Zinc Supplementation and Strength Exercise in Rats with Type 2 Diabetes: Akt and PTP1B Phosphorylation in Nonalcoholic Fatty Liver
Type 2 diabetes mellitus (T2D) is a metabolic disorder caused by chronic hyperglycemia due to a deficiency in the secretion and/or action of insulin. Zinc (Zn) supplementation and strength exercise increases insulin signaling. We evaluate the effect of Zn supplementation and strength exercise on ins...
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| Veröffentlicht in: | Biological trace element research 2021-06, Vol.199 (6), p.2215-2224 |
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| creator | Vivero, Ariel Ruz, Manuel Rivera, Matías Miranda, Karen Sacristán, Camila Espinosa, Alejandra Codoceo, Juana Inostroza, Jorge Vásquez, Karla Pérez, Álvaro García-Díaz, Diego Arredondo, Miguel |
| description | Type 2 diabetes mellitus (T2D) is a metabolic disorder caused by chronic hyperglycemia due to a deficiency in the secretion and/or action of insulin. Zinc (Zn) supplementation and strength exercise increases insulin signaling. We evaluate the effect of Zn supplementation and strength exercise on insulin resistance in the liver of rats with diet-induced T2D through the study of phosphorylation of Akt and protein tyrosine phosphatase 1B (PTP1B). Rats were fed with a high-fat diet (HFD) for 18 weeks to induce T2D and then assigned in four experimental groups: HFD, HFD-Zn (Zn), HFD-strength exercise (Ex), and HFD-Zn/strength exercise (ZnEx) and treated during 12 weeks. Serum Zn, lipid profile, transaminases, glucose, and insulin were measured. In the liver with/without insulin stimuli, total and phosphorylated Akt (pAkt
Ser473
) and PTP1B (pPTP1B
Ser50
) were determined by western blot. Hepatic steatosis was evaluated by histological staining with red oil and intrahepatic triglyceride (IHTG) content. There were no differences in biochemical and body-related variables. The ZnEx group showed a higher level of pAkt, both with/without insulin. The ZnEx group also showed higher levels of pPTP1B with respect to HFD and Zn groups. The ZnEx group had higher levels of pPTP1B than groups treated with insulin. Liver histology showed a better integrity and less IHTG in Ex and ZnEx with respect to the HFD group. The Ex and ZnEx groups had lower IHTG with respect to the HFD group. Our results showed that Zn supplementation and strength exercise together improved insulin signaling and attenuated nonalcoholic liver disease in a T2D rat model. |
| doi_str_mv | 10.1007/s12011-020-02324-3 |
| format | Article |
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Ser473
) and PTP1B (pPTP1B
Ser50
) were determined by western blot. Hepatic steatosis was evaluated by histological staining with red oil and intrahepatic triglyceride (IHTG) content. There were no differences in biochemical and body-related variables. The ZnEx group showed a higher level of pAkt, both with/without insulin. The ZnEx group also showed higher levels of pPTP1B with respect to HFD and Zn groups. The ZnEx group had higher levels of pPTP1B than groups treated with insulin. Liver histology showed a better integrity and less IHTG in Ex and ZnEx with respect to the HFD group. The Ex and ZnEx groups had lower IHTG with respect to the HFD group. Our results showed that Zn supplementation and strength exercise together improved insulin signaling and attenuated nonalcoholic liver disease in a T2D rat model.