Wheat germ supplementation alleviates insulin resistance and cardiac mitochondrial dysfunction in an animal model of diet-induced obesity
Obesity is strongly associated with insulin resistance (IR), along with mitochondrial dysfunction to metabolically active tissues and increased production of reactive O2 species (ROS). Foods rich in antioxidants such as wheat germ (WG), protect tissues from damage due to ROS and modulate some negati...
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| Veröffentlicht in: | British journal of nutrition 2017-08, Vol.118 (4), p.241-249 |
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| creator | Ojo, Babajide Simenson, Ashley J. O’Hara, Crystal Wu, Lei Gou, Xin Peterson, Sandra K. Lin, Daniel Smith, Brenda J. Lucas, Edralin A. |
| description | Obesity is strongly associated with insulin resistance (IR), along with mitochondrial dysfunction to metabolically active tissues and increased production of reactive O2 species (ROS). Foods rich in antioxidants such as wheat germ (WG), protect tissues from damage due to ROS and modulate some negative effects of obesity. This study examined the effects of WG supplementation on markers of IR, mitochondrial substrate metabolism and innate antioxidant markers in two metabolically active tissues (i.e. liver and heart) of C57BL/6 mice fed a high-fat–high-sucrose (HFS) diet. Male C57BL/6 mice, 6-week-old, were randomised into four dietary treatment groups (n 12 mice/group): control (C, 10 % fat kcal), C+10 % WG, HFS (60 % fat kcal) or HFS+10 % WG (HFS+WG). After 12 weeks of treatment, HFS+WG mice had significantly less visceral fat (−16 %, P=0·006) compared with the HFS group. WG significantly reduced serum insulin (P=0·009), the insulinotropic hormone, gastric inhibitory peptide (P=0·0003), and the surrogate measure of IR, homoeostatic model assessment of IR (P=0·006). HFS diet significantly elevated (45 %, P=0·02) cardiac complex 2 mitochondrial VO2, suggesting increased metabolic stress, whereas WG stabilised this effect to the level of control. Consequently, genes which mediate antioxidant defense and mitochondrial biogenesis (superoxide dismutase 2 (Sod2) and PPARγ coactivator 1-α (Pgc1a), respectively) were significantly reduced (P |
| doi_str_mv | 10.1017/S0007114517002082 |
| format | Article |
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Foods rich in antioxidants such as wheat germ (WG), protect tissues from damage due to ROS and modulate some negative effects of obesity. This study examined the effects of WG supplementation on markers of IR, mitochondrial substrate metabolism and innate antioxidant markers in two metabolically active tissues (i.e. liver and heart) of C57BL/6 mice fed a high-fat–high-sucrose (HFS) diet. Male C57BL/6 mice, 6-week-old, were randomised into four dietary treatment groups (n 12 mice/group): control (C, 10 % fat kcal), C+10 % WG, HFS (60 % fat kcal) or HFS+10 % WG (HFS+WG). After 12 weeks of treatment, HFS+WG mice had significantly less visceral fat (−16 %, P=0·006) compared with the HFS group. WG significantly reduced serum insulin (P=0·009), the insulinotropic hormone, gastric inhibitory peptide (P=0·0003), and the surrogate measure of IR, homoeostatic model assessment of IR (P=0·006). HFS diet significantly elevated (45 %, P=0·02) cardiac complex 2 mitochondrial VO2, suggesting increased metabolic stress, whereas WG stabilised this effect to the level of control. Consequently, genes which mediate antioxidant defense and mitochondrial biogenesis (superoxide dismutase 2 (Sod2) and PPARγ coactivator 1-α (Pgc1a), respectively) were significantly reduced (P<0·05) in the heart of the HFS group, whereas WG supplementation tended to up-regulate both genes. WG significantly increased hepatic gene expression of Sod2 (P=0·048) but not Pgc1a. Together, these results showed that WG supplementation in HFS diet, reduced IR and improved cardiac mitochondrial metabolic functions.