Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hunger”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources
PubMed1985

Physiological determinant of hunger, satiation, and satiety.

The initiation and cessation of feeding behavior is explained on the basis of the ischymetric hypothesis (from ISCHYROS meaning "Mighty One" or power). Cellular production of power or "Metabolisme de Fond" (MF) is measured continuously in terms of total body metabolism minus the metabolic costs of locomotion. A drop in MF signals the onset of eating. Eating initiates a rise in MF and when this signal peaks, the feeding process stops. Control of satiation is described in terms of recent neurophysiologic and neuroendrologic factors that influence MF.

Animals↗
PubMedDate not supplied

Hunger and appetite.

Explore the source record for details and available documents.

Appetite↗
PubMed1976

Glucose antimetabolites and hunger (theoretical article).

A decrease in the cellular utilization of glucose produced by several glucose antimetabolites and especially by 2 deoxy-D-glucose considerably stimulates food intake. An analysis of this phenomenon is presented in terms of the available experimental evidence. Experiments in which glucose antimetabolites have been administered so as to influence selectively the central and peripheral glucosensitive loci suggest a possible mechanism for the action of the substances. The mechanisms by which glucose antimetabolites and exogenous insulin induce cellular glucoprivation and the subsequent changes in food intake are compared and discussed.

Animals↗
PubMed1979

Hepatic-portal glucose and insulin levels: relationship to glucose-induced satiety and hunger.

The hepatic-portal infusions of both smaller and larger glucose loads, which had no significant effect on food intake in chronic feeding experiments, produced only a brief dose-dependent peak-like elevation in glucose and insulin levels. In contrast, metabolic changes produced by duodenal infusions were greater and considerably longer in duration. The maximal level and duration of glucose and insulin increase further differentiated two feeding phenomena induced by duodenal infusions: 1) the metabolic satiety of smaller glucose loads associated with blunted and delayed glucose and insulin increases within normal physiological range; 2) paradoxical antiregulatory stimulation of food intake induced by larger glucose loads associated with a gradually intensified, exaggerated and prolonged insulin increase. This increase was significantly larger than corresponding preinfusion value even at the end of 3 hour test period. Present results thus demonstrate that various glucose-induced feeding phenomena are associated and apparently dependent for their expression on distinct, prolonged changes in glycemia and insulin levels.

Animals↗