Protection against diet-induced obesity and obesity- related insulin resistance in Group 1B PLA2-deficient mice
Center for Lipid and Arteriosclerosis Studies, Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267 Group 1B phospholipase A 2 (PLA 2 ) is an abundant lipolytic enzyme that is well characterized biochemically and structurally. Because...
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| Veröffentlicht in: | American journal of physiology: endocrinology and metabolism 2002-11, Vol.283 (5), p.E994-E1001 |
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| container_title | American journal of physiology: endocrinology and metabolism |
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| creator | Huggins, Kevin W Boileau, Amy C Hui, David Y |
| description | Center for Lipid and Arteriosclerosis Studies, Department
of Pathology and Laboratory Medicine, University of Cincinnati
College of Medicine, Cincinnati, Ohio 45267
Group 1B
phospholipase A 2 (PLA 2 ) is an abundant
lipolytic enzyme that is well characterized biochemically and
structurally. Because of its high level of expression in the pancreas,
it has been presumed that PLA 2 plays a role in the
digestion of dietary lipids, but in vivo data have been lacking to
support this theory. Our initial study on mice lacking PLA 2
demonstrated no abnormalities in dietary lipid absorption in mice
consuming a chow diet. However, the effects of PLA 2
deficiency on animals consuming a high-fat diet have not been studied.
To investigate this, PLA 2 +/+ and
PLA 2 / mice were fed a western
diet for 16 wk. The results showed that PLA 2 / mice were resistant to
high-fat diet-induced obesity. This observed weight difference was due
to decreased adiposity present in the PLA 2 / mice. Compared with
PLA 2 +/+ mice, the
PLA 2 / mice had 60% lower plasma
insulin and 72% lower plasma leptin levels after high-fat diet
feeding. The PLA 2 / mice also did
not exhibit impaired glucose tolerance associated with the development
of obesity-related insulin resistance as observed in the
PLA 2 +/+ mice. To investigate the
mechanism by which PLA 2 / mice
exhibit decreased weight gain while on a high-fat diet, fat absorption
studies were performed. The
PLA 2 / mice displayed 50 and 35%
decreased plasma [ 3 H]triglyceride concentrations 4 and
6 h, respectively, after feeding on a lipid-rich meal containing
[ 3 H]triolein. The PLA 2 /
mice also displayed increased lipid content in the stool, thus indicating decreased fat absorption in these animals. These results suggest a novel role for PLA 2 in the protection against
diet-induced obesity and obesity-related insulin resistance, thereby
offering a new target for treatment of obesity and diabetes.
phospholipase A 2 ; lipase; pancreatic enzymes; animal
models; lipid absorption |
| doi_str_mv | 10.1152/ajpendo.00110.2002 |
| format | Article |
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of Pathology and Laboratory Medicine, University of Cincinnati
College of Medicine, Cincinnati, Ohio 45267
Group 1B
phospholipase A 2 (PLA 2 ) is an abundant
lipolytic enzyme that is well characterized biochemically and
structurally. Because of its high level of expression in the pancreas,
it has been presumed that PLA 2 plays a role in the
digestion of dietary lipids, but in vivo data have been lacking to
support this theory. Our initial study on mice lacking PLA 2
demonstrated no abnormalities in dietary lipid absorption in mice
consuming a chow diet. However, the effects of PLA 2
deficiency on animals consuming a high-fat diet have not been studied.
To investigate this, PLA 2 +/+ and
PLA 2 / mice were fed a western
diet for 16 wk. The results showed that PLA 2 / mice were resistant to
high-fat diet-induced obesity. This observed weight difference was due
to decreased adiposity present in the PLA 2 / mice. Compared with
PLA 2 +/+ mice, the
PLA 2 / mice had 60% lower plasma
insulin and 72% lower plasma leptin levels after high-fat diet
feeding. The PLA 2 / mice also did
not exhibit impaired glucose tolerance associated with the development
of obesity-related insulin resistance as observed in the
PLA 2 +/+ mice. To investigate the
mechanism by which PLA 2 / mice
exhibit decreased weight gain while on a high-fat diet, fat absorption
studies were performed. The
PLA 2 / mice displayed 50 and 35%
decreased plasma [ 3 H]triglyceride concentrations 4 and
6 h, respectively, after feeding on a lipid-rich meal containing
[ 3 H]triolein. The PLA 2 /
mice also displayed increased lipid content in the stool, thus indicating decreased fat absorption in these animals. These results suggest a novel role for PLA 2 in the protection against
diet-induced obesity and obesity-related insulin resistance, thereby
offering a new target for treatment of obesity and diabetes.
phospholipase A 2 ; lipase; pancreatic enzymes; animal
models; lipid absorption</description><identifier>ISSN: 0193-1849</identifier><identifier>EISSN: 1522-1555</identifier><identifier>DOI: 10.1152/ajpendo.00110.2002</identifier><identifier>PMID: 12376327</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Dietary Fats - pharmacokinetics ; Disease Models, Animal ; Insulin Resistance - genetics ; Intestinal Absorption - genetics ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Obesity - genetics ; Obesity - metabolism ; Pancreas - enzymology ; Phospholipases A - genetics ; Phospholipases A2 ; Weight Gain - genetics</subject><ispartof>American journal of physiology: endocrinology and metabolism, 2002-11, Vol.283 (5), p.E994-E1001</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12376327$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huggins, Kevin W</creatorcontrib><creatorcontrib>Boileau, Amy C</creatorcontrib><creatorcontrib>Hui, David Y</creatorcontrib><title>Protection against diet-induced obesity and obesity- related insulin resistance in Group 1B PLA2-deficient mice</title><title>American journal of physiology: endocrinology and metabolism</title><addtitle>Am J Physiol Endocrinol Metab</addtitle><description>Center for Lipid and Arteriosclerosis Studies, Department
of Pathology and Laboratory Medicine, University of Cincinnati
College of Medicine, Cincinnati, Ohio 45267
Group 1B
phospholipase A 2 (PLA 2 ) is an abundant
lipolytic enzyme that is well characterized biochemically and
structurally. Because of its high level of expression in the pancreas,
it has been presumed that PLA 2 plays a role in the
digestion of dietary lipids, but in vivo data have been lacking to
support this theory. Our initial study on mice lacking PLA 2
demonstrated no abnormalities in dietary lipid absorption in mice
consuming a chow diet. However, the effects of PLA 2
deficiency on animals consuming a high-fat diet have not been studied.
To investigate this, PLA 2 +/+ and
PLA 2 / mice were fed a western
diet for 16 wk. The results showed that PLA 2 / mice were resistant to
high-fat diet-induced obesity. This observed weight difference was due
to decreased adiposity present in the PLA 2 / mice. Compared with
PLA 2 +/+ mice, the
PLA 2 / mice had 60% lower plasma
insulin and 72% lower plasma leptin levels after high-fat diet
feeding. The PLA 2 / mice also did
not exhibit impaired glucose tolerance associated with the development
of obesity-related insulin resistance as observed in the
PLA 2 +/+ mice. To investigate the
mechanism by which PLA 2 / mice
exhibit decreased weight gain while on a high-fat diet, fat absorption
studies were performed. The
PLA 2 / mice displayed 50 and 35%
decreased plasma [ 3 H]triglyceride concentrations 4 and
6 h, respectively, after feeding on a lipid-rich meal containing
[ 3 H]triolein. The PLA 2 /
mice also displayed increased lipid content in the stool, thus indicating decreased fat absorption in these animals. These results suggest a novel role for PLA 2 in the protection against
diet-induced obesity and obesity-related insulin resistance, thereby
offering a new target for treatment of obesity and diabetes.
phospholipase A 2 ; lipase; pancreatic enzymes; animal
models; lipid absorption</description><subject>Animals</subject><subject>Dietary Fats - pharmacokinetics</subject><subject>Disease Models, Animal</subject><subject>Insulin Resistance - genetics</subject><subject>Intestinal Absorption - genetics</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Mutant Strains</subject><subject>Obesity - genetics</subject><subject>Obesity - metabolism</subject><subject>Pancreas - enzymology</subject><subject>Phospholipases A - genetics</subject><subject>Phospholipases A2</subject><subject>Weight Gain - genetics</subject><issn>0193-1849</issn><issn>1522-1555</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU1vFDEMhiMEokvhD3BAOXFLycd4sjmWqi1IK9FDOUeZxLObajYZJhnB_nsidYETJ9uvn9eSbULeC34lBMhP7mnGFPIV56JJknP5gmxaQzIBAC_JhgujmNh25oK8KeWJc66hk6_JhZBK90rqDckPS67oa8yJur2LqVQaIlYWU1g9BpoHLLGeqEt_c0YXnFxtzYavU0ytLrFUlzw2id4veZ2p-EwfdteSBRyjj5gqPUaPb8mr0U0F353jJfl-d_t484Xtvt1_vbnesYPUfWWGaxz1aMCHDsAAcN-3NX0PwflBoJODAsMDhz6AdMIPynM1gETdbUMAdUk-Ps-dl_xjxVLtMRaP0-QS5rVYLYVWgvMGfjiD63DEYOclHt1ysn9O1ADzDBzi_vAzLmjnw6nEPOX9yd6t0_SIv6o9_0JulQV7a0xn5zA2L_u_92yx_zzqN_Ymj8U</recordid><startdate>20021101</startdate><enddate>20021101</enddate><creator>Huggins, Kevin W</creator><creator>Boileau, Amy C</creator><creator>Hui, David Y</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20021101</creationdate><title>Protection against diet-induced obesity and obesity- related insulin resistance in Group 1B PLA2-deficient mice</title><author>Huggins, Kevin W ; Boileau, Amy C ; Hui, David Y</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h276t-907ef7f95cd4559550c6001c65dacb1ea2b3590d056d52a1cb3c03b52e748dd53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Dietary Fats - pharmacokinetics</topic><topic>Disease Models, Animal</topic><topic>Insulin Resistance - genetics</topic><topic>Intestinal Absorption - genetics</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Mutant Strains</topic><topic>Obesity - genetics</topic><topic>Obesity - metabolism</topic><topic>Pancreas - enzymology</topic><topic>Phospholipases A - genetics</topic><topic>Phospholipases A2</topic><topic>Weight Gain - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huggins, Kevin W</creatorcontrib><creatorcontrib>Boileau, Amy C</creatorcontrib><creatorcontrib>Hui, David Y</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology: endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huggins, Kevin W</au><au>Boileau, Amy C</au><au>Hui, David Y</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protection against diet-induced obesity and obesity- related insulin resistance in Group 1B PLA2-deficient mice</atitle><jtitle>American journal of physiology: endocrinology and metabolism</jtitle><addtitle>Am J Physiol Endocrinol Metab</addtitle><date>2002-11-01</date><risdate>2002</risdate><volume>283</volume><issue>5</issue><spage>E994</spage><epage>E1001</epage><pages>E994-E1001</pages><issn>0193-1849</issn><eissn>1522-1555</eissn><abstract>Center for Lipid and Arteriosclerosis Studies, Department
of Pathology and Laboratory Medicine, University of Cincinnati
College of Medicine, Cincinnati, Ohio 45267
Group 1B
phospholipase A 2 (PLA 2 ) is an abundant
lipolytic enzyme that is well characterized biochemically and
structurally. Because of its high level of expression in the pancreas,
it has been presumed that PLA 2 plays a role in the
digestion of dietary lipids, but in vivo data have been lacking to
support this theory. Our initial study on mice lacking PLA 2
demonstrated no abnormalities in dietary lipid absorption in mice
consuming a chow diet. However, the effects of PLA 2
deficiency on animals consuming a high-fat diet have not been studied.
To investigate this, PLA 2 +/+ and
PLA 2 / mice were fed a western
diet for 16 wk. The results showed that PLA 2 / mice were resistant to
high-fat diet-induced obesity. This observed weight difference was due
to decreased adiposity present in the PLA 2 / mice. Compared with
PLA 2 +/+ mice, the
PLA 2 / mice had 60% lower plasma
insulin and 72% lower plasma leptin levels after high-fat diet
feeding. The PLA 2 / mice also did
not exhibit impaired glucose tolerance associated with the development
of obesity-related insulin resistance as observed in the
PLA 2 +/+ mice. To investigate the
mechanism by which PLA 2 / mice
exhibit decreased weight gain while on a high-fat diet, fat absorption
studies were performed. The
PLA 2 / mice displayed 50 and 35%
decreased plasma [ 3 H]triglyceride concentrations 4 and
6 h, respectively, after feeding on a lipid-rich meal containing
[ 3 H]triolein. The PLA 2 /
mice also displayed increased lipid content in the stool, thus indicating decreased fat absorption in these animals. These results suggest a novel role for PLA 2 in the protection against
diet-induced obesity and obesity-related insulin resistance, thereby
offering a new target for treatment of obesity and diabetes.
phospholipase A 2 ; lipase; pancreatic enzymes; animal
models; lipid absorption</abstract><cop>United States</cop><pmid>12376327</pmid><doi>10.1152/ajpendo.00110.2002</doi></addata></record> |
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| identifier | ISSN: 0193-1849 |
| ispartof | American journal of physiology: endocrinology and metabolism, 2002-11, Vol.283 (5), p.E994-E1001 |
| issn | 0193-1849 1522-1555 |
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| recordid | cdi_highwire_physiology_ajpendo_283_5_E994 |
| source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Dietary Fats - pharmacokinetics Disease Models, Animal Insulin Resistance - genetics Intestinal Absorption - genetics Mice Mice, Inbred C57BL Mice, Mutant Strains Obesity - genetics Obesity - metabolism Pancreas - enzymology Phospholipases A - genetics Phospholipases A2 Weight Gain - genetics |
| title | Protection against diet-induced obesity and obesity- related insulin resistance in Group 1B PLA2-deficient mice |
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