</description><identifier>ISSN: 0007-1145</identifier><identifier>EISSN: 1475-2662</identifier><identifier>DOI: 10.1017/S0007114517002082</identifier><identifier>PMID: 28875871</identifier><language>eng</language><publisher>Cambridge, UK: Cambridge University Press</publisher><subject>Animal models ; Animals ; Antioxidants ; Antioxidants - metabolism ; Antioxidants - pharmacology ; Antioxidants - therapeutic use ; Cholesterol ; Diabetes ; Diet ; Diet, High-Fat ; Dietary Supplements ; Disease Models, Animal ; Drug dosages ; Fatty acids ; Gastric Inhibitory Polypeptide - blood ; Gene expression ; Gene Expression - drug effects ; Genes ; Glucose ; Heart ; Heart - drug effects ; High fat diet ; Insulin ; Insulin - blood ; Insulin Resistance ; Intra-Abdominal Fat - metabolism ; Laboratory animals ; Lipids ; Liver ; Liver - drug effects ; Liver - metabolism ; Male ; Markers ; Metabolism ; Metabolism and Metabolic Studies ; Mice ; Mice, Inbred C57BL ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; Musculoskeletal system ; Myocardium - metabolism ; Obesity ; Obesity - complications ; Obesity - drug therapy ; Obesity - etiology ; Obesity - metabolism ; Oxidative stress ; Oxidative Stress - drug effects ; Peptides ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism ; Plant Preparations - pharmacology ; Plant Preparations - therapeutic use ; Reactive Oxygen Species ; Substrates ; Sucrose ; Sugar ; Superoxide dismutase ; Superoxide Dismutase - genetics ; Superoxide Dismutase - metabolism ; Triticum ; Wheat ; Wheat germ</subject><ispartof>British journal of nutrition, 2017-08, Vol.118 (4), p.241-249</ispartof><rights>Copyright © The Authors 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c373t-d9a708f1dcd7d64e310b88ff2ded31663392c29a0ef2a1d2c89acf409438eace3</citedby><cites>FETCH-LOGICAL-c373t-d9a708f1dcd7d64e310b88ff2ded31663392c29a0ef2a1d2c89acf409438eace3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.cambridge.org/core/product/identifier/S0007114517002082/type/journal_article$$EHTML$$P50$$Gcambridge$$H</linktohtml><link.rule.ids>164,314,776,780,27901,27902,55603</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28875871$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ojo, Babajide</creatorcontrib><creatorcontrib>Simenson, Ashley J.</creatorcontrib><creatorcontrib>O’Hara, Crystal</creatorcontrib><creatorcontrib>Wu, Lei</creatorcontrib><creatorcontrib>Gou, Xin</creatorcontrib><creatorcontrib>Peterson, Sandra K.</creatorcontrib><creatorcontrib>Lin, Daniel</creatorcontrib><creatorcontrib>Smith, Brenda J.</creatorcontrib><creatorcontrib>Lucas, Edralin A.</creatorcontrib><title>Wheat germ supplementation alleviates insulin resistance and cardiac mitochondrial dysfunction in an animal model of diet-induced obesity</title><title>British journal of nutrition</title><addtitle>Br J Nutr</addtitle><description>Obesity is strongly associated with insulin resistance (IR), along with mitochondrial dysfunction to metabolically active tissues and increased production of reactive O2 species (ROS). Foods rich in antioxidants such as wheat germ (WG), protect tissues from damage due to ROS and modulate some negative effects of obesity. This study examined the effects of WG supplementation on markers of IR, mitochondrial substrate metabolism and innate antioxidant markers in two metabolically active tissues (i.e. liver and heart) of C57BL/6 mice fed a high-fat–high-sucrose (HFS) diet. Male C57BL/6 mice, 6-week-old, were randomised into four dietary treatment groups (n 12 mice/group): control (C, 10 % fat kcal), C+10 % WG, HFS (60 % fat kcal) or HFS+10 % WG (HFS+WG). After 12 weeks of treatment, HFS+WG mice had significantly less visceral fat (−16 %, P=0·006) compared with the HFS group. WG significantly reduced serum insulin (P=0·009), the