Perilipin Ablation Results in a Lean Mouse with Aberrant Adipocyte Lipolysis, Enhanced Leptin Production, and Resistance to Diet-Induced Obesity
Perilipin coats the lipid droplets of adipocytes and is thought to have a role in regulating triacylglycerol hydrolysis. To study the role of perilipin in vivo, we have created a perilipin knockout mouse. Perilipin null (peri-/-) and wild-type (peri+/+) mice consume equal amounts of food, but the ad...
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| creator | Tansey, J. T. Sztalryd, C. Gruia-Gray, J. Roush, D. L. Zee, J. V. Gavrilova, O. Reitman, M. L. C.-X. Deng Li, C. Kimmel, A. R. Londos, C. |
| description | Perilipin coats the lipid droplets of adipocytes and is thought to have a role in regulating triacylglycerol hydrolysis. To study the role of perilipin in vivo, we have created a perilipin knockout mouse. Perilipin null (peri-/-) and wild-type (peri+/+) mice consume equal amounts of food, but the adipose tissue mass in the null animals is reduced to ≈30% of that in wild-type animals. Isolated adipocytes of perilipin null mice exhibit elevated basal lipolysis because of the loss of the protective function of perilipin. They also exhibit dramatically attenuated stimulated lipolytic activity, indicating that perilipin is required for maximal lipolytic activity. Plasma leptin concentrations in null animals were greater than expected for the reduced adipose mass. The peri-/-animals have a greater lean body mass and increased metabolic rate but they also show an increased tendency to develop glucose intolerance and peripheral insulin resistance. When fed a high-fat diet, the perilipin null animals are resistant to diet-induced obesity but not to glucose intolerance. The data reveal a major role for perilipin in adipose lipid metabolism and suggest perilipin as a potential target for attacking problems associated with obesity. |
| doi_str_mv | 10.1073/pnas.101042998 |
| format | Article |
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T. ; Sztalryd, C. ; Gruia-Gray, J. ; Roush, D. L. ; Zee, J. V. ; Gavrilova, O. ; Reitman, M. L. ; C.-X. Deng ; Li, C. ; Kimmel, A. R. ; Londos, C.</creator><creatorcontrib>Tansey, J. T. ; Sztalryd, C. ; Gruia-Gray, J. ; Roush, D. L. ; Zee, J. V. ; Gavrilova, O. ; Reitman, M. L. ; C.-X. Deng ; Li, C. ; Kimmel, A. R. ; Londos, C.</creatorcontrib><description>Perilipin coats the lipid droplets of adipocytes and is thought to have a role in regulating triacylglycerol hydrolysis. To study the role of perilipin in vivo, we have created a perilipin knockout mouse. Perilipin null (peri-/-) and wild-type (peri+/+) mice consume equal amounts of food, but the adipose tissue mass in the null animals is reduced to ≈30% of that in wild-type animals. Isolated adipocytes of perilipin null mice exhibit elevated basal lipolysis because of the loss of the protective function of perilipin. They also exhibit dramatically attenuated stimulated lipolytic activity, indicating that perilipin is required for maximal lipolytic activity. Plasma leptin concentrations in null animals were greater than expected for the reduced adipose mass. The peri-/-animals have a greater lean body mass and increased metabolic rate but they also show an increased tendency to develop glucose intolerance and peripheral insulin resistance. When fed a high-fat diet, the perilipin null animals are resistant to diet-induced obesity but not to glucose intolerance. The data reveal a major role for perilipin in adipose lipid metabolism and suggest perilipin as a potential target for attacking problems associated with obesity.