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Lipid metabolism and resistin gene expression in insulin-resistant Fischer 344 rats

1  Section of Endocrinology and Metabolism, McGuire Veterans Administration Medical Center and 2  Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23249 The interrelationship between insulin and leptin resistance in young Fischer 344 (F344) rats was studied. Young F3...

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Published in:American journal of physiology: endocrinology and metabolism 2002-03, Vol.282 (3), p.E626-E633
Main Authors: Levy, James R, Davenport, Byrd, Clore, John N, Stevens, Wayne
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container_title American journal of physiology: endocrinology and metabolism
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creator Levy, James R
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Stevens, Wayne
description 1  Section of Endocrinology and Metabolism, McGuire Veterans Administration Medical Center and 2  Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23249 The interrelationship between insulin and leptin resistance in young Fischer 344 (F344) rats was studied. Young F344 and Sprague-Dawley (SD) rats were fed regular chow. F344 animals had two- to threefold higher insulin and triglyceride concentrations and increased stores of triglycerides within liver and muscle. F344 animals gained more body fat. Both acyl-CoA oxidase (ACO) and carnitine palmitoyltransferase I gene expression were 20-50% less in F344 animals than in age-matched SD animals. Peroxisome proliferator-activated receptor- gene expression was reduced in 70-day-old F344 animals. Finally, resistin gene expression was similar in 70-day-old SD and F344 animals. Resistin gene expression increased fivefold in F344 animals and twofold in SD animals from 70 to 130 days, without a change in insulin sensitivity. We conclude that young F344 animals have both insulin and leptin resistance, which may lead to diminished fatty oxidation and accumulation of triglycerides in insulin-sensitive target tissues. We did not detect a role for resistin in the etiology of insulin resistance in F344 animals. Fischer 344 rats; acyl-coenzyme A oxidase; carnitine palmitoyltransferase I; peroxisome proliferator-activated receptor-
doi_str_mv 10.1152/ajpendo.00346.2001
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Young F344 and Sprague-Dawley (SD) rats were fed regular chow. F344 animals had two- to threefold higher insulin and triglyceride concentrations and increased stores of triglycerides within liver and muscle. F344 animals gained more body fat. Both acyl-CoA oxidase (ACO) and carnitine palmitoyltransferase I gene expression were 20-50% less in F344 animals than in age-matched SD animals. Peroxisome proliferator-activated receptor- gene expression was reduced in 70-day-old F344 animals. Finally, resistin gene expression was similar in 70-day-old SD and F344 animals. Resistin gene expression increased fivefold in F344 animals and twofold in SD animals from 70 to 130 days, without a change in insulin sensitivity. We conclude that young F344 animals have both insulin and leptin resistance, which may lead to diminished fatty oxidation and accumulation of triglycerides in insulin-sensitive target tissues. We did not detect a role for resistin in the etiology of insulin resistance in F344 animals. 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We did not detect a role for resistin in the etiology of insulin resistance in F344 animals. 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Young F344 and Sprague-Dawley (SD) rats were fed regular chow. F344 animals had two- to threefold higher insulin and triglyceride concentrations and increased stores of triglycerides within liver and muscle. F344 animals gained more body fat. Both acyl-CoA oxidase (ACO) and carnitine palmitoyltransferase I gene expression were 20-50% less in F344 animals than in age-matched SD animals. Peroxisome proliferator-activated receptor- gene expression was reduced in 70-day-old F344 animals. Finally, resistin gene expression was similar in 70-day-old SD and F344 animals. Resistin gene expression increased fivefold in F344 animals and twofold in SD animals from 70 to 130 days, without a change in insulin sensitivity. We conclude that young F344 animals have both insulin and leptin resistance, which may lead to diminished fatty oxidation and accumulation of triglycerides in insulin-sensitive target tissues. We did not detect a role for resistin in the etiology of insulin resistance in F344 animals. Fischer 344 rats; acyl-coenzyme A oxidase; carnitine palmitoyltransferase I; peroxisome proliferator-activated receptor-</abstract><cop>United States</cop><pmid>11832366</pmid><doi>10.1152/ajpendo.00346.2001</doi></addata></record>
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source American Physiological Society Free
subjects Acyl-CoA Oxidase
Animals
Blood Glucose - analysis
Body Composition
Body Weight
Carnitine O-Palmitoyltransferase - genetics
Drug Resistance
Gene Expression
Glucose Tolerance Test
Hormones, Ectopic - genetics
Insulin - analysis
Insulin - blood
Insulin Resistance - genetics
Kinetics
Leptin - blood
Leptin - pharmacology
Lipid Metabolism
Lipids - blood
Liver - chemistry
Muscle, Skeletal - chemistry
Nerve Growth Factor
Oxidoreductases - genetics
Proteins
Rats
Rats, Inbred F344
Rats, Sprague-Dawley
Receptors, Cytoplasmic and Nuclear - genetics
Resistin
Transcription Factors - genetics
Triglycerides - analysis
title Lipid metabolism and resistin gene expression in insulin-resistant Fischer 344 rats
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