Abstract
The ob gene product, leptin, causes significant and dose-dependent inhibition of basal and insulin-stimulated glycogen synthesis in isolated soleus muscle from ob/ob mice, and a smaller, non-significant inhibition in muscle from wild-type mice. Leptin had no inhibitory effect on glycogen synthesis in soleus muscle from the diabetic (db/db) mice, which lack the functional leptin receptor. The full-length leptin receptor (Ob-Rb), is expressed in soleus muscle of both ob/ob and wild-type mice, however with no detectable differences in expression level. These results suggest that hyperleptinaemia may attenuate insulin action on glucose storage in skeletal muscle.
MeSH terms
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Animals
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Carrier Proteins / genetics
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Carrier Proteins / metabolism
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Female
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Gene Expression Regulation
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Glucose / metabolism
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Glycogen / biosynthesis*
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Glycogen / metabolism
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Insulin / pharmacology
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Leptin
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Mice
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Mice, Inbred DBA
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Mice, Mutant Strains
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Mice, Obese
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Muscle, Skeletal / metabolism*
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Obesity / metabolism*
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Polymerase Chain Reaction
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Proteins / pharmacology*
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RNA, Messenger / analysis
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RNA, Messenger / genetics
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Receptors, Cell Surface*
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Receptors, Leptin
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Recombinant Proteins / pharmacology
Substances
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Carrier Proteins
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Insulin
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Leptin
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Proteins
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RNA, Messenger
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Receptors, Cell Surface
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Receptors, Leptin
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Recombinant Proteins
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leptin receptor, mouse
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Glycogen
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Glucose