Diet-induced Obese Mice Are Leptin Insufficient After Weight Reduction
Behavioral therapies aimed at reducing excess body fat result in limited fat loss after dieting. To understand the causes for maintenance of adiposity, high‐fat (HF) diet–induced obese (DIO) mice were switched to a low‐fat chow diet, and the effects of chow on histological and molecular alterations...
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Veröffentlicht in: | Obesity (Silver Spring, Md.) Md.), 2009-09, Vol.17 (9), p.1702-1709 |
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description | Behavioral therapies aimed at reducing excess body fat result in limited fat loss after dieting. To understand the causes for maintenance of adiposity, high‐fat (HF) diet–induced obese (DIO) mice were switched to a low‐fat chow diet, and the effects of chow on histological and molecular alterations of adipose tissue and metabolic parameters were examined. DIO mice reduced and stabilized their body weights after being switched to chow (HF‐chow), but retained a greater amount of adiposity than chow‐fed mice. Reduction in adipocyte volume, not number, caused a decrease in fat mass. HF‐chow mice showed normalized circulating insulin and leptin levels, improved glucose tolerance, and reduced inflammatory status in white adipose tissue (WAT). Circulating leptin levels corrected for fat mass were lower in HF‐chow mice. Leptin administration was used to test whether reduced leptin level of HF‐chow mice inhibited further fat loss. Leptin treatment led to an additional reduction in adiposity. Finally, HF‐HF mice had lower mRNA levels of β3 adrenergic receptor (β3‐AR) in epididymal WAT (EWAT) compared to chow‐fed mice, and diet change led to an increase in the WAT β3‐AR mRNA levels that were similar to the levels of chow‐fed mice, suggesting an elevation in sympathetic activation of WAT during diet switch relative to HF‐HF mice leading to the reduced leptin level and proinflammatory cytokine content. In summary, HF‐chow mice were resistant to further fat loss due to leptin insufficiency. Diet alteration from HF to low fat improved metabolic state of DIO mice, although their adiposity was defended at a higher level. |
doi_str_mv | 10.1038/oby.2009.106 |
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Chrissy ; Foster, Michelle T ; Seeley, Randy J ; Reizes, Ofer</creator><creatorcontrib>Shi, Haifei ; Akunuru, Shailaja ; Bierman, John C ; Hodge, Karen M ; Mitchell, M. Chrissy ; Foster, Michelle T ; Seeley, Randy J ; Reizes, Ofer</creatorcontrib><description>Behavioral therapies aimed at reducing excess body fat result in limited fat loss after dieting. To understand the causes for maintenance of adiposity, high‐fat (HF) diet–induced obese (DIO) mice were switched to a low‐fat chow diet, and the effects of chow on histological and molecular alterations of adipose tissue and metabolic parameters were examined. DIO mice reduced and stabilized their body weights after being switched to chow (HF‐chow), but retained a greater amount of adiposity than chow‐fed mice. Reduction in adipocyte volume, not number, caused a decrease in fat mass. HF‐chow mice showed normalized circulating insulin and leptin levels, improved glucose tolerance, and reduced inflammatory status in white adipose tissue (WAT). Circulating leptin levels corrected for fat mass were lower in HF‐chow mice. Leptin administration was used to test whether reduced leptin level of HF‐chow mice inhibited further fat loss. Leptin treatment led to an additional reduction in adiposity. Finally, HF‐HF mice had lower mRNA levels of β3 adrenergic receptor (β3‐AR) in epididymal WAT (EWAT) compared to chow‐fed mice, and diet change led to an increase in the WAT β3‐AR mRNA levels that were similar to the levels of chow‐fed mice, suggesting an elevation in sympathetic activation of WAT during diet switch relative to HF‐HF mice leading to the reduced leptin level and proinflammatory cytokine content. In summary, HF‐chow mice were resistant to further fat loss due to leptin insufficiency. Diet alteration from HF to low fat improved metabolic state of DIO mice, although their adiposity was defended at a higher level.