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Biomedical subjects

D Novin

Publications and source records attributed to D Novin.

At least 73 records · Page 4Linked to original sources
PubMed1977

Hepatic-portal nutrient infustion: effect on feeding in intact and vagotomized rabbits.

Hepatic-portal infusions of isotonic glucose did not influence food intake in free-feeding rabbits. In contrast, several other macronutrients and some of their metabolites, infused via the same route, cause anorexia followed by prolonged hypophagia. Its duration was generally decreased when the same infusions were performed during the nocturnal period. Vagotomy did not significantly alter the food intake responses to hepatic-portal infusions of either glucose or the other experimental substances. The results of related experiments have demonstrated that prolonged anorexia was not a consequence of the fast infusion rate or the generalized behavioral mallaise. However, when the infusions of most anorexigenic substances were followed by intraperitoneal administration of insulin, the duration of anorexia was shortened and food consumption was elevated. The results provided indirect evidence for the vagally mediated regulatory contribution of the previously studied neural and humoral intestinal mechanisms which are bypassed by infusing nutrient loads directly into the hepatic-portal circulation.

Ammonium Chloride↗
PubMed1976

Duodenal nutrient infusion: effects on feeding in intact and vagotomized rabbits.

A comparative study on the satiating effect of duodenal infusions of glycerol, casein and glucose was performed in intact and vagotomized rabbits during both diuranal and nocturnal periods. All duodenally infused substances had satiating effects. Glycerol infusions produced the largest reduction of food intake during the day while casein hydrolysate infusion was most effective in this respect during the night. The most apparent and consistent effect of vagotomy was the elimination of hypophagic effect of diurnal and nocturnal infusions of glucose. Pretreatment with atropine methyl nitrate, which prevented the evoked gastric contractions in response to electrical stimulation of the efferent cervical vagus nerve in acute preparations but did not influence spontaneous intake in free-feeding animals, had no effect on duodenal glucose induced satiety. This result indicates that afferent vagal mediation of information from peripheral metabolic organs is vital to the short-term glucostatic regulation of food intake.

Afferent Pathways↗
PubMed1976

Paradoxical increased feeding following glucose infusions in recovered lateral rats.

Glucose infusions increased feeding in recovered lateral hypothalamic (LH) lesioned rats in constrast to its suppressant effect in sham-lesioned rats and in rats with lesions unilateral, asymmetrical or anterior to LH. This paradoxical enhancement of eating by glucose was predicted from similar effects seen in vagotomized rabbits and general parallels observed in ingestive behavior after LH lesions and vagotomy. We conclude that an important component in the short-term control of food intake is a vagal-LH circuit and that a modification of the classic notion of the LH as an excitatory "feeding center" is needed.

Animals↗
PubMed1976

Glycogen levels and peripheral mechanisms of glucose-induced spppression of feeding.

Rabbits deprived of food for 0, 2, 4, 6, 8, 16, and 24 h were assessed for glucose-induced feeding suppression, refeeding after deprivation, and liver glycogen. In previous research, we hypothesized a relationship between liver glycogen and the transition from duodenal to hepatic glucose suppression. In duodenally cannulated rabbits, the infusion of 10 ml of isotonic glucose in awake, free-feeding animals significantly suppressed food intake but did not do so in those food deprived for 2, 4, 6, 8, or 24 h. In hepatic-cannulated rabbits, similar amounts of glucose significantly suppressed food intake in 4-, 6-, 16-, and 24-h-deprived animals. Also, refeeding after deprivation increased as a function of continued deprivation until 6 or 8 h, when refeeding reached asymptote, or decreased through 24-h deprivations. In agreement with these observations, liver glycogen showed a sharp decline between 4, 6, and 8 h of deprivation (depending on circadian cycle). It is proposed that liver glycogen depletion, or some correlate, alters liver glucostatic regulation and determines refeeding after deprivation.

Animals↗
PubMed1975

The effects of serotonin on feeding in the rabbit.

Serotonin infused through hepatic-portal cannulae of rabbits decreased food intake in a free-feeding condition. Following a 12 hr food deprivation period similar doses of serotonin increased food intake. Other investigators have shown release of serotonin to food and related stimuli. Our results demonstrate that serotonin is not a simple "satiety hormone" but suggest that it may be importantly involved in short-term regulatory mechanisms of feeding.

Animals↗
PubMed1975

Satiety and hunger induced by small and large duodenal loads of isotonic glucose.

Hepatic-portal infusions of small or large flucose loads in the rabbit had little or no stimulating effect on postinfusion food intake. However, marked differential changes in appetite were observed when small and large glucose loads were infused into the duodenum. The satiating effect of small glucose loads contrasted sharply with an unusually high increase in food intake triggered by the infusions of larger amounts of glucose into the duodenum. The results are interpreted in terms of a possible involvement of the enteroinsular mechanism in the regulation of food intake. This mechanism is bypassed and its influence on food intake eliminated when glucose is infused directly into the portal circulation. The positive relationship between large amounts of alimentary carbohydrates and overeating is seen as a factor that may actively promote the development of obesity and diabetes mellitus.

Animals↗
PubMed1973

Infusion of 2-deoxy-D-glucose into the hepatic-portal system causes eating: evidence for peripheral glucoreceptors.

Injections of 2-deoxyglucose into the hepatic-portal system of normal rabbits increased eating to a greater extent and with shorter latency than comparable injections of 2-deoxyglucose into the jugular vein or into the hepaticportal circulation of the vagotomized rabbit. These differences suggest the existence of vagally mediated peripheral glucoreceptors important in the initiation of food intake.

Animals↗