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Biomedical subjects

N Geary

Publications and source records attributed to N Geary.

At least 73 records · Page 4Linked to original sources
PubMed1986

Pancreatic glucagon's effects on satiety and hepatic glucose production are independently affected by diet composition.

We tested whether pancreatic glucagon's effects on satiety and hepatic glycogenolysis depend on variations in the macronutrient composition of the diet. Rats were kept on high carbohydrate, high fat, or high protein diets (HC-, HF- or HP-rats, respectively) and adapted to a 5 hour feeding (11:00-16:00)-19 hour deprivation (16:00-11:00) schedule. Glucagon (540 mcg/kg body weight) was intraperitoneally injected at 14:00. Glucagon stimulated similar amounts of hepatic glycogenolysis in HC- and in HF-rats and less glycogenolysis in HP-rats, but glucagon decreased food intake only in HC-rats. When HF- or HP-rats were prefed the HC-diet once for 1 hour (11:00-12:00) prior to injection, glucagon stimulated hepatic glycogenolysis similarly in both groups but decreased food intake only in HF-rats. Therefore, stimulation of hepatic glycogenolysis by glucagon is not sufficient to elicit satiety under all feeding conditions. The results also suggest that glucagon-induced satiety is not limited to carbohydrate intake.

Animals↗
PubMed1986

Pancreatic glucagon and bombesin inhibit meal size in ventromedial hypothalamus-lesioned rats.

The effects of intraperitoneal injections of pancreatic glucagon and bombesin on meal size were tested in female rats in the dynamic phase of ventromedial hypothalamic (VMH) hyperphagia. Both pancreatic glucagon (100-2500 micrograms/kg) and bombesin (4-16 micrograms/kg) inhibited meal size in a dose-related manner. Percent inhibitions of meal size in VMH-lesioned and control rats did not differ significantly. These results suggest that the VMH is not necessary for peripheral administration of either pancreatic glucagon or bombesin to elicit postprandial satiety.

Animals↗
PubMed1986

Combined injection potentiates the satiety effects of pancreatic glucagon, cholecystokinin, and bombesin.

Pancreatic glucagon (PG), cholecystokinin (CCK), and bombesin (BBS) were injected individually and in combination before nondeprived rats were offered condensed milk test meals. Peptide doses that were individually below the threshold for reliable inhibition of meal size (0.15 microgram/kg CCK, 0.75 microgram/kg BBS, 100 micrograms/kg PG) combined to inhibit meal size 19-40%. The inhibitions produced by combinations including CCK were 16-21% more than the sum of the inhibitions elicited by individual injections. This indicates a potentiation of inhibition. In contrast, when peptide doses were increased, the inhibitory effects of the combinations were similar to the sum of the individual injections. None of the peptide treatments disrupted the normal behavioral sequence of postprandial satiety, and they did not reliably affect water intake in water-deprived rats. We conclude that exogenous CCK, BBS, and PG can interact to potentiate postprandial satiety.

Animals↗
PubMed1985

Partial liver denervations dissociate the inhibitory effects of pancreatic glucagon and epinephrine on feeding.

We compared the roles of different components of the liver's innervation in the inhibitory effects of pancreatic glucagon and epinephrine on feeding by testing the effects on meal size of intraperitoneal injections of these hormones in rats with selective abdominal vagotomies of only the hepatic branch, with partial liver denervations that spared only the hepatic branch of the vagus, and with sham operations. Pancreatic glucagon (100-400 micrograms/kg) inhibited size of evaporated milk test meals equally in rats with partial liver denervations sparing the hepatic vagus and in sham-operated rats, but had no effect on feeding in rats with selective hepatic vagotomies. In contrast, epinephrine (25-100 micrograms/kg) inhibited meal size equally in all rats. These data suggest that the hepatic vagus is the necessary and sufficient contribution of the liver's innervation to pancreatic glucagon's satiety effect and that hepatic innervation does not contribute to epinephrine's inhibitory effect on meal size. Thus, different peripheral neural mechanisms appear to mediate the effects of these hormones on feeding. Further, the data fail to support the hypothesis that abdominal vagotomies and coeliac ganglionectomies attenuate epinephrine's effect on feeding by disconnecting hepatic afferents.

Animals↗
PubMed1985

Pimozide decreases the positive reinforcing effect of sham fed sucrose in the rat.

Rats with chronic gastric cannulas were intraperitoneally injected with the dopamine receptor antagonist pimozide (0.25 mg/kg) before sham feeding 5, 10, 20, or 40% (w/v) sucrose solutions. Amount of sham intake after control injections increased as a function of sucrose concentration. At each concentration, the rate of sham feeding was greatest during the initial 3 min of sham feeding and subsequently decelerated. Pimozide inhibited sham feeding rate, and the temporal pattern of decreases in sham feeding rate after pimozide were similar to those produced by decreasing the concentration of sucrose sham fed. These data extend previous reports of the inhibitory effect of pimozide on ingestion of sweet fluids by eliminating the possibility that the effect was the result of pimozide facilitating postingestional inhibitory mechanisms. Further, pimozide did not appear to produce fatigue or sedation, or to reduce the rats' motor capacity to sham feed. Therefore, these data are consistent with the hypothesis that central dopaminergic synaptic activity mediates the reinforcing effects of sweet taste that drive sham feeding.

Animals↗
PubMed1984

Late surgical decompression for compartment syndrome of the forearm.

Two cases are reported of the late diagnosis of compartment syndrome secondary to alcohol and drug overdose. Surgical decompression at two and a half days and at six days, respectively, produced worthwhile recovery. Other reports are reviewed and a case is made for the value of decompression even when performed late, and for delayed and minimal excision of apparently necrotic muscle.

Adult↗
PubMed1983

Selective hepatic vagotomy blocks pancreatic glucagon's satiety effect.

To test the hypothesis that hepatic vagal afferents mediate the satiety effect of pancreatic glucagon, we tested the effects of selective surgical and pharmacological lesions of the abdominal vagus on glucagon's potency to inhibit feeding. Surgical disconnection of only the hepatic branch of the abdominal vagus blocked glucagon's satiety effect as well as total abdominal vagotomy. However, abdominal vagotomy that spared the hepatic branch did not change glucagon's satiety effect. Glucagon also inhibited feeding after pharmacological blockade of peripheral postganglionic muscarinic receptors with atropine methylnitrate. All these results are consistent with the hypothesis that hepatic vagal afferents mediate the satiety effect of pancreatic glucagon.

Animals↗
PubMed1982

Stimulation of feeding in rats by intraperitoneal injection of antibodies to glucagon.

Intraperitoneal injections of antibodies to pancreatic glucagon at the onset of the first meal after 12 hours of food deprivation increased meal size 63 percent and meal duration 74 percent in rats. The antibodies also reduced the increase in hepatic vein blood glucose that occurred during meals in control rats, but did not affect the prandial increase in portal vein blood glucose. These results suggest that, under these conditions, pancreatic glucagon is necessary for the normal termination of meals.

Animals↗
PubMed1982

Pancreatic glucagon and postprandial satiety in the rat.

The hypothesis that administration of pancreatic glucagon inhibits feeding by eliciting satiety for food was tested against several behavioral and physiological criteria of specificity. The effects of intraperitoneal glucagon injections on intake of a palatable milk diet were tested in rats maintained with ad lib access to pelleted diet. Injections of 25--800 micrograms/kg glucagon administered at meal onset inhibited meal