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.101042998</identifier><identifier>PMID: 11371650</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Adipocytes ; Adipocytes - cytology ; Adipocytes - metabolism ; Adipose Tissue - metabolism ; Adipose tissues ; Animals ; Biological Sciences ; Blood Glucose - analysis ; Blood plasma ; Carrier Proteins ; Cell Differentiation ; Cells ; Diet ; Dietary Fats - metabolism ; Female ; Genotypes ; glucose intolerance ; Leptin - biosynthesis ; Lipids ; Lipolysis ; Male ; Male animals ; Membrane Proteins - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Obesity ; Obesity - metabolism ; Oxygen Consumption ; Peptides - metabolism ; perilipin ; Perilipin-1 ; Perilipin-2 ; Phosphoproteins - genetics ; Phosphoproteins - physiology ; RNA ; Rodents ; Sterol Esterase - metabolism ; Thinness ; Triglycerides - metabolism</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2001-05, Vol.98 (11), p.6494-6499</ispartof><rights>Copyright 1993-2001 National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences May 22, 2001</rights><rights>Copyright © 2001, The National Academy of Sciences 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c520t-fba10498bee00e252c0218306edd0cabfa9465235e5369e62c441b4e66abe37d3</citedby><cites>FETCH-LOGICAL-c520t-fba10498bee00e252c0218306edd0cabfa9465235e5369e62c441b4e66abe37d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/98/11.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3055833$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3055833$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,885,27924,27925,53791,53793,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11371650$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tansey, J. T.</creatorcontrib><creatorcontrib>Sztalryd, C.</creatorcontrib><creatorcontrib>Gruia-Gray, J.</creatorcontrib><creatorcontrib>Roush, D. L.</creatorcontrib><creatorcontrib>Zee, J. V.</creatorcontrib><creatorcontrib>Gavrilova, O.</creatorcontrib><creatorcontrib>Reitman, M. L.</creatorcontrib><creatorcontrib>C.-X. Deng</creatorcontrib><creatorcontrib>Li, C.</creatorcontrib><creatorcontrib>Kimmel, A. R.</creatorcontrib><creatorcontrib>Londos, C.</creatorcontrib><title>Perilipin Ablation Results in a Lean Mouse with Aberrant Adipocyte Lipolysis, Enhanced Leptin Production, and Resistance to Diet-Induced Obesity</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Perilipin coats the lipid droplets of adipocytes and is thought to have a role in regulating triacylglycerol hydrolysis. To study the role of perilipin in vivo, we have created a perilipin knockout mouse. Perilipin null (peri-/-) and wild-type (peri+/+) mice consume equal amounts of food, but the adipose tissue mass in the null animals is reduced to ≈30% of that in wild-type animals. Isolated adipocytes of perilipin null mice exhibit elevated basal lipolysis because of the loss of the protective function of perilipin. They also exhibit dramatically attenuated stimulated lipolytic activity, indicating that perilipin is required for maximal lipolytic activity. Plasma leptin concentrations in null animals were greater than expected for the reduced adipose mass. The peri-/-animals have a greater lean body mass and increased metabolic rate but they also show an increased tendency to develop glucose intolerance and peripheral insulin resistance. When fed a high-fat diet, the perilipin null animals are resistant to diet-induced obesity but not to glucose intolerance. The data reveal a major role for perilipin in adipose lipid metabolism and suggest perilipin as a potential target for attacking problems associated with obesity.</description><subject>Adipocytes</subject><subject>Adipocytes - cytology</subject><subject>Adipocytes - metabolism</subject><subject>Adipose Tissue - metabolism</subject><subject>Adipose tissues</subject><subject>Animals</subject><subject>Biological Sciences</subject><subject>Blood Glucose - analysis</subject><subject>Blood plasma</subject><subject>Carrier Proteins</subject><subject>Cell Differentiation</subject><subject>Cells</subject><subject>Diet</subject><subject>Dietary Fats - metabolism</subject><subject>Female</subject><subject>Genotypes</subject><subject>glucose intolerance</subject><subject>Leptin - biosynthesis</subject><subject>Lipids</subject><subject>Lipolysis</subject><subject>Male</subject><subject>Male animals</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Obesity</subject><subject>Obesity - metabolism</subject><subject>Oxygen