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Dietary Tomato Pectin Attenuates Hepatic Insulin Resistance and Inflammation in High-Fat-Diet Mice by Regulating the PI3K/AKT Pathway
Chronic metabolic disease is a serious global health issue, which is accompanied by impaired insulin resistance. Tomato pectin (TP) is a naturally soluble complex hetero-polysaccharide with various biological functions. However, the impact of TP on hepatic insulin resistance in a high-fat diet (HFD)...
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Published in: | Foods 2024-01, Vol.13 (3), p.444 |
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description | Chronic metabolic disease is a serious global health issue, which is accompanied by impaired insulin resistance. Tomato pectin (TP) is a naturally soluble complex hetero-polysaccharide with various biological functions. However, the impact of TP on hepatic insulin resistance in a high-fat diet (HFD) and its potential mechanism remains largely unknown. The results revealed that TP treatment significantly decreased the liver weight, hepatic fat accumulation and hepatic injury in HFD-fed mice. TP also improved fasting blood glucose levels and glucose tolerance in HFD-fed mice. The underlying mechanisms involved in the inflammation, oxidative stress and insulin signaling in the liver were also investigated by RT-qPCR and western blot, which indicated that TP ameliorated hepatic insulin resistance by regulating the PI3K/AKT/GSK-3β pathway, increasing the expression of GLUT4, decreasing the expression of PECK and G6P as well as restoring antioxidant activities and suppressing the inflammation statues in HFD-fed mice. Our data showed that dietary TP has profound effects on hepatic insulin resistance, inflammation and oxidative stress, demonstrating that TP might be a promising therapeutic agent against insulin resistance and related chronic metabolic disease. |
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Tomato pectin (TP) is a naturally soluble complex hetero-polysaccharide with various biological functions. However, the impact of TP on hepatic insulin resistance in a high-fat diet (HFD) and its potential mechanism remains largely unknown. The results revealed that TP treatment significantly decreased the liver weight, hepatic fat accumulation and hepatic injury in HFD-fed mice. TP also improved fasting blood glucose levels and glucose tolerance in HFD-fed mice. The underlying mechanisms involved in the inflammation, oxidative stress and insulin signaling in the liver were also investigated by RT-qPCR and western blot, which indicated that TP ameliorated hepatic insulin resistance by regulating the PI3K/AKT/GSK-3β pathway, increasing the expression of GLUT4, decreasing the expression of PECK and G6P as well as restoring antioxidant activities and suppressing the inflammation statues in HFD-fed mice. Our data showed that dietary TP has profound effects on hepatic insulin resistance, inflammation and oxidative stress, demonstrating that TP might be a promising therapeutic agent against insulin resistance and related chronic metabolic disease.</description><identifier>ISSN: 2304-8158</identifier><identifier>EISSN: 2304-8158</identifier><identifier>DOI: 10.3390/foods13030444</identifier><identifier>PMID: 38338579</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Blood levels ; Blood sugar ; Diet ; Ethylenediaminetetraacetic acid ; Global health ; Glucose ; Glucose tolerance ; Health aspects ; High fat diet ; Homeostasis ; Inflammation ; Insulin ; Insulin resistance ; Kinases ; Laboratory animals ; Lipids ; Liver ; Liver diseases ; Metabolic disorders ; Obesity ; Oils & fats ; Oxidation resistance ; Oxidative stress ; Pectin ; Pharmacology ; PI3K/AKT pathway ; Polysaccharides ; Proteins ; Public health ; tomato pectin ; Tomatoes ; Tumor necrosis factor-TNF ; World health</subject><ispartof>Foods, 2024-01, Vol.13 (3), p.444</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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Tomato pectin (TP) is a naturally soluble complex hetero-polysaccharide with various biological functions. However, the impact of TP on hepatic insulin resistance in a high-fat diet (HFD) and its potential mechanism remains largely unknown. The results revealed that TP treatment significantly decreased the liver weight, hepatic fat accumulation and hepatic injury in HFD-fed mice. TP also improved fasting blood glucose levels and glucose tolerance in HFD-fed mice. The underlying mechanisms involved in the inflammation, oxidative stress and insulin signaling in the liver were also investigated by RT-qPCR and western blot, which indicated that TP ameliorated hepatic insulin resistance by regulating the PI3K/AKT/GSK-3β pathway, increasing the expression of GLUT4, decreasing the expression of PECK and G6P as well as restoring antioxidant activities and suppressing the inflammation statues in HFD-fed mice. Our data showed that dietary TP has profound effects on hepatic insulin resistance, inflammation and oxidative stress, demonstrating that TP might be a promising therapeutic agent against insulin resistance and related chronic metabolic disease.