n-3 Fatty acids preserve insulin sensitivity in vivo in a peroxisome proliferator-activated receptor-alpha-dependent manner.

n-3 Fatty acids preserve insulin sensitivity in vivo in a peroxisome proliferator-activated receptor-alpha-dependent manner. Research Abstract Details 

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n-3 Fatty acids preserve insulin sensitivity in vivo in a peroxisome proliferator-activated receptor-alpha-dependent manner. Abstract Text:

Susanne Neschen,Katsutaro Morino,Jianying Dong,Yanlin Wang-Fischer,Gary W Cline,Anthony J Romanelli, Rossbacher,Irene K Moore,Werner Regittnig,David S Munoz,Jung H Kim,Gerald I Shulman,

Recent studies have suggested that n-3 fatty acids, abundant in fish oil, protect against high-fat diet-induced insulin resistance through peroxisome proliferator-activated receptor (PPAR)-alpha activation and a subsequent decrease in intracellular lipid abundance. To directly test this hypothesis, we fed PPAR-alpha null and wild-type mice for 2 weeks with isocaloric high-fat diets containing 27% fat from either safflower oil or safflower oil with an 8% fish oil replacement (fish oil diet). In both genotypes the safflower oil diet blunted insulin-mediated suppression of hepatic glucose production (P < 0.02 vs. genotype control) and PEPCK gene expression. Feeding wild-type mice a fish oil diet restored hepatic insulin sensitivity (hepatic glucose production [HGP], P < 0.002 vs. wild-type mice fed safflower oil), whereas in contrast, in PPAR-alpha null mice failed to counteract hepatic insulin resistance (HGP, P = NS vs. PPAR-alpha null safflower oil-fed mice). In PPAR-alpha null mice fed the fish oil diet, safflower oil plus fish oil, hepatic insulin resistance was dissociated from increases in hepatic triacylglycerol and acyl-CoA but accompanied by a more than threefold increase in hepatic diacylglycerol concentration (P < 0.0001 vs. genotype control). These data support the hypothesis that n-3 fatty acids protect from high-fat diet-induced hepatic insulin resistance in a PPAR-alpha-and diacylglycerol-dependent manner.

n-3 Fatty acids preserve insulin sensitivity in vivo in a peroxisome proliferator-activated receptor-alpha-dependent manner. Publishing Authors By Initials

S Neschen,K Morino,J Dong,Y Wang-Fischer,GW Cline,AJ Romanelli,JC Rossbacher,IK Moore,W Regittnig,DS Munoz,JH Kim,GI Shulman,

For similar lipids: glycerides: triglycerides research abstracts see: lipids: glycerides: triglycerides research

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n-3 Fatty acids preserve insulin sensitivity in vivo in a peroxisome proliferator-activated receptor-alpha-dependent manner. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Diabetes

VOLUME: 56

Page Numbers: 1034-41

Journal Abbreviation: Diabetes

ISSN: 0012-1797

DAY: 24

MONTH: 01

YEAR: 2007

n-3 Fatty acids preserve insulin sensitivity in vivo in a peroxisome proliferator-activated receptor-alpha-dependent manner. Information

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LANGUAGE: eng

NlmUniqueID: 372763

n-3 Fatty acids preserve insulin sensitivity in vivo in a peroxisome proliferator-activated receptor-alpha-dependent manner. Keywords Mesh Terms:

KEYWORDS: Triglycerides

MESH TERMS: metabolism

Chemical & Substance for Abstract: n-3 Fatty acids preserve insulin sensitivity in vivo in a peroxisome proliferator-activated receptor-alpha-dependent manner. Information

Substance Name: Insulin

Registry Number: 11061-68-0

Grant and Affiliation Information for n-3 Fatty acids preserve insulin sensitivity in vivo in a peroxisome proliferator-activated receptor-alpha-dependent manner.

AFFILIATION: Yale University School of Medicine, Howard Hughes Medical Institute, Departments of Internal Medicine, The Anlyan Center, P.O. Box 9812, New Haven, CT 06536-8012, USA.

Country: United States

AGENCY: United States NIDDK

GRANT: U24 DK-59635

ACRONYM: DK

MEDLINETA: Diabetes

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