insulinotropic hormone, gastric inhibitory peptide (P=0·0003), and the surrogate measure of IR, homoeostatic model assessment of IR (P=0·006). HFS diet significantly elevated (45 %, P=0·02) cardiac complex 2 mitochondrial VO2, suggesting increased metabolic stress, whereas WG stabilised this effect to the level of control. Consequently, genes which mediate antioxidant defense and mitochondrial biogenesis (superoxide dismutase 2 (Sod2) and PPARγ coactivator 1-α (Pgc1a), respectively) were significantly reduced (P<0·05) in the heart of the HFS group, whereas WG supplementation tended to up-regulate both genes. WG significantly increased hepatic gene expression of Sod2 (P=0·048) but not Pgc1a. Together, these results showed that WG supplementation in HFS diet, reduced IR and improved cardiac mitochondrial metabolic functions.</description><subject>Animal models</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - metabolism</subject><subject>Antioxidants - pharmacology</subject><subject>Antioxidants - therapeutic use</subject><subject>Cholesterol</subject><subject>Diabetes</subject><subject>Diet</subject><subject>Diet, High-Fat</subject><subject>Dietary Supplements</subject><subject>Disease Models, Animal</subject><subject>Drug dosages</subject><subject>Fatty acids</subject><subject>Gastric Inhibitory Polypeptide - blood</subject><subject>Gene expression</subject><subject>Gene Expression - drug effects</subject><subject>Genes</subject><subject>Glucose</subject><subject>Heart</subject><subject>Heart - drug effects</subject><subject>High fat diet</subject><subject>Insulin</subject><subject>Insulin - blood</subject><subject>Insulin Resistance</subject><subject>Intra-Abdominal Fat - metabolism</subject><subject>Laboratory animals</subject><subject>Lipids</subject><subject>Liver</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Markers</subject><subject>Metabolism</subject><subject>Metabolism and Metabolic Studies</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Musculoskeletal system</subject><subject>Myocardium - metabolism</subject><subject>Obesity</subject><subject>Obesity - complications</subject><subject>Obesity - drug therapy</subject><subject>Obesity - etiology</subject><subject>Obesity - metabolism</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Peptides</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism</subject><subject>Plant Preparations - pharmacology</subject><subject>Plant Preparations - therapeutic use</subject><subject>Reactive Oxygen Species</subject><subject>Substrates</subject><subject>Sucrose</subject><subject>Sugar</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - genetics</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Triticum</subject><subject>Wheat</subject><subject>Wheat germ</subject><issn>0007-1145</issn><issn>1475-2662</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kU1rFTEUhoMo9lr9AW4k4MbN2HzMTJKllFqFgosqLodzkzNtSia5Jhnh_gT_tbntVUERAiG8z_sk4RDykrO3nHF1ds0YU5z3A1eMCabFI7LhvRo6MY7iMdkc4u6Qn5Bnpdy1o-bMPCUnQms1aMU35MfXW4RKbzAvtKy7XcAFY4XqU6QQAn73ULFQH8safKQZiy8VokUK0VEL2XmwdPE12dsUXfYQqNuXeY323tE6cFh-acGSHAaaZuo81s5Ht1p0NG2btO6fkyczhIIvjvsp-fL-4vP5h-7q0-XH83dXnZVK1s4ZUEzP3Fmn3Nij5Gyr9TwLh07ycZTSCCsMMJwFcCesNmDnnpleagSL8pS8efDucvq2YqnT4ovFECBiWsvEjRzFOIxKNfT1X-hdWnNsr5tEw4wZhBkaxR8om1MpGedpl9t3837ibDrMafpnTq3z6mhetwu6341fg2mAPEph2WbvbvDP3f_X_gRt-Z-d</recordid><startdate>20170801</startdate><enddate>20170801</enddate><creator>Ojo, Babajide</creator><creator>Simenson, Ashley J.</creator><creator>O’Hara, Crystal</creator><creator>Wu, Lei</creator><creator>Gou, Xin</creator><creator>Peterson, Sandra K.</creator><creator>Lin, Daniel</creator><creator>Smith, Brenda J.</creator><creator>Lucas, Edralin A.