Abstract
Tumor necrosis factor-alpha (TNF-alpha) has been shown to have certain catabolic effects on fat cells and whole animals. An induction of TNF-alpha messenger RNA expression was observed in adipose tissue from four different rodent models of obesity and diabetes. TNF-alpha protein was also elevated locally and systemically. Neutralization of TNF-alpha in obese fa/fa rats caused a significant increase in the peripheral uptake of glucose in response to insulin. These results indicate a role for TNF-alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity.
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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3T3 Cells
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Adipose Tissue / physiology
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Adipose Tissue / physiopathology*
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Animals
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Blood Glucose / metabolism
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Blotting, Northern
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Diabetes Mellitus, Experimental / physiopathology
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Glucose Clamp Technique
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Homeostasis
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Immunoglobulin G / genetics
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Immunoglobulin G / pharmacology
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Insulin / pharmacology
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Insulin Infusion Systems
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Insulin Resistance / genetics*
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Male
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Mice
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Mice, Obese
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Obesity / chemically induced
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Obesity / genetics*
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Obesity / physiopathology*
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RNA / genetics
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RNA / isolation & purification
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RNA, Messenger / biosynthesis*
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RNA, Messenger / isolation & purification
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Rats
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Rats, Zucker
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Receptors, Cell Surface / genetics
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Receptors, Cell Surface / physiology
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Receptors, Tumor Necrosis Factor
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Recombinant Fusion Proteins / pharmacology
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Reference Values
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Sodium Glutamate
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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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Immunoglobulin G
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Insulin
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RNA, Messenger
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Receptors, Cell Surface
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Receptors, Tumor Necrosis Factor
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Recombinant Fusion Proteins
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Tumor Necrosis Factor-alpha
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RNA
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Sodium Glutamate