“Super Food” upgrade again?Blood glucose and blood lipids can also improve oxidation stress!
In recent years, the global public health issue of obesity has continued to spread rapidly. As a chronic metabolic disease, obesity is caused by the interaction of many factors (such as diet, environment and genetics), such as intracellular stress and inflammation caused by metabolic disorders. Diet intervention can help treat obesity and overweight.
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The chronic activation of the internal quality network (ER) stress has proven to play an important role in the development of obese insulin resistance. The internal quality mesh stress is considered an important feature of insulin resistance in molecular, cells, and body levels. Therefore, maintaining the stability of the internal quality network is essential for the normal function and survival of the cell.
In recent years, quinoa seeds have quickly attracted people’s attention due to its high -quality protein and broad amino acid spectrum. In addition, quinoa has the characteristics of cold, salt resistance and drought resistance, and can be widely planted around the world. Therefore, from the perspective of the nutrition and functional characteristics of quinoa protein, it can be used as an ideal choice for human food. Quinoa can produce a variety of metabolites with extensive biological activity, including saponin, plant alcohol, phenol, and biological activated peptides, which makes the seeds of quinoa a candidate against obesity, metabolic syndrome and T2DM dietary intervention. A clinical study shows that ingesting 50 grams of quinoa daily can reduce the incidence of serum triglycerides and metabolic syndrome of overweight and obesity participants. Animal experiments also show that quinoa can significantly improve the accumulation of liver lipids and sugar stability of obese mice, which causes animal Homa-IR and blood lipids to change, and sugar lipid metabolism changes. In addition, cell experiments have shown that quinoa polysaccharides can inhibit fat transcription factors (such as PPAR+, C/EBP?, C/EBP+, C/EBP+, SREBP1C, and AP2 expression, which significantly inhibits the differentiation of 3T3-L1. The specific mechanism of role is unclear.
This study aims to clarify the influence of quinoa diet on high -fat diet (HFD) to induce obese mice, as well as the regulating role of quinoa diet on ERS, and reveal the mechanism of quinoa resistance to obesity.
1. Supplement of quinoa will reduce the weight, food intake and liver index of obesity mice
In order to observe the inhibitory effect of quinoa on obesity, he first feeds HFD for 12 weeks, and then feeds the quinoa with 2 G/KG weight for 12 weeks. Obesity mice weigh higher than the control group mice (Figure 1A). After 12 weeks of quinoa and MET treatment, the weight and weight gain of mice were significantly reduced (P <0.01, Figure 1A), while the quinoa treatment effectively reduced the liver index and food intake of obese mice (Figure 1C 1C To. Compared with the obese model group, the quinoa group's feeding in the 6th to 10th week is decreased (P <0.01, Figure 1B). Compared with the model group mice, quinoa significantly reduces the weight, food intake and liver index of obese mice.
2. The impact of quinoa on the characteristics of obese mice’s blood glucose characteristics
In the experiment, the FBG level in the model control group is significantly higher than the normal control group. Compared with the model control group, the quinoa and the two -meta are significantly reduced the FBG (P <0.05) of obese mice (Figure 2D). Figure 2A, B shows the result of OGTT in the 12th week. Compared with the model control group, quinoa and two -septic twin can significantly reduce the level of blood glucose (P <0.05), 30, 60, 90, and 120 min after giving sugar, which is similar to the normal control group level. The AUC of the quinoa group and the two -metal dual -tadpoles is significantly smaller than the model control group in the 6th and 12th weeks (P <0.05). The results showed that quinoa reduced the FBG of obese mice and improved insulin sensitivity. As shown in Figure 2C, the level of obese mice's serum FINS level is significantly higher than normal mice (P <0.01). After 12 weeks of quinoa treatments, the level of serum FINS and FBG (P <0.01, Figure 2D). Taking Quinoa for 12 weeks to strengthen insulin sensitivity.