</creator><general>Cambridge University Press</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>7QP</scope><scope>7RV</scope><scope>7T5</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20170801</creationdate><title>Wheat germ supplementation alleviates insulin resistance and cardiac mitochondrial dysfunction in an animal model of diet-induced obesity</title><author>Ojo, Babajide ; Simenson, Ashley J. ; O’Hara, Crystal ; Wu, Lei ; Gou, Xin ; Peterson, Sandra K. ; Lin, Daniel ; Smith, Brenda J. ; Lucas, Edralin A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c373t-d9a708f1dcd7d64e310b88ff2ded31663392c29a0ef2a1d2c89acf409438eace3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animal models</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Antioxidants - metabolism</topic><topic>Antioxidants - pharmacology</topic><topic>Antioxidants - therapeutic use</topic><topic>Cholesterol</topic><topic>Diabetes</topic><topic>Diet</topic><topic>Diet, High-Fat</topic><topic>Dietary Supplements</topic><topic>Disease Models, Animal</topic><topic>Drug dosages</topic><topic>Fatty acids</topic><topic>Gastric Inhibitory Polypeptide - blood</topic><topic>Gene expression</topic><topic>Gene Expression - drug effects</topic><topic>Genes</topic><topic>Glucose</topic><topic>Heart</topic><topic>Heart - drug effects</topic><topic>High fat diet</topic><topic>Insulin</topic><topic>Insulin - blood</topic><topic>Insulin Resistance</topic><topic>Intra-Abdominal Fat - metabolism</topic><topic>Laboratory animals</topic><topic>Lipids</topic><topic>Liver</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>Markers</topic><topic>Metabolism</topic><topic>Metabolism and Metabolic Studies</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Musculoskeletal system</topic><topic>Myocardium - metabolism</topic><topic>Obesity</topic><topic>Obesity - complications</topic><topic>Obesity - drug therapy</topic><topic>Obesity - etiology</topic><topic>Obesity - metabolism</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Peptides</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism</topic><topic>Plant Preparations - pharmacology</topic><topic>Plant Preparations - therapeutic use</topic><topic>Reactive Oxygen Species</topic><topic>Substrates</topic><topic>Sucrose</topic><topic>Sugar</topic><topic>Superoxide dismutase</topic><topic>Superoxide Dismutase - genetics</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Triticum</topic><topic>Wheat</topic><topic>Wheat germ</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ojo, Babajide</creatorcontrib><creatorcontrib>Simenson, Ashley J.</creatorcontrib><creatorcontrib>O’Hara, Crystal</creatorcontrib><creatorcontrib>Wu, Lei</creatorcontrib><creatorcontrib>Gou, Xin</creatorcontrib><creatorcontrib>Peterson, Sandra K.</creatorcontrib><creatorcontrib>Lin, Daniel</creatorcontrib><creatorcontrib>Smith, Brenda J.</creatorcontrib><creatorcontrib>Lucas, Edralin A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ojo, Babajide</au><au>Simenson, Ashley J.</au><au>O’Hara, Crystal</au><au>Wu, Lei</au><au>Gou, Xin</au><au>Peterson, Sandra K.</au><au>Lin, Daniel</au><au>Smith, Brenda J.</au><au>Lucas, Edralin A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Wheat germ supplementation alleviates insulin resistance and cardiac mitochondrial dysfunction in an animal model of diet-induced obesity</atitle><jtitle>British journal of nutrition</jtitle><addtitle>Br J Nutr</addtitle><date>2017-08-01</date><risdate>2017</risdate><volume>118</volume><issue>4</issue><spage>241</spage><epage>249</epage><pages>241-249</pages><issn>0007-1145</issn><eissn>1475-2662</eissn><abstract>Obesity is strongly associated with insulin resistance (IR), along with mitochondrial dysfunction to metabolically active tissues and increased production of reactive O2 species (ROS). Foods rich in antioxidants such as wheat germ (WG), protect tissues from damage due to ROS and modulate some negative effects of obesity. This study examined the effects of WG supplementation on markers of