Glucose metabolism in rat hypothalamus.
In vitro glucose oxidation and glucose transport in the rat medial (MH) and lateral (LH) hypothalamic areas was measured. Glucose oxidation was calculated from the conversion of [U-14C]glucose to 14CO2 and glucose transport from 14CO2 produced from [1-14C]glucose in the presence of phenazine and methosulphate and NaF. Increasing glucose in the medium from 1 mM to 20 mM enhanced glucose oxidation two-fold in MH and 40% in LH. Addition of insulin, 100 microU/ml, to the medium decreased glucose oxidation 30% both in MH and LH at both 4 mM and 20 mM glucose. Fasting did not affect glucose oxidation in either of these hypothalamic areas. Glucose transport was not affected by insulin, but was increased significantly when glucose was raised from 0.25 mM to 1.0 mM. Fasting also increased glucose transport in both hypothalamic areas. In conclusion, extracellular glucose concentration seems to be the major regulator of glucose utilization by the rat hypothalamus. Insulin, rather than increasing, seems to decrease glucose oxidation while having no effect on glucose transport.
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D005215:Fasting; D005947:Glucose / Q000378:metabolism*; D007031:Hypothalamus / Q000378:metabolism*; D007328:Insulin / Q000494:pharmacology; D008297:Male; D010084:Oxidation-Reduction / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D005947:Glucose