3. The effect of quinoa on the blood lipids and fat quality of obesity mice
The concentration of serum TG, TC and LDL-C in the obesity model group is significantly higher than that of the control group. Compared with the model control group, the treatment of quinoa and two-meta duality reduces the concentration of serum TG, TC and LDL-C (Figure 3A-C). Compared with the model control group, the concentration of serum HDL-C in the quinoa group and the two-metal dual-tadpoles (P <0.01, Figure 3D). In the 6th and 12th weeks, the fat content of the model control group is about twice the normal control group (P <0.05). In the 6th and 12th weeks, the treatment of quinoa reduced the amount of fat (P <0.05) compared with the model control group. Compared with the model control group, the dual -dual -dual -double also significantly reduces the amount of fat (P <0.05) (Figure 3E, F). The results show that quinoa can inhibit the accumulation of fat mice fed by HFD and has time dependence.
3. The effect of quinoa on the oxidation stress and liver function of obesity mice
As shown in Figure 4A, HFD induced the MDA content in the serum of obesity mice is significantly higher than normal mice (P <0.05), and GSH activity was significantly lower than normal mice (P <0.05, 4B). After 12 weeks of intervention, quinoa can effectively reduce the serum MDA content (P <0.05) and improve GSH activity (P <0.01). In addition, we observe the impact of quinoa on obese mice and liver and kidney function. As shown in Figure 4C and D, the liver function -related indicators of obese mice are significantly higher than normal mice (P <0.05). After 12 weeks of administration, the quinoa group and the two -metal dual -dual -tadpole group can significantly reduce the serum AlT and AST content (P <0.05), which shows that quinoa supplements can reduce liver cell damage to a certain extent. Similar phenomena were found in the kidneys ((Figure 4E, F). After 12 weeks of intervention, quinoa can significantly reduce serum urea nitrogen and creatinine levels, and have good kidney protection effect while resisting to obesity. Figure 4G. Normal mice's liver and lobular structure are clear, liver cables are arranged in the center of the central vein, and liver cell arrangement is arranged. Compared with normal mice, the liver structure of obesity mice is not treated Cell hypertrophy, lymphocyte infiltration and microvascular fat degeneration. After 12 weeks of treatment of quinoa treatment, the tissue pathological performance of the liver tissue has been improved.
4. The expression of EIF2α and GRP78 of phosphorylation in liver immunohistochemistry
Observe GRP78 (Figure 5A, B) and P-EIF2α (Figure 5C, D) expression. Compared with normal ICR mice, obese mice P-EIF2α (Figure 5D) and GRP78 (Figure 5B) have increased. After 12 weeks of quinoa treatment, EIF2α and GRP78 in the liver IHC decreased.
5. The expression of P-EIF2α, GRP78 and CHOP protein in obesity mice
The expression of P-EIF2α, GRP78 and Chop in obese mice than normal mice (Figure 6). Compared with the unused T2DM mice, after the treatment of quinoa, the expression of all internal quality networks should be reduced.
6. The effect of quinoa on the expression of mRNA expression on obesity mice internal quality network
As shown in Figure 7, the relative expression volume of the obese model group GRP78, EIF2α, and Chop MRNA is significantly higher than that of the control group (P <0.01). Compared with obese mice that have not taken medicine, quinoa treatment has reduced gene expression of EIF2+, GRP78 and Chop. In particular, 12 weeks of low -dose quinoa treatment have significantly reduced the relative expression of EIF2+, GRP78 and Chop (P <0.01).
In summary, quinoa diet can significantly reduce blood glucose, triglyceride, cholesterol, and low density lipoprotein levels, improve glucose tolerance, and improve the tissue changes of obese mouse liver tissues. In addition, quinoa can improve oxidation stress indicators such as GSH and MDA. In addition, quinoa can reduce the expression of EIF2+, GRP78 and Chop’s MRNA expression in the liver stress label of obesity mice.
In general, our research results show that high -fat consumption can change the steady state of the liver network. In addition, the results of the study show that quinoa treatment can reduce weight and body fat, and improve the blood glucose and blood lipid distribution of high -fat diets inducing obesity mice models. Its potential mechanism is related to quinoa through EIF2α, GRP78, and CHOP to regulate the internal quality of the liver tissue. Therefore, we believe that quinoa has the potential to become a drug that treats obesity and its related metabolic abnormalities, including hyperlipidemia, hyperglycemia and insulin resistance.
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Original source:
An et al. Supplementation of quinoa regulaters GlyColipid Metabolism and Endoplasmic Reticulum Stress in the High-Fat Diet-Induced FEMALED FEMALED FEMALED.
https://doi.org/10.1186/s12986-021-00622-8
