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Free fatty acids (FFAs) suppress appetite when injected into the hypothalamus.
To examine whether lipoprotein lipase (LPL), a serine hydrolase that releases
FFAs from circulating triglyceride (TG)-rich lipoproteins, might contribute to
FFA-mediated signaling in the brain, we created neuron-specific LPL-deficient
mice. Homozygous mutant (NEXLPL-/-) mice were hyperphagic and became obese by 16
weeks of age. These traits were accompanied by elevations in the hypothalamic
orexigenic neuropeptides, AgRP and NPY, and were followed by reductions in
metabolic rate. The uptake of TG-rich lipoprotein fatty acids was reduced in the
hypothalamus of 3-month-old NEXLPL-/- mice. Moreover, deficiencies in essential
fatty acids in the hypothalamus were evident by 3 months, with major
deficiencies of long-chain n-3 fatty acids by 12 months. These results indicate
that TG-rich lipoproteins are sensed in the brain by an LPL-dependent mechanism
and provide lipid signals for the central regulation of body weight and energy
Applicable research area(s): Diabetes, Obesity, Metabolism, Neurobiology
Data will not be collected for this catalog item
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Experimental Factor: Experimental Group
This animal belongs to the control group for the experiment.
This animal belongs to the experimental group and is heterozygous wild type/mutation for the affected locus.
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energy intake (24 hr)
energy intake (24 hr)
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respiratory exchange ratio (Light Period)
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oxygen consumption (Dark Period)
carbon dioxide production Light Period
carbon dioxide production Dark Period
respiratory exchange ratio (Dark Period)
heat (Dark Period)
carbon dioxide production
respiratory exchange ratio
energy intake (Ligth Period)
energy intake -light
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energy intake - dark
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) under the MICROMouse Program, grants DK076169.
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