</description><identifier>ISSN: 1930-7381</identifier><identifier>EISSN: 1930-739X</identifier><identifier>DOI: 10.1038/oby.2009.106</identifier><identifier>PMID: 19373220</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adipocytes ; adipose tissue ; Adipose Tissue, Brown - metabolism ; Adipose Tissue, Brown - pathology ; Adipose Tissue, Brown - physiopathology ; Adipose Tissue, White - metabolism ; Adipose Tissue, White - pathology ; Adipose Tissue, White - physiopathology ; Adiposity ; animal models ; Animals ; Blood Glucose - metabolism ; Body fat ; body weight ; Cell Size ; Diet ; Diet, Fat-Restricted ; diet-related diseases ; Dietary Fats - administration & dosage ; Digitization ; Disease Models, Animal ; Eating ; Fatty Liver - etiology ; Fatty Liver - metabolism ; Fatty Liver - physiopathology ; Feeding Behavior ; Glucose ; high fat diet ; Histology ; human diseases ; Inflammation - etiology ; Inflammation - metabolism ; Inflammation - physiopathology ; Insulin - blood ; Insulin resistance ; leptin ; Leptin - blood ; Leptin - deficiency ; low fat diet ; Macrophages - metabolism ; Male ; Metabolism ; Mice ; Mice, Inbred C57BL ; Obesity ; Obesity - diet therapy ; Obesity - etiology ; Obesity - metabolism ; Obesity - physiopathology ; Physiology ; quantitative analysis ; Receptors, Adrenergic, beta-3 - genetics ; RNA, Messenger - metabolism ; Time Factors ; Weight control ; Weight Loss</subject><ispartof>Obesity (Silver Spring, Md.), 2009-09, Vol.17 (9), p.1702-1709</ispartof><rights>2009 North American Association for the Study of Obesity (NAASO)</rights><rights>Copyright Nature Publishing Group Sep 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5420-6c7750645d44d4a4bc2e585120a5e0ccaae6a2fa31cc239968c2bc85652e4c343</citedby><cites>FETCH-LOGICAL-c5420-6c7750645d44d4a4bc2e585120a5e0ccaae6a2fa31cc239968c2bc85652e4c343</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1038%2Foby.2009.106$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1038%2Foby.2009.106$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19373220$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, Haifei</creatorcontrib><creatorcontrib>Akunuru, Shailaja</creatorcontrib><creatorcontrib>Bierman, John C</creatorcontrib><creatorcontrib>Hodge, Karen M</creatorcontrib><creatorcontrib>Mitchell, M. Chrissy</creatorcontrib><creatorcontrib>Foster, Michelle T</creatorcontrib><creatorcontrib>Seeley, Randy J</creatorcontrib><creatorcontrib>Reizes, Ofer</creatorcontrib><title>Diet-induced Obese Mice Are Leptin Insufficient After Weight Reduction</title><title>Obesity (Silver Spring, Md.)</title><addtitle>Obesity (Silver Spring)</addtitle><description>Behavioral therapies aimed at reducing excess body fat result in limited fat loss after dieting. To understand the causes for maintenance of adiposity, high‐fat (HF) diet–induced obese (DIO) mice were switched to a low‐fat chow diet, and the effects of chow on histological and molecular alterations of adipose tissue and metabolic parameters were examined. DIO mice reduced and stabilized their body weights after being switched to chow (HF‐chow), but retained a greater amount of adiposity than chow‐fed mice. Reduction in adipocyte volume, not number, caused a decrease in fat mass. HF‐chow mice showed normalized circulating insulin and leptin levels, improved glucose tolerance, and reduced inflammatory status in white adipose tissue (WAT). Circulating leptin levels corrected for fat mass were lower in HF‐chow mice. Leptin administration was used to test whether reduced leptin level of HF‐chow mice inhibited further fat loss. Leptin treatment led to an additional reduction in adiposity. Finally, HF‐HF mice had lower mRNA levels of β3 adrenergic receptor (β3‐AR) in epididymal WAT (EWAT) compared to chow‐fed mice, and diet change led to an increase in the WAT β3‐AR mRNA levels that were similar to the levels of chow‐fed mice, suggesting an elevation in sympathetic activation of WAT during diet switch relative to HF‐HF mice leading to the reduced leptin level and proinflammatory cytokine content. In summary, HF‐chow mice were resistant to further fat loss due to leptin insufficiency. Diet alteration from HF to low fat improved metabolic state of DIO mice, although their adiposity was defended at a higher level.