</description><identifier>ISSN: 0163-4984</identifier><identifier>EISSN: 1559-0720</identifier><identifier>DOI: 10.1007/s12011-020-02324-3</identifier><identifier>PMID: 32939643</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>AKT protein ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Biotechnology ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 2 - metabolism ; Diet ; Diet, High-Fat ; Dietary Supplements ; Evaluation ; Fatty liver ; High fat diet ; Histology ; Hyperglycemia ; Insulin ; Insulin - metabolism ; Insulin Resistance ; Life Sciences ; Lipids ; Liver ; Liver - metabolism ; Liver diseases ; Metabolic disorders ; Non-alcoholic Fatty Liver Disease - metabolism ; Nutrition ; Oncology ; Phosphatase ; Phosphorylation ; Physical Conditioning, Animal ; Protein Tyrosine Phosphatase, Non-Receptor Type 1 - metabolism ; Protein-tyrosine-phosphatase ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Secretion ; Serum ; Signaling ; Steatosis ; Strength ; Triglycerides ; Tyrosine ; Zinc ; Zinc - metabolism ; Zinc - pharmacology</subject><ispartof>Biological trace element research, 2021-06, Vol.199 (6), p.2215-2224</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-2fee627f963180d3078db906ce15b601eadc775ff295cb331d4657177c43d6fb3</citedby><cites>FETCH-LOGICAL-c375t-2fee627f963180d3078db906ce15b601eadc775ff295cb331d4657177c43d6fb3</cites><orcidid>0000-0002-6277-4090</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12011-020-02324-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12011-020-02324-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32939643$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vivero, Ariel</creatorcontrib><creatorcontrib>Ruz, Manuel</creatorcontrib><creatorcontrib>Rivera, Matías</creatorcontrib><creatorcontrib>Miranda, Karen</creatorcontrib><creatorcontrib>Sacristán, Camila</creatorcontrib><creatorcontrib>Espinosa, Alejandra</creatorcontrib><creatorcontrib>Codoceo, Juana</creatorcontrib><creatorcontrib>Inostroza, Jorge</creatorcontrib><creatorcontrib>Vásquez, Karla</creatorcontrib><creatorcontrib>Pérez, Álvaro</creatorcontrib><creatorcontrib>García-Díaz, Diego</creatorcontrib><creatorcontrib>Arredondo, Miguel</creatorcontrib><title>Zinc Supplementation and Strength Exercise in Rats with Type 2 Diabetes: Akt and PTP1B Phosphorylation in Nonalcoholic Fatty Liver</title><title>Biological trace element research</title><addtitle>Biol Trace Elem Res</addtitle><addtitle>Biol Trace Elem Res</addtitle><description>Type 2 diabetes mellitus (T2D) is a metabolic disorder caused by chronic hyperglycemia due to a deficiency in the secretion and/or action of insulin. Zinc (Zn) supplementation and strength exercise increases insulin signaling. We evaluate the effect of Zn supplementation and strength exercise on insulin resistance in the liver of rats with diet-induced T2D through the study of phosphorylation of Akt and protein tyrosine phosphatase 1B (PTP1B). Rats were fed with a high-fat diet (HFD) for 18 weeks to induce T2D and then assigned in four experimental groups: HFD, HFD-Zn (Zn), HFD-strength exercise (Ex), and HFD-Zn/strength exercise (ZnEx) and treated during 12 weeks. Serum Zn, lipid profile, transaminases, glucose, and insulin were measured. In the liver with/without insulin stimuli, total and phosphorylated Akt (pAkt
Ser473
) and PTP1B (pPTP1B
Ser50
) were determined by western blot. Hepatic steatosis was evaluated by histological staining with red oil and intrahepatic triglyceride (IHTG) content. There were no differences in biochemical and body-related variables. The ZnEx group showed a higher level of pAkt, both with/without insulin. The ZnEx group also showed higher levels of pPTP1B with respect to HFD and Zn groups. The ZnEx group had higher levels of pPTP1B than groups treated with insulin. Liver histology showed a better integrity and less IHTG in Ex and ZnEx with respect to the HFD group. The Ex and ZnEx groups had lower IHTG with respect to the HFD group. Our results showed that Zn supplementation and strength exercise together improved insulin signaling and attenuated nonalcoholic liver disease in a T2D rat model.