Abstract
Transgenic mice ubiquitously overexpressing murine gamma-aminobutyric acid transporter subtype I were created. Unexpectedly, these mice markedly exhibited heritable obesity, which features significantly increased body weight and fat deposition. Behavioral examination revealed that transgenic mice have slightly reduced spontaneous locomotive capacity and altered feeding pattern. This preliminary finding indicates that the inappropriate level of gamma-aminobutyric acid transporters may be directly or indirectly involved in the pathogenic mechanism underlying certain types of obesity.
MeSH terms
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Animals
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Body Weight
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Carrier Proteins / genetics
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Carrier Proteins / metabolism*
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Cholesterol / blood
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Eating
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GABA Plasma Membrane Transport Proteins
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Humans
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Lipoproteins, HDL / blood
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Lipoproteins, LDL / blood
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Membrane Proteins / genetics
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Membrane Proteins / metabolism*
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Membrane Transport Proteins*
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Mice
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Mice, Transgenic
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Motor Activity
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Nerve Tissue Proteins / genetics
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Nerve Tissue Proteins / metabolism*
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Obesity / genetics*
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Obesity / metabolism*
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Organic Anion Transporters*
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Triglycerides / blood
Substances
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Carrier Proteins
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GABA Plasma Membrane Transport Proteins
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Lipoproteins, HDL
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Lipoproteins, LDL
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Membrane Proteins
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Membrane Transport Proteins
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Nerve Tissue Proteins
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Organic Anion Transporters
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Triglycerides
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Cholesterol