)2D3; the liver Cyp2r1 expression was significantly decreased; while the kidney Cyp27b1 and Cyp27b1 and There was no significant change in Cyp24 expression
.
In the process of high-fat diet leading to obesity, the blood levels of cholesterol, triglycerides, fatty acids, glucose and insulin rise successively
.
These changes occurred before the decrease in liver Cyp2r1 expression and the decrease in blood 25(OH)D3 concentration
.
The expression of Cyp2r1 in the liver of obese mice induced by high-fat and high-sugar diet was also significantly lower than that of mice with normal diet
.
High cholesterol diet mice showed a significant increase in blood cholesterol levels and a significant decrease in liver Cyp2r1 expression after 2 days.
These changes all occurred before the blood 25(OH)D3 concentration decreased
.
Further in vitro experiments found that high concentrations of cholesterol, glucose, and insulin alone can inhibit the expression of Cyp2r1 in mouse liver cells, while fatty acids have no significant effect on the expression of Cyp2r1
.
These results suggest that the increase in blood cholesterol, blood sugar, and insulin in obese mice induced by high-fat diet, and the increase in blood cholesterol in mice caused by high-cholesterol diet can all reduce liver Cyp2r1 levels and reduce liver 25(OH)D synthesis.
, Resulting in a decrease in blood 25(OH)D levels
.
The researchers further used high-fat diet-induced obesity and metabolic disorder model mice to observe whether reducing body weight and improving glucose and lipid metabolism disorders by restricting diet can improve vitamin D metabolism.
They found that the food intake of mice was reduced to that of control mice.
Ten weeks later, the weight of the mice was significantly reduced, hypercholesterolemia and hyperglycemia were significantly reduced, and the expression of liver Cyp2r1 and blood 25(OH)D levels were significantly increased
.
In summary, the study used diet-induced obesity and glucose and lipid metabolism animal models, combined with in vitro experiments and diet restriction experiments, and found that blood cholesterol, blood sugar, and insulin increased by inhibiting liver Cyp2r1 expression led to a decrease in blood circulation 25(OH)D ; It is suggested to avoid high-fat and high-cholesterol diet, and treat obesity and glucose and lipid metabolism disorders not only to improve vitamin D metabolism and vitamin D deficiency, but also to enhance vitamin D supplementation by increasing liver Cyp2r1 levels
.
The research was funded by the National Natural Science Foundation of China and the Ministry of Science and Technology
.
High-fat, high-cholesterol diet interferes with vitamin D metabolism and limits the improvement of vitamin D metabolism in obese mice.
Links to papers: https://onlinelibrary.
wiley.
com/doi/10.
1002/mnfr.
202100220 2020 Hot Article Selection 1.
The cup is ready! A full paper cup of hot coffee, full of plastic particles.
.
.
2.
Scientists from the United States, Britain and Australia “Natural Medicine” further prove that the new coronavirus is a natural evolution product, or has two origins.
.
.
3.
NEJM: Intermittent fasting is right The impact of health, aging and disease 4.
Heal insomnia within one year! The study found that: to improve sleep, you may only need a heavy blanket.
5.
New Harvard study: Only 12 minutes of vigorous exercise can bring huge metabolic benefits to health.
6.
The first human intervention experiment: in nature.
"Feeling and rolling" for 28 days is enough to improve immunity.
7.
Junk food is "real rubbish"! It takes away telomere length and makes people grow old faster! 8.
Cell puzzle: you can really die if you don't sleep! But the lethal changes do not occur in the brain, but in the intestines.
.
.
9.
The super large-scale study of "Nature Communications": The level of iron in the blood is the key to health and aging! 10.
Unbelievable! Scientists reversed the "permanent" brain damage in animals overnight, and restored the old brain to a young state.
.
.