Consumption</subject><subject>Peptides - metabolism</subject><subject>perilipin</subject><subject>Perilipin-1</subject><subject>Perilipin-2</subject><subject>Phosphoproteins - genetics</subject><subject>Phosphoproteins - physiology</subject><subject>RNA</subject><subject>Rodents</subject><subject>Sterol Esterase - metabolism</subject><subject>Thinness</subject><subject>Triglycerides - metabolism</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkk1v1DAQhiMEokvhygkhiwNcmjKOnS-Jy6oUqLSoFYKz5SQT1qusHWwH2H_BT2aiXZbCAU4eeZ53NB9vkjzmcM6hFC9HqwNFHGRW19WdZMGh5mkha7ibLACyMq1kJk-SByFsAKDOK7ifnHAuSl7ksEh-3KA3gxmNZctm0NE4yz5gmIYYGP1ptkJt2Xs3BWTfTFwThd5rG9myM6NrdxHZioJhF0w4Y5d2rW2LHcnGSPob77qpnaueMW27ubQJcUZYdOy1wZheWSJIcd1QLu4eJvd6PQR8dHhPk09vLj9evEtX12-vLpartM0ziGnfaJq5rhpEAMzyrIWMVwIK7DpoddPrWhZ5JnLMRVFjkbVS8kZiUegGRdmJ0-TVvu44NVvsWrTR60GN3my13ymnjfozY81afXZflRCyLkj-_CD37suEIaqtCS0Og7ZIy1IlVLmsqYH_gbysiopOR-Czv8CNm7ylHagMuAQpBRB0voda70Lw2B8b5qBmQ6jZEOpoCBI8vT3mb_zggFvALPyVrisiFNlIEvDin4Dqp2GI-D0S-WRPbkJ0_ogKyPNKCPETXNbU_g</recordid><startdate>20010522</startdate><enddate>20010522</enddate><creator>Tansey, J. 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T.</au><au>Sztalryd, C.</au><au>Gruia-Gray, J.</au><au>Roush, D. L.</au><au>Zee, J. V.</au><au>Gavrilova, O.</au><au>Reitman, M. L.</au><au>C.-X. Deng</au><au>Li, C.</au><au>Kimmel, A. R.</au><au>Londos, C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Perilipin Ablation Results in a Lean Mouse with Aberrant Adipocyte Lipolysis, Enhanced Leptin Production, and Resistance to Diet-Induced Obesity</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2001-05-22</date><risdate>2001</risdate><volume>98</volume><issue>11</issue><spage>6494</spage><epage>6499</epage><pages>6494-6499</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Perilipin coats the lipid droplets of adipocytes and is thought to have a role in regulating triacylglycerol hydrolysis. To study the role of perilipin in vivo, we have created a perilipin knockout mouse. Perilipin null (peri-/-) and wild-type (peri+/+) mice consume equal amounts of food, but the adipose tissue mass in the null animals is reduced to ≈30% of that in wild-type animals. Isolated adipocytes of perilipin null mice exhibit elevated basal lipolysis because of the loss of the protective function of perilipin. They also exhibit dramatically attenuated stimulated lipolytic activity, indicating that perilipin is required for maximal lipolytic activity. Plasma leptin concentrations in null animals were greater than expected for the reduced adipose mass. The peri-/-animals have a greater lean body mass and increased metabolic rate but they also show an increased tendency to develop glucose intolerance and peripheral insulin resistance. When fed a high-fat diet, the perilipin null animals are resistant to diet-induced obesity but not to glucose intolerance. The data reveal a major role for perilipin in adipose lipid metabolism and suggest perilipin as a potential target for attacking problems associated with obesity.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>11371650</pmid><doi>10.1073/pnas.101042998</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adipocytes Adipocytes - cytology Adipocytes - metabolism Adipose Tissue - metabolism Adipose tissues Animals Biological Sciences Blood Glucose - analysis Blood plasma Carrier Proteins Cell Differentiation Cells Diet Dietary Fats - metabolism Female Genotypes glucose intolerance Leptin - biosynthesis Lipids Lipolysis Male Male animals Membrane Proteins - metabolism Mice Mice, Inbred C57BL Mice, Knockout Obesity Obesity - metabolism Oxygen Consumption Peptides - metabolism perilipin Perilipin-1 Perilipin-2 Phosphoproteins - genetics Phosphoproteins - physiology RNA Rodents Sterol Esterase - metabolism Thinness Triglycerides - metabolism |
| title | Perilipin Ablation Results in a Lean Mouse with Aberrant Adipocyte Lipolysis, Enhanced Leptin Production, and Resistance to Diet-Induced Obesity |
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