</description><subject>AKT protein</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biotechnology</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diet</subject><subject>Diet, High-Fat</subject><subject>Dietary Supplements</subject><subject>Evaluation</subject><subject>Fatty liver</subject><subject>High fat diet</subject><subject>Histology</subject><subject>Hyperglycemia</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Insulin Resistance</subject><subject>Life Sciences</subject><subject>Lipids</subject><subject>Liver</subject><subject>Liver - metabolism</subject><subject>Liver diseases</subject><subject>Metabolic disorders</subject><subject>Non-alcoholic Fatty Liver Disease - metabolism</subject><subject>Nutrition</subject><subject>Oncology</subject><subject>Phosphatase</subject><subject>Phosphorylation</subject><subject>Physical Conditioning, Animal</subject><subject>Protein Tyrosine Phosphatase, Non-Receptor Type 1 - metabolism</subject><subject>Protein-tyrosine-phosphatase</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Secretion</subject><subject>Serum</subject><subject>Signaling</subject><subject>Steatosis</subject><subject>Strength</subject><subject>Triglycerides</subject><subject>Tyrosine</subject><subject>Zinc</subject><subject>Zinc - metabolism</subject><subject>Zinc - pharmacology</subject><issn>0163-4984</issn><issn>1559-0720</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc1u1DAURi0EokPhBVggS2zYBPwbJ-za0gLSCEZ02LCxHOem45Kxg-0As-XJMU0BiQUL60r2-T5bPgg9puQ5JUS9SJQRSivCSFmciYrfQSsqZVsRxchdtCK05pVoG3GEHqR0TQhVrOX30REvo60FX6Efn5y3-HKephH24LPJLnhsfI8vcwR_lXf4_DtE6xJg5_EHkxP-5sru9jABZviVMx1kSC_xyed8k9tsN_QUb3YhTbsQD-PSWLLvgjejDbswOosvTM4HvHZfIT5E9wYzJnh0O4_Rx4vz7dmbav3-9duzk3VluZK5YgNAzdTQ1pw2pOdENX3XktoClV1NKJjeKiWHgbXSdpzTXtRSUaWs4H09dPwYPVt6pxi-zJCy3rtkYRyNhzAnzYTgTSOpEgV9-g96HeZYnl8oSUWjyv_TQrGFsjGkFGHQU3R7Ew-aEv3LkF4M6WJI3xjSvISe3FbP3R76P5HfSgrAFyCVI38F8e_d_6n9CaokmvY</recordid><startdate>20210601</startdate><enddate>20210601</enddate><creator>Vivero, Ariel</creator><creator>Ruz, Manuel</creator><creator>Rivera, Matías</creator><creator>Miranda, Karen</creator><creator>Sacristán, Camila</creator><creator>Espinosa, Alejandra</creator><creator>Codoceo, Juana</creator><creator>Inostroza, Jorge</creator><creator>Vásquez, Karla</creator><creator>Pérez, Álvaro</creator><creator>García-Díaz, Diego</creator><creator>Arredondo, Miguel</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QH</scope><scope>7QP</scope><scope>7TN</scope><scope>7U7</scope><scope>7UA</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>F1W</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H97</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>L.G</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PCBAR</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6277-4090</orcidid></search><sort><creationdate>20210601</creationdate><title>Zinc Supplementation and Strength Exercise in Rats with Type 2 Diabetes: Akt and PTP1B Phosphorylation in Nonalcoholic Fatty Liver</title><author>Vivero, Ariel ; Ruz, Manuel ; Rivera, Matías ; Miranda, Karen ; Sacristán, Camila ; Espinosa, Alejandra ; Codoceo, Juana ; Inostroza, Jorge ; Vásquez, Karla ; Pérez, Álvaro ; García-Díaz, Diego ; Arredondo, Miguel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-2fee627f963180d3078db906ce15b601eadc775ff295cb331d4657177c43d6fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>AKT protein</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biotechnology</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diet</topic><topic>Diet, High-Fat</topic><topic>Dietary Supplements</topic><topic>Evaluation</topic><topic>Fatty liver</topic><topic>High fat diet</topic><topic>Histology</topic><topic>Hyperglycemia</topic><topic>Insulin</topic><topic>Insulin - metabolism</topic><topic>Insulin Resistance</topic><topic>Life Sciences</topic><topic>Lipids</topic><topic>Liver</topic><topic>Liver - metabolism</topic><topic>Liver diseases</topic><topic>Metabolic disorders</topic><topic>Non-alcoholic Fatty Liver Disease - metabolism</topic><topic>Nutrition</topic><topic>Oncology</topic><topic>Phosphatase</topic><topic>Phosphorylation</topic><topic>Physical Conditioning, Animal</topic><topic>Protein Tyrosine Phosphatase, Non-Receptor Type 1 - metabolism</topic><topic>Protein-tyrosine-phosphatase</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>Secretion</topic><topic>Serum</topic><topic>Signaling</topic><topic>Steatosis</topic><topic>Strength</topic><topic>Triglycerides</topic><topic>Tyrosine</topic><topic>Zinc</topic><topic>Zinc - 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Academic</collection><jtitle>Biological trace element research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vivero, Ariel</au><au>Ruz, Manuel</au><au>Rivera, Matías</au><au>Miranda, Karen</au><au>Sacristán, Camila</au><au>Espinosa, Alejandra</au><au>Codoceo, Juana</au><au>Inostroza, Jorge</au><au>Vásquez, Karla</au><au>Pérez, Álvaro</au><au>García-Díaz, Diego</au><au>Arredondo, Miguel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Zinc Supplementation and Strength Exercise in Rats with Type 2 Diabetes: Akt and PTP1B Phosphorylation in Nonalcoholic Fatty Liver</atitle><jtitle>Biological trace element research</jtitle><stitle>Biol Trace Elem Res</stitle><addtitle>Biol Trace Elem Res</addtitle><date>2021-06-01</date><risdate>2021</risdate><volume>199</volume><issue>6</issue><spage>2215</spage><epage>2224</epage><pages>2215-2224</pages><issn>0163-4984</issn><eissn>1559-0720</eissn><abstract>Type 2 diabetes mellitus (T2D) is a metabolic disorder caused by chronic hyperglycemia due to a deficiency in the secretion and/or action of insulin. Zinc (Zn) supplementation and strength exercise increases insulin signaling. We evaluate the effect of Zn supplementation and strength exercise on insulin resistance in the liver of rats with diet-induced T2D through the study of phosphorylation of Akt and protein tyrosine phosphatase 1B (PTP1B). Rats were fed with a high-fat diet (HFD) for 18 weeks to induce T2D and then assigned in four experimental groups: HFD, HFD-Zn (Zn), HFD-strength exercise (Ex), and HFD-Zn/strength exercise (ZnEx) and treated during 12 weeks. Serum Zn, lipid profile, transaminases, glucose, and insulin were measured. In the liver with/without insulin stimuli, total and phosphorylated Akt (pAkt
Ser473
) and PTP1B (pPTP1B
Ser50
) were determined by western blot. Hepatic steatosis was evaluated by histological staining with red oil and intrahepatic triglyceride (IHTG) content. There were no differences in biochemical and body-related variables. The ZnEx group showed a higher level of pAkt, both with/without insulin. The ZnEx group also showed higher levels of pPTP1B with respect to HFD and Zn groups. The ZnEx group had higher levels of pPTP1B than groups treated with insulin. Liver histology showed a better integrity and less IHTG in Ex and ZnEx with respect to the HFD group. The Ex and ZnEx groups had lower IHTG with respect to the HFD group. Our results showed that Zn supplementation and strength exercise together improved insulin signaling and attenuated nonalcoholic liver disease in a T2D rat model.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>32939643</pmid><doi>10.1007/s12011-020-02324-3</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-6277-4090</orcidid></addata></record> |
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| subjects | AKT protein Animals Biochemistry Biomedical and Life Sciences Biotechnology Diabetes Diabetes mellitus Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - metabolism Diet Diet, High-Fat Dietary Supplements Evaluation Fatty liver High fat diet Histology Hyperglycemia Insulin Insulin - metabolism Insulin Resistance Life Sciences Lipids Liver Liver - metabolism Liver diseases Metabolic disorders Non-alcoholic Fatty Liver Disease - metabolism Nutrition Oncology Phosphatase Phosphorylation Physical Conditioning, Animal Protein Tyrosine Phosphatase, Non-Receptor Type 1 - metabolism Protein-tyrosine-phosphatase Proto-Oncogene Proteins c-akt - metabolism Rats Secretion Serum Signaling Steatosis Strength Triglycerides Tyrosine Zinc Zinc - metabolism Zinc - pharmacology |
| title | Zinc Supplementation and Strength Exercise in Rats with Type 2 Diabetes: Akt and PTP1B Phosphorylation in Nonalcoholic Fatty Liver |
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