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D Novin

Publications and source records attributed to D Novin.

At least 55 records · Page 3Linked to original sources
PubMed1980

Physiological and morphological changes in the gastrointestinal tract induced by hypothalamic intervention: an overview.

Neural control and modulation of gastric secretion is well established. The role of the parasympathetic vagal system as a final motor pathway in gastric acid secretion is clearer than the involvement of the sympathetic nervous system. Both portions of the autonomic nervous system, however, appear to play an important role in the pathogenesis of at least experimentally induced gastric erosions. With respect to higher neural control there are numerous reports of hypothalamic effects on gastric secretion, motility, and morphology, yet the results of many of these reports appear equivocal. This ambiguity can be attributed in part to species differences, time course of observations, and differences in stimulation and lesion parameters. However, a mcal description of the sites of central lesions and stimulation. Implications of several of the studies concerning hypothalamic involvement in gastric functions are reviewed and recent methodological advances including neural fiber transection, relatively specific neural cell damage with neurotoxins (e.g., 6-OHDA, kainic acid), histochemistry and intracerebral infusions of gut hormones are suggested as alternative approaches to studying brain-gut relationships.

Animals↗
PubMed1980

Multivariate analysis of meal patterning in intact and vagotomized rabbits.

Meal patterns of female rabbits were measured throughout a 12:12 hr light/dark cycle and subjected to a multivariate-univariate analysis. Increased food intake occurring during the first 6 hr of dark was attributed to increased meal frequency and feeding rate, while that found during the last 6 hr of dark was attributed to increased meal duration and meal size. Meal patterning was also nonhomogeneous between the 6-hr periods in the light portion of the cycle. Experiment 2 demonstrated the times of day when feeding patterns of vagotomized animals are different from those of intact animals and, further, delineated the relevant variables that are altered by vagotomy. Immediately following light offset, vagotomized animals were distinguished from intact animals by sloer feeding rate and decreased food intake. Immediately following light onset, vagotomized animals were distinguished from intact animals by decreased feeding frequency, increased meal duration, and increased satiety ratio. During the 6 hr immediately preceding light onset or offset, none of the variables could discriminate the feeding patterns of intact animals from those of vagotomized animals.

Animals↗
PubMed1979

Pancreatic glucagon, food deprivation and feeding in intact and vagotomized rabbits.

Thirty New-Zealand female rabbits were implanted with hepatic-portal cannulas and six simultaneously underwent bilateral subdiaphragmatic vagotomy. When recovered, all animals received pancreatic glucagon infused at 1.0 cc/min for a total dosage of 12 microgram in 3.0 cc of isotonic saline. On alternate days, isotonic saline alone was infused as a control. Twelve intact and six vagotomized animals received infusions terminating food deprivations of 4, 8, and 24 hr while the remaining animals received the infusions only when free feeding. The feeding behavior of all animals was measured at 0.5, 1 and 2 hr postinfusion. Glucagon significantly suppressed feeding relative to saline only in 0- and 4-hr-food-deprived intact rabbits. Longer deprivations followed by glucagon did not produce suppression, and glucagon was completely ineffective in suppressing feeding in vagotomized animals. Although glucagon infusion in 4-hr food-deprived intact rabbits produced 38% suppression of food intake during the first hr postadministration, glycogen analysis revealed no significant reduction under the behavioral testing paradigm. These results indicate that glucagon can suppress food intake without depletion of liver glycogen. It is suggested that glucagon is not a satiety signal but can probably suppress feeding through initiating glycogenolysis.

Animals↗
PubMed1979

Electrophysiological and neuroanatomical studies of hepatic portal osmo- and sodium-receptive afferent projections within the brain.

Previous investigations concerning the function of hepatic sodium and osmoreceptors indicated that the activation of these chemoreceptive structures significantly affected physiological and behavioral mechanisms related to water and electrolyte homeostasis. Though anatomical studies predicted that such information should follow the previously described gustatory afferent pathy, until recently, the precise course taken by higher order hepatic afferents was unknown. The studies described herein verify anatomical predictions with regard to the central course of vagal-visceral afferents, as hepatically activated neurons were localized to two areas known to relay gustatory input. Further, horseradish peroxidase histochemical studies verified that a path between the nucleus of the solitary tract, the parabrachial nucleus and the ventrobasal complex certainly exists. In the light of recent findings regarding projections from the ventrobasal complex to the supraoptic nuclei, from the parabrachial nucleus to the supraoptic nuclei and from the nucleus of the solitary tract to the paraventricular and supraoptic nuclei it seems likely that the viscero-gustatory path which carries hepatic afferent information is the pathway responsible for the physiological and perhaps the behavioral consequences of hepatic sodium or osmotic stimulation.

Afferent Pathways↗
PubMed1978

Loss of glucagon suppression of feeding after vagotomy in rats.

Infusion of pancreatic glucagon through the hepatic-portal vein decreased short-term food intake in sham-vagotomized but not in subdiaphragmatically vagotomized rats. Measurement of hepatic glycogen storage showed that vagotomized rats maintain a lower glycogen level than control animals over the four fasting periods evaluated. To determine whether the absence of a glucagon effect on feeding in vagotomized rats was the result of the reduced amount of substrate for glycogenolysis, vagotomized rats were not fasted and control animals were food deprived for 8h to produce comparable hepatic glycogen levels. Hepatic-portal infusion of glucagon into these differentially fasted animals suppressed feeding in control rats but not in vagotomized rats. It is concluded that the ineffectiveness of glucagon in suppressing feeding in vagotomized rats is not due to reduced concentration of hepatic glycogen. Instead, it is likely that glucagon induces glycogenolysis, but the glucose, or some other correlate of glycogen breakdown, loses its ability to produce satiety subsequent to vagotomy.

Animals↗