Injection with gold thioglucose impairs sensitivity to glucose: evidence that glucose-responsive neurons are important for long-term regulation of body weight.
It has been proposed, but never demonstrated, that glucose-responsive neurons are essential for the long-term regulation of body weight, and that mice injected with gold-thio-glucose (GTG) become obese due to destruction of glucose-responsive neurons. To assess these hypotheses, mice were injected with either saline (control) or a dose of GTG that produces obesity, and the effects on feeding of peripheral injection of saline, glucose, 2-deoxyglucose (2-DG), or cholecystokinin (CCK) were measured. In control mice, 2-DG increased, whereas glucose and CCK decreased, food intake significantly. In contrast, in GTG-treated mice, 2-DG and glucose did not have a significant effect on food intake. The GTG-treated mice remained sensitive to the inhibitory effect of CCK on food intake. These data indicate that i.p. injection of GTG, which produces obesity, also destroys glucose-responsive neurons, consistent with the hypothesis that glucose-responsive neurons contribute to the long-term regulation of body weight.
Bergen
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HT
Department of Anatomy, University of Manitoba, Winnipeg, Canada. bergen@bldghsc.lan1.umanitoba.ca
Monkman
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Mobbs
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CV
D000818:Animals; D006051:Aurothioglucose / Q000494:pharmacology*; D001835:Body Weight / Q000502:physiology*; D002766:Cholecystokinin / Q000494:pharmacology; D003847:Deoxyglucose / Q000494:pharmacology; D004351:Drug Resistance; D004435:Eating / Q000187:drug effects; D005947:Glucose / Q000494:pharmacology*; D007274:Injections, Intraperitoneal; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D013997:Time Factors; D014697:Ventromedial Hypothalamic Nucleus / Q000187:drug effects* / Q000473:pathology / Q000502:physiology*
D006051:Aurothioglucose; D002766:Cholecystokinin; D003847:Deoxyglucose; D005947:Glucose