1978
DOI: 10.1079/pns19780023
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Neurochemistry of appetite mechanisms

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Cited by 41 publications
(8 citation statements)
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“…At the level of the body's energy economy certainly, and even perhaps at the neural sensor level, I find it difficult to distinguish Le Magnen's view of liporegulatory "modulation" of glucose sensors controlling hunger from the view he opposes to it -that hunger/satiety is controlled by metabolizable fuels globally, through sensors that remain to be satisfactorily identified. Our calculations presuppose the classical integration of carbohydrate, protein, and fat oxidation in most of the high-energy phosphate generation occurring in many cells and the glucose-sparing action of lipid and amino acid substrates in the liver (Booth 1972c,d;Booth et al 1976;Booth 1978). Processing lags and sensor specialisations are likely to limit the universal "interchangeability of fuels" (Friedman & Strieker 1976).…”
Section: Department Of Psychology University Of Birmingham Po Boxmentioning
confidence: 84%
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“…At the level of the body's energy economy certainly, and even perhaps at the neural sensor level, I find it difficult to distinguish Le Magnen's view of liporegulatory "modulation" of glucose sensors controlling hunger from the view he opposes to it -that hunger/satiety is controlled by metabolizable fuels globally, through sensors that remain to be satisfactorily identified. Our calculations presuppose the classical integration of carbohydrate, protein, and fat oxidation in most of the high-energy phosphate generation occurring in many cells and the glucose-sparing action of lipid and amino acid substrates in the liver (Booth 1972c,d;Booth et al 1976;Booth 1978). Processing lags and sensor specialisations are likely to limit the universal "interchangeability of fuels" (Friedman & Strieker 1976).…”
Section: Department Of Psychology University Of Birmingham Po Boxmentioning
confidence: 84%
“…The glucose utilization rate, which is increased during nocturnal lipogenesis and slowed during diurnal lipolysis, determines the frequency of the glucose shortage that triggers hunger arousal and the onset of feeding. It is also assumed that only glucose shortage is involved, as substantiated by the occurrence of a preprandial decline in blood glucose rather than a drop in the overall availability of other energy metabolites (as suggested by various investigators ;Booth 1972dBooth , 1978Danguir & Nicolaidis 1980b). No indication exists that insufficient availability of free fatty acids or aminoacids per se, or as elements of a global deficit of metabolizable fuel, can be a stimulus for eating.…”
Section: The Lateral Hypothalamus Feeding Systemmentioning
confidence: 99%
“…Another possibility consists in some possible changes in the basal metabolizm and macronutrient utilization due to the post-absorptive action of the EAA-deficient diet. Such metabolic changes were shown to induce reductions in feeding (Booth, 1978;Nicolaïdis & Even, 1984).…”
Section: Dmentioning
confidence: 99%
“…Tews et al (1979) suggested that altered competition among plasma amino acids for cerebral transport is the cause of reduced feed consumption. The results of many imbalance studies led Booth (1978) to report the possible existence of an amino acid-regulated appetite-control center in the brain.…”
Section: Imbalance and Antagonismmentioning
confidence: 99%