Abstract
Fatty acid binding proteins (FABPs) are small cytoplasmic proteins that are expressed in a highly tissue-specific manner and bind to fatty acids such as oleic and retinoic acid. Mice with a null mutation in aP2, the gene encoding the adipocyte FABP, were developmentally and metabolically normal. The aP2-deficient mice developed dietary obesity but, unlike control mice, they did not develop insulin resistance or diabetes. Also unlike their obese wild-type counterparts, obese aP2-/- animals failed to express in adipose tissue tumor necrosis factor-alpha (TNF-alpha), a molecule implicated in obesity-related insulin resistance. These results indicate that aP2 is central to the pathway that links obesity to insulin resistance, possibly by linking fatty acid metabolism to expression of TNF-alpha.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adipose Tissue / metabolism*
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Animals
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Blood Glucose / metabolism
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Carrier Proteins / genetics
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Carrier Proteins / metabolism
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Carrier Proteins / physiology*
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Dietary Fats / administration & dosage
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Fatty Acid-Binding Protein 7
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Fatty Acid-Binding Proteins
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Fatty Acids / metabolism*
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Female
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Gene Expression Regulation
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Gene Targeting
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Glucose Tolerance Test
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Homeostasis
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Insulin / blood
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Insulin Resistance*
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Male
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Mice
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Mice, Inbred C57BL
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Mutation
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Myelin P2 Protein / genetics
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Myelin P2 Protein / metabolism
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Myelin P2 Protein / physiology*
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Neoplasm Proteins*
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Nerve Tissue Proteins*
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Obesity / metabolism*
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Triglycerides / blood
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Tumor Necrosis Factor-alpha / biosynthesis*
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Tumor Necrosis Factor-alpha / genetics
Substances
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Blood Glucose
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Carrier Proteins
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Dietary Fats
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Fabp5 protein, mouse
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Fabp7 protein, mouse
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Fatty Acid-Binding Protein 7
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Fatty Acid-Binding Proteins
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Fatty Acids
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Insulin
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Myelin P2 Protein
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Neoplasm Proteins
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Nerve Tissue Proteins
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Triglycerides
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Tumor Necrosis Factor-alpha