The mechanism exploration of the non‐colonic toxicity and obesity inhibition of food‐grade κ‐carrageenan by transcriptome
Abstract Previous study has suggested the colonic nontoxicity and obesity inhibition of food‐grade κ‐carrageenan in obese mice. Further study using transcriptome is important to provide further understanding on the gene expressions of inflammation and obesity. Here, the obese mice without any treatm...
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2021
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oai:doaj.org-article:7fb8766cf0ca4bf5960290114c9736a12021-11-04T13:06:43ZThe mechanism exploration of the non‐colonic toxicity and obesity inhibition of food‐grade κ‐carrageenan by transcriptome2048-717710.1002/fsn3.2581https://doaj.org/article/7fb8766cf0ca4bf5960290114c9736a12021-11-01T00:00:00Zhttps://doi.org/10.1002/fsn3.2581https://doaj.org/toc/2048-7177Abstract Previous study has suggested the colonic nontoxicity and obesity inhibition of food‐grade κ‐carrageenan in obese mice. Further study using transcriptome is important to provide further understanding on the gene expressions of inflammation and obesity. Here, the obese mice without any treatment (HFD) or with 5% food‐grade κ‐carrageenan diet intervention (H5%) were used to perform colonic transcriptome sequencing. The results showed that genes involved in the inflammatory pathways or tight junction protein encoding were not significantly dysregulated by 5% carrageenan. However, the expression of lipid metabolism genes meaningfully changed as evidenced by the decreased gene levels of adipocytokines, lipogenesis, lipid absorption and transport, and the increased adipolysis and oxidation. In addition, the carrageenan metabolism experiments by toluidine blue (TB) staining of colon and high‐performance size exclusion chromatography (HPSEC) of feces supernatant showed that the food‐grade κ‐carrageenan was not absorbed or significantly degraded in the digestive tract of obese mice. Hence, the fact that food‐grade κ‐carrageenan was not significantly metabolized by the organism and did not cause obvious dysregulation of colonic inflammatory genes provided evidences for its noncolonic toxicity in obese mice. An anti‐obesity potential of food‐grade κ‐carrageenan was probably mediated by the regulation of lipids metabolism‐related genes.Hui ZhangWanxiu CaoFang LiuYuan GaoYaoguang ChangChanghu XueQingjuan TangWileyarticleanti‐obesitycarrageenan metabolismcolitisdegradationfat accumulationfood‐grade κ‐carrageenanNutrition. Foods and food supplyTX341-641ENFood Science & Nutrition, Vol 9, Iss 11, Pp 6232-6244 (2021) |
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anti‐obesity carrageenan metabolism colitis degradation fat accumulation food‐grade κ‐carrageenan Nutrition. Foods and food supply TX341-641 |
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anti‐obesity carrageenan metabolism colitis degradation fat accumulation food‐grade κ‐carrageenan Nutrition. Foods and food supply TX341-641 Hui Zhang Wanxiu Cao Fang Liu Yuan Gao Yaoguang Chang Changhu Xue Qingjuan Tang The mechanism exploration of the non‐colonic toxicity and obesity inhibition of food‐grade κ‐carrageenan by transcriptome |
| description |
Abstract Previous study has suggested the colonic nontoxicity and obesity inhibition of food‐grade κ‐carrageenan in obese mice. Further study using transcriptome is important to provide further understanding on the gene expressions of inflammation and obesity. Here, the obese mice without any treatment (HFD) or with 5% food‐grade κ‐carrageenan diet intervention (H5%) were used to perform colonic transcriptome sequencing. The results showed that genes involved in the inflammatory pathways or tight junction protein encoding were not significantly dysregulated by 5% carrageenan. However, the expression of lipid metabolism genes meaningfully changed as evidenced by the decreased gene levels of adipocytokines, lipogenesis, lipid absorption and transport, and the increased adipolysis and oxidation. In addition, the carrageenan metabolism experiments by toluidine blue (TB) staining of colon and high‐performance size exclusion chromatography (HPSEC) of feces supernatant showed that the food‐grade κ‐carrageenan was not absorbed or significantly degraded in the digestive tract of obese mice. Hence, the fact that food‐grade κ‐carrageenan was not significantly metabolized by the organism and did not cause obvious dysregulation of colonic inflammatory genes provided evidences for its noncolonic toxicity in obese mice. An anti‐obesity potential of food‐grade κ‐carrageenan was probably mediated by the regulation of lipids metabolism‐related genes. |
| format |
article |
| author |
Hui Zhang Wanxiu Cao Fang Liu Yuan Gao Yaoguang Chang Changhu Xue Qingjuan Tang |
| author_facet |
Hui Zhang Wanxiu Cao Fang Liu Yuan Gao Yaoguang Chang Changhu Xue Qingjuan Tang |
| author_sort |
Hui Zhang |
| title |
The mechanism exploration of the non‐colonic toxicity and obesity inhibition of food‐grade κ‐carrageenan by transcriptome |
| title_short |
The mechanism exploration of the non‐colonic toxicity and obesity inhibition of food‐grade κ‐carrageenan by transcriptome |
| title_full |
The mechanism exploration of the non‐colonic toxicity and obesity inhibition of food‐grade κ‐carrageenan by transcriptome |
| title_fullStr |
The mechanism exploration of the non‐colonic toxicity and obesity inhibition of food‐grade κ‐carrageenan by transcriptome |
| title_full_unstemmed |
The mechanism exploration of the non‐colonic toxicity and obesity inhibition of food‐grade κ‐carrageenan by transcriptome |
| title_sort |
mechanism exploration of the non‐colonic toxicity and obesity inhibition of food‐grade κ‐carrageenan by transcriptome |
| publisher |
Wiley |
| publishDate |
2021 |
| url |
https://doaj.org/article/7fb8766cf0ca4bf5960290114c9736a1 |
| work_keys_str_mv |
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1718444911779381248 |