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Blood levels</subject><subject>Blood sugar</subject><subject>Diet</subject><subject>Ethylenediaminetetraacetic acid</subject><subject>Global health</subject><subject>Glucose</subject><subject>Glucose tolerance</subject><subject>Health aspects</subject><subject>High fat diet</subject><subject>Homeostasis</subject><subject>Inflammation</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Lipids</subject><subject>Liver</subject><subject>Liver diseases</subject><subject>Metabolic disorders</subject><subject>Obesity</subject><subject>Oils & fats</subject><subject>Oxidation resistance</subject><subject>Oxidative stress</subject><subject>Pectin</subject><subject>Pharmacology</subject><subject>PI3K/AKT pathway</subject><subject>Polysaccharides</subject><subject>Proteins</subject><subject>Public health</subject><subject>tomato pectin</subject><subject>Tomatoes</subject><subject>Tumor necrosis factor-TNF</subject><subject>World health</subject><issn>2304-8158</issn><issn>2304-8158</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptklFv0zAQxyMEYtPYI6_IEi-8ZHPspIkfq8FotSEqVJ6ji31uXSV2iR2hfgC-N1c6BkPYlu5097u_ffJl2euCX0mp-LUNwcRCcsnLsnyWnQty8qaomud_-WfZZYw7TksVspHiZXZGRjZVrc6zH-8dJhgPbB0GSIGtUCfn2Twl9BMkjGyBe0hOs6WPU0-pLxhdTOA1MvCGwraHgWpd8IzSC7fZ5reQ8qMw--QI6w5UtJl6YvyGpS2y1VLeXc_v1mwFafsdDq-yFxb6iJcP9iL7evthfbPI7z9_XN7M73NdKplyqLXVWhrFqwoUgNCFLbqZrQ0HtGg5qAZVB6YSsjHEYaOsBVHPatVZRHmRLU-6JsCu3Y9uoNbbAK79FQjjpoWRmu2x7QrUNQJCaXSJ3KpO1I0uhSq56BQa0np30tqP4duEMbWDixr7HjyGKbZCiYrLGR1C3_6D7sI0eur0SElVylrJP9QG6H7nbUgj6KNoO68bwRWnLyfq6j8UbYOD08GjdRR_UpCfCvQYYhzRPvZd8PY4Re2TKSL-zcNjp25A80j_nhn5Ez21wq0</recordid><startdate>20240101</startdate><enddate>20240101</enddate><creator>Sun, Jing</creator><creator>Wu, Kongyan</creator><creator>Wang, Pan</creator><creator>Wang, Yubin</creator><creator>Wang, Dan</creator><creator>Zhao, Wenting</creator><creator>Zhao, Yuanyuan</creator><creator>Zhang, Chunhong</creator><creator>Zhao, Xiaoyan</creator><general>MDPI AG</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QR</scope><scope>7T7</scope><scope>7X2</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>HCIFZ</scope><scope>M0K</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20240101</creationdate><title>Dietary Tomato Pectin Attenuates Hepatic Insulin Resistance and Inflammation in High-Fat-Diet Mice by Regulating the PI3K/AKT Pathway</title><author>Sun, Jing ; 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Tomato pectin (TP) is a naturally soluble complex hetero-polysaccharide with various biological functions. However, the impact of TP on hepatic insulin resistance in a high-fat diet (HFD) and its potential mechanism remains largely unknown. The results revealed that TP treatment significantly decreased the liver weight, hepatic fat accumulation and hepatic injury in HFD-fed mice. TP also improved fasting blood glucose levels and glucose tolerance in HFD-fed mice. The underlying mechanisms involved in the inflammation, oxidative stress and insulin signaling in the liver were also investigated by RT-qPCR and western blot, which indicated that TP ameliorated hepatic insulin resistance by regulating the PI3K/AKT/GSK-3β pathway, increasing the expression of GLUT4, decreasing the expression of PECK and G6P as well as restoring antioxidant activities and suppressing the inflammation statues in HFD-fed mice. Our data showed that dietary TP has profound effects on hepatic insulin resistance, inflammation and oxidative stress, demonstrating that TP might be a promising therapeutic agent against insulin resistance and related chronic metabolic disease.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>38338579</pmid><doi>10.3390/foods13030444</doi><oa>free_for_read</oa></addata></record> |
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subjects | 1-Phosphatidylinositol 3-kinase AKT protein Blood levels Blood sugar Diet Ethylenediaminetetraacetic acid Global health Glucose Glucose tolerance Health aspects High fat diet Homeostasis Inflammation Insulin Insulin resistance Kinases Laboratory animals Lipids Liver Liver diseases Metabolic disorders Obesity Oils & fats Oxidation resistance Oxidative stress Pectin Pharmacology PI3K/AKT pathway Polysaccharides Proteins Public health tomato pectin Tomatoes Tumor necrosis factor-TNF World health |
title | Dietary Tomato Pectin Attenuates Hepatic Insulin Resistance and Inflammation in High-Fat-Diet Mice by Regulating the PI3K/AKT Pathway |
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