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Rosiglitazone Enhances Glucose Tolerance by Mechanisms Other than Reduction of Fatty Acid Accumulation within Skeletal Muscle

We hypothesized that improved glucose tolerance with rosiglitazone treatment would coincide with decreased levels of im triacylglycerol (IMTG), diacylglycerol, and ceramide. Obese Zucker rats were randomly divided into two experimental groups: control (n = 9) and rosiglitazone (n = 9), with lean Zuc...

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Published in:Endocrinology (Philadelphia) 2004-12, Vol.145 (12), p.5665-5670
Main Authors: Lessard, Sarah J, Giudice, Sonia L. Lo, Lau, Winnie, Reid, Julianne J, Turner, Nigel, Febbraio, Mark A, Hawley, John A, Watt, Matthew J
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description We hypothesized that improved glucose tolerance with rosiglitazone treatment would coincide with decreased levels of im triacylglycerol (IMTG), diacylglycerol, and ceramide. Obese Zucker rats were randomly divided into two experimental groups: control (n = 9) and rosiglitazone (n = 9), with lean Zucker rats (n = 9) acting as a control group for obese controls. Rats received either vehicle or 3 mg/kg rosiglitazone for 6 wk. Glucose tolerance was impaired (P < 0.01) in obese compared with lean rats, but was normalized after rosiglitazone treatment. IMTG content was higher in obese compared with lean rats (70.5 ± 5.1 vs. 27.5 ± 2.0 μmol/g dry mass; P < 0.05) and increased an additional 30% (P < 0.05) with rosiglitazone treatment. Intramuscular fatty acid composition shifted toward a higher proportion of monounsaturates (P < 0.05) in obese rosiglitazone-treated rats due to an increase in palmitoleate (16:1; P < 0.05). Rosiglitazone treatment increased (P < 0.05) skeletal muscle diacylglycerol and ceramide levels by 65% and 100%, respectively, compared with obese rats, but elevated muscle diacylglycerol was not associated with changes in the total or membrane contents of the diacylglycerol-sensitive protein kinase C isoforms θ, δ, α, and β. In summary, we observed a disassociation among skeletal muscle IMTG, diacylglycerol and ceramide content, and glucose tolerance with rosiglitazone treatment in obese Zucker rats. Our data suggest, therefore, that rosiglitazone enhances glucose tolerance by mechanisms other than reduction of fatty acid accumulation within skeletal muscle.
doi_str_mv 10.1210/en.2004-0659
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Lo ; Lau, Winnie ; Reid, Julianne J ; Turner, Nigel ; Febbraio, Mark A ; Hawley, John A ; Watt, Matthew J</creator><creatorcontrib>Lessard, Sarah J ; Giudice, Sonia L. Lo ; Lau, Winnie ; Reid, Julianne J ; Turner, Nigel ; Febbraio, Mark A ; Hawley, John A ; Watt, Matthew J</creatorcontrib><description><![CDATA[We hypothesized that improved glucose tolerance with rosiglitazone treatment would coincide with decreased levels of im triacylglycerol (IMTG), diacylglycerol, and ceramide. Obese Zucker rats were randomly divided into two experimental groups: control (n = 9) and rosiglitazone (n = 9), with lean Zucker rats (n = 9) acting as a control group for obese controls. Rats received either vehicle or 3 mg/kg rosiglitazone for 6 wk. Glucose tolerance was impaired (P < 0.01) in obese compared with lean rats, but was normalized after rosiglitazone treatment. IMTG content was higher in obese compared with lean rats (70.5 ± 5.1 vs. 27.5 ± 2.0 μmol/g dry mass; P < 0.05) and increased an additional 30% (P < 0.05) with rosiglitazone treatment. Intramuscular fatty acid composition shifted toward a higher proportion of monounsaturates (P < 0.05) in obese rosiglitazone-treated rats due to an increase in palmitoleate (16:1; P < 0.05). Rosiglitazone treatment increased (P < 0.05) skeletal muscle diacylglycerol and ceramide levels by 65% and 100%, respectively, compared with obese rats, but elevated muscle diacylglycerol was not associated with changes in the total or membrane contents of the diacylglycerol-sensitive protein kinase C isoforms θ, δ, α, and β. In summary, we observed a disassociation among skeletal muscle IMTG, diacylglycerol and ceramide content, and glucose tolerance with rosiglitazone treatment in obese Zucker rats. 