Abstract
Rats were injected acutely with antimetabolites of either glucose (2 deoxy- d-glucose, 2DG), fat (methylpalmoxirate, MP or mercaptoacetate, MAC), or the combination of these agents, in dosages known to stimulate food intake. Norepinephrine (NE) turnover in hypothalamus and brainstem was determined after these treatments by the method of synthesis inhibition. Glucoprivation (2DG) increased NE turnover in hypothalamus, confirming previous studies. Fat antimetabolites alone had no effect on NE turnover, nor did a peripherally-acting fructose antimetabolite. Combination of MP and 2DG, but not MAC and 2DG, produced a greater NE turnover than 2DG alone. These data suggest that peripheral signals of metabolic emergency do not activate brain NE systems, except when these systems are already activated by an ongoing cerebral metabolic emergency. The role of hypothalamic NE in metabolic integration of feeding is discussed, and possible hemispheric differences.
Published Version
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