</description><subject>Adipocytes</subject><subject>adipose tissue</subject><subject>Adipose Tissue, Brown - metabolism</subject><subject>Adipose Tissue, Brown - pathology</subject><subject>Adipose Tissue, Brown - physiopathology</subject><subject>Adipose Tissue, White - metabolism</subject><subject>Adipose Tissue, White - pathology</subject><subject>Adipose Tissue, White - physiopathology</subject><subject>Adiposity</subject><subject>animal models</subject><subject>Animals</subject><subject>Blood Glucose - metabolism</subject><subject>Body fat</subject><subject>body weight</subject><subject>Cell Size</subject><subject>Diet</subject><subject>Diet, Fat-Restricted</subject><subject>diet-related diseases</subject><subject>Dietary Fats - administration & dosage</subject><subject>Digitization</subject><subject>Disease Models, Animal</subject><subject>Eating</subject><subject>Fatty Liver - etiology</subject><subject>Fatty Liver - metabolism</subject><subject>Fatty Liver - physiopathology</subject><subject>Feeding Behavior</subject><subject>Glucose</subject><subject>high fat diet</subject><subject>Histology</subject><subject>human diseases</subject><subject>Inflammation - etiology</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - physiopathology</subject><subject>Insulin - blood</subject><subject>Insulin resistance</subject><subject>leptin</subject><subject>Leptin - blood</subject><subject>Leptin - deficiency</subject><subject>low fat diet</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Obesity</subject><subject>Obesity - diet therapy</subject><subject>Obesity - etiology</subject><subject>Obesity - metabolism</subject><subject>Obesity - physiopathology</subject><subject>Physiology</subject><subject>quantitative analysis</subject><subject>Receptors, Adrenergic, beta-3 - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Time Factors</subject><subject>Weight control</subject><subject>Weight Loss</subject><issn>1930-7381</issn><issn>1930-739X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUtv1DAUhS1ERR-wYw2RkLoi5fqdbJCGQh_SoJGAClhZjnMzdZWJBzsBzb_Hoxm1wIKVfXW_c3ysQ8hzCmcUePUmNJszBlDnST0iR7TmUGpef3t8f6_oITlO6Q5AKJD0CTnMC80ZgyNy8d7jWPqhnRy2xaLBhMVH77CYRSzmuB79UFwPaeo67zwOYzHrRozFV_TL27H4hFk3-jA8JQed7RM-258n5Obiw5fzq3K-uLw-n81LJwWDUjmtJSghWyFaYUXjGMpKUgZWIjhnLSrLOsupc4zXtaoca1wllWQoHBf8hLzd-a6nZoWty4mi7c06-pWNGxOsN39vBn9rluGnEZUSgqlscLo3iOHHhGk0K58c9r0dMEzJKK045JAZfPUPeBemOOTPGQoCKq60rjL1eke5GFKK2N1HoWC29Zhcj9nWk6ft6y_-jP8A7_vIAN0Bv3yPm_-amcW771TyreblTtPZYOwy-mRuPjOgHKhmUkPNfwMVuqMR</recordid><startdate>200909</startdate><enddate>200909</enddate><creator>Shi, Haifei</creator><creator>Akunuru, Shailaja</creator><creator>Bierman, John C</creator><creator>Hodge, Karen M</creator><creator>Mitchell, M. Chrissy</creator><creator>Foster, Michelle T</creator><creator>Seeley, Randy J</creator><creator>Reizes, Ofer</creator><general>Blackwell Publishing Ltd</general><scope>FBQ</scope><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>K9.</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200909</creationdate><title>Diet-induced Obese Mice Are Leptin Insufficient After Weight Reduction</title><author>Shi, Haifei ; Akunuru, Shailaja ; Bierman, John C ; Hodge, Karen M ; Mitchell, M. Chrissy ; Foster, Michelle T ; Seeley, Randy J ; Reizes, Ofer</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5420-6c7750645d44d4a4bc2e585120a5e0ccaae6a2fa31cc239968c2bc85652e4c343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adipocytes</topic><topic>adipose tissue</topic><topic>Adipose Tissue, Brown - metabolism</topic><topic>Adipose Tissue, Brown - pathology</topic><topic>Adipose Tissue, Brown - physiopathology</topic><topic>Adipose Tissue, White - metabolism</topic><topic>Adipose Tissue, White - pathology</topic><topic>Adipose Tissue, White - physiopathology</topic><topic>Adiposity</topic><topic>animal models</topic><topic>Animals</topic><topic>Blood Glucose - metabolism</topic><topic>Body fat</topic><topic>body weight</topic><topic>Cell Size</topic><topic>Diet</topic><topic>Diet, Fat-Restricted</topic><topic>diet-related diseases</topic><topic>Dietary Fats - administration & dosage</topic><topic>Digitization</topic><topic>Disease Models, Animal</topic><topic>Eating</topic><topic>Fatty Liver - etiology</topic><topic>Fatty Liver - metabolism</topic><topic>Fatty Liver - physiopathology</topic><topic>Feeding Behavior</topic><topic>Glucose</topic><topic>high fat diet</topic><topic>Histology</topic><topic>human diseases</topic><topic>Inflammation - etiology</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - physiopathology</topic><topic>Insulin - blood</topic><topic>Insulin resistance</topic><topic>leptin</topic><topic>Leptin - blood</topic><topic>Leptin - deficiency</topic><topic>low fat diet</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Obesity</topic><topic>Obesity - diet therapy</topic><topic>Obesity - etiology</topic><topic>Obesity - metabolism</topic><topic>Obesity - physiopathology</topic><topic>Physiology</topic><topic>quantitative analysis</topic><topic>Receptors, Adrenergic, beta-3 - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Time Factors</topic><topic>Weight control</topic><topic>Weight Loss</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shi, Haifei</creatorcontrib><creatorcontrib>Akunuru, Shailaja</creatorcontrib><creatorcontrib>Bierman, John C</creatorcontrib><creatorcontrib>Hodge, Karen M</creatorcontrib><creatorcontrib>Mitchell, M. 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Chrissy</au><au>Foster, Michelle T</au><au>Seeley, Randy J</au><au>Reizes, Ofer</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Diet-induced Obese Mice Are Leptin Insufficient After Weight Reduction</atitle><jtitle>Obesity (Silver Spring, Md.)</jtitle><addtitle>Obesity (Silver Spring)</addtitle><date>2009-09</date><risdate>2009</risdate><volume>17</volume><issue>9</issue><spage>1702</spage><epage>1709</epage><pages>1702-1709</pages><issn>1930-7381</issn><eissn>1930-739X</eissn><abstract>Behavioral therapies aimed at reducing excess body fat result in limited fat loss after dieting. To understand the causes for maintenance of adiposity, high‐fat (HF) diet–induced obese (DIO) mice were switched to a low‐fat chow diet, and the effects of chow on histological and molecular alterations of adipose tissue and metabolic parameters were examined. DIO mice reduced and stabilized their body weights after being switched to chow (HF‐chow), but retained a greater amount of adiposity than chow‐fed mice. Reduction in adipocyte volume, not number, caused a decrease in fat mass. HF‐chow mice showed normalized circulating insulin and leptin levels, improved glucose tolerance, and reduced inflammatory status in white adipose tissue (WAT). Circulating leptin levels corrected for fat mass were lower in HF‐chow mice. Leptin administration was used to test whether reduced leptin level of HF‐chow mice inhibited further fat loss. Leptin treatment led to an additional reduction in adiposity. Finally, HF‐HF mice had lower mRNA levels of β3 adrenergic receptor (β3‐AR) in epididymal WAT (EWAT) compared to chow‐fed mice, and diet change led to an increase in the WAT β3‐AR mRNA levels that were similar to the levels of chow‐fed mice, suggesting an elevation in sympathetic activation of WAT during diet switch relative to HF‐HF mice leading to the reduced leptin level and proinflammatory cytokine content. In summary, HF‐chow mice were resistant to further fat loss due to leptin insufficiency. Diet alteration from HF to low fat improved metabolic state of DIO mice, although their adiposity was defended at a higher level.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>19373220</pmid><doi>10.1038/oby.2009.106</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adipocytes adipose tissue Adipose Tissue, Brown - metabolism Adipose Tissue, Brown - pathology Adipose Tissue, Brown - physiopathology Adipose Tissue, White - metabolism Adipose Tissue, White - pathology Adipose Tissue, White - physiopathology Adiposity animal models Animals Blood Glucose - metabolism Body fat body weight Cell Size Diet Diet, Fat-Restricted diet-related diseases Dietary Fats - administration & dosage Digitization Disease Models, Animal Eating Fatty Liver - etiology Fatty Liver - metabolism Fatty Liver - physiopathology Feeding Behavior Glucose high fat diet Histology human diseases Inflammation - etiology Inflammation - metabolism Inflammation - physiopathology Insulin - blood Insulin resistance leptin Leptin - blood Leptin - deficiency low fat diet Macrophages - metabolism Male Metabolism Mice Mice, Inbred C57BL Obesity Obesity - diet therapy Obesity - etiology Obesity - metabolism Obesity - physiopathology Physiology quantitative analysis Receptors, Adrenergic, beta-3 - genetics RNA, Messenger - metabolism Time Factors Weight control Weight Loss |
title | Diet-induced Obese Mice Are Leptin Insufficient After Weight Reduction |
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