IR, mitochondrial substrate metabolism and innate antioxidant markers in two metabolically active tissues (i.e. liver and heart) of C57BL/6 mice fed a high-fat–high-sucrose (HFS) diet. Male C57BL/6 mice, 6-week-old, were randomised into four dietary treatment groups (n 12 mice/group): control (C, 10 % fat kcal), C+10 % WG, HFS (60 % fat kcal) or HFS+10 % WG (HFS+WG). After 12 weeks of treatment, HFS+WG mice had significantly less visceral fat (−16 %, P=0·006) compared with the HFS group. WG significantly reduced serum insulin (P=0·009), the insulinotropic hormone, gastric inhibitory peptide (P=0·0003), and the surrogate measure of IR, homoeostatic model assessment of IR (P=0·006). HFS diet significantly elevated (45 %, P=0·02) cardiac complex 2 mitochondrial VO2, suggesting increased metabolic stress, whereas WG stabilised this effect to the level of control. Consequently, genes which mediate antioxidant defense and mitochondrial biogenesis (superoxide dismutase 2 (Sod2) and PPARγ coactivator 1-α (Pgc1a), respectively) were significantly reduced (P<0·05) in the heart of the HFS group, whereas WG supplementation tended to up-regulate both genes. WG significantly increased hepatic gene expression of Sod2 (P=0·048) but not Pgc1a. Together, these results showed that WG supplementation in HFS diet, reduced IR and improved cardiac mitochondrial metabolic functions.</abstract><cop>Cambridge, UK</cop><pub>Cambridge University Press</pub><pmid>28875871</pmid><doi>10.1017/S0007114517002082</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0007-1145 |
| ispartof | British journal of nutrition, 2017-08, Vol.118 (4), p.241-249 |
| issn | 0007-1145 1475-2662 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1936265677 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Cambridge Journals; Free Full-Text Journals in Chemistry |
| subjects | Animal models Animals Antioxidants Antioxidants - metabolism Antioxidants - pharmacology Antioxidants - therapeutic use Cholesterol Diabetes Diet Diet, High-Fat Dietary Supplements Disease Models, Animal Drug dosages Fatty acids Gastric Inhibitory Polypeptide - blood Gene expression Gene Expression - drug effects Genes Glucose Heart Heart - drug effects High fat diet Insulin Insulin - blood Insulin Resistance Intra-Abdominal Fat - metabolism Laboratory animals Lipids Liver Liver - drug effects Liver - metabolism Male Markers Metabolism Metabolism and Metabolic Studies Mice Mice, Inbred C57BL Mitochondria Mitochondria - drug effects Mitochondria - metabolism Musculoskeletal system Myocardium - metabolism Obesity Obesity - complications Obesity - drug therapy Obesity - etiology Obesity - metabolism Oxidative stress Oxidative Stress - drug effects Peptides Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism Plant Preparations - pharmacology Plant Preparations - therapeutic use Reactive Oxygen Species Substrates Sucrose Sugar Superoxide dismutase Superoxide Dismutase - genetics Superoxide Dismutase - metabolism Triticum Wheat Wheat germ |
| title | Wheat germ supplementation alleviates insulin resistance and cardiac mitochondrial dysfunction in an animal model of diet-induced obesity |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-13T21%3A12%3A28IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Wheat%20germ%20supplementation%20alleviates%20insulin%20resistance%20and%20cardiac%20mitochondrial%20dysfunction%20in%20an%20animal%20model%20of%20diet-induced%20obesity&rft.jtitle=British%20journal%20of%20nutrition&rft.au=Ojo,%20Babajide&rft.date=2017-08-01&rft.volume=118&rft.issue=4&rft.spage=241&rft.epage=249&rft.pages=241-249&rft.issn=0007-1145&rft.eissn=1475-2662&rft_id=info:doi/10.1017/S0007114517002082&rft_dat=%3Cproquest_cross%3E1936265677%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2193995295&rft_id=info:pmid/28875871&rft_cupid=10_1017_S0007114517002082&rfr_iscdi=true |