Abstract
2-Deoxy-D-glucose (2-DG) elicits significant and prolonged hypothermia in a variety of animals when administered either peripherally or centrally. From our current studies it would appear that, in high concentrations (250 mg/kg or more, ip), 2-DG can act directly on peripheral tissues in the rat by competitively interfering with glucose metabolism and consequently with normal heat producing mechanisms. When a low concentration of 2-DG (20 micrograms) is injected centrally, the ensuing glucopenia results in vagal stimulation and subsequent diminution of peripheral heat production. Vagal involvement is concluded from studies with atropine, which demonstrated total inhibition of the usual 2-DG depression of body temperature by administration to the ventral premammillary nucleus (PMV), a site that is normally extremely sensitive to this analog of glucose. Additionally, from studies with PMV-lesioned rats, it was concluded that an intact nucleus is necessary for thermoregulation in a normal, a hot, or a cold environment.
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