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Lo</creatorcontrib><creatorcontrib>Lau, Winnie</creatorcontrib><creatorcontrib>Reid, Julianne J</creatorcontrib><creatorcontrib>Turner, Nigel</creatorcontrib><creatorcontrib>Febbraio, Mark A</creatorcontrib><creatorcontrib>Hawley, John A</creatorcontrib><creatorcontrib>Watt, Matthew J</creatorcontrib><title>Rosiglitazone Enhances Glucose Tolerance by Mechanisms Other than Reduction of Fatty Acid Accumulation within Skeletal Muscle</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description><![CDATA[We hypothesized that improved glucose tolerance with rosiglitazone treatment would coincide with decreased levels of im triacylglycerol (IMTG), diacylglycerol, and ceramide. Obese Zucker rats were randomly divided into two experimental groups: control (n = 9) and rosiglitazone (n = 9), with lean Zucker rats (n = 9) acting as a control group for obese controls. Rats received either vehicle or 3 mg/kg rosiglitazone for 6 wk. 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Obese Zucker rats were randomly divided into two experimental groups: control (n = 9) and rosiglitazone (n = 9), with lean Zucker rats (n = 9) acting as a control group for obese controls. Rats received either vehicle or 3 mg/kg rosiglitazone for 6 wk. Glucose tolerance was impaired (P < 0.01) in obese compared with lean rats, but was normalized after rosiglitazone treatment. IMTG content was higher in obese compared with lean rats (70.5 ± 5.1 vs. 27.5 ± 2.0 μmol/g dry mass; P < 0.05) and increased an additional 30% (P < 0.05) with rosiglitazone treatment. Intramuscular fatty acid composition shifted toward a higher proportion of monounsaturates (P < 0.05) in obese rosiglitazone-treated rats due to an increase in palmitoleate (16:1; P < 0.05). Rosiglitazone treatment increased (P < 0.05) skeletal muscle diacylglycerol and ceramide levels by 65% and 100%, respectively, compared with obese rats, but elevated muscle diacylglycerol was not associated with changes in the total or membrane contents of the diacylglycerol-sensitive protein kinase C isoforms θ, δ, α, and β. In summary, we observed a disassociation among skeletal muscle IMTG, diacylglycerol and ceramide content, and glucose tolerance with rosiglitazone treatment in obese Zucker rats. Our data suggest, therefore, that rosiglitazone enhances glucose tolerance by mechanisms other than reduction of fatty acid accumulation within skeletal muscle.]]></abstract><cop>Bethesda, MD</cop><pub>Endocrine Society</pub><pmid>15375026</pmid><doi>10.1210/en.2004-0659</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
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source Oxford Journals Online
subjects Accumulation
Animals
Biological and medical sciences
Ceramide
Diglycerides
Diglycerides - metabolism
Fatty acid composition
Fatty acids
Fatty Acids - metabolism
Female
Fundamental and applied biological sciences. Psychology
Glucose
Glucose Intolerance - drug therapy
Glucose Intolerance - metabolism
Glucose tolerance
Hypoglycemic Agents - pharmacology
Isoforms
Kinases
Muscle, Skeletal - metabolism
Muscles
Musculoskeletal system
Obesity - metabolism
Protein kinase C
Rats
Rats, Zucker
Rosiglitazone
Skeletal muscle
Striated muscle. Tendons
Thiazolidinediones - pharmacology
Triglycerides
Triglycerides - metabolism
Vertebrates: endocrinology
Vertebrates: osteoarticular system, musculoskeletal system
title Rosiglitazone Enhances Glucose Tolerance by Mechanisms Other than Reduction of Fatty Acid Accumulation within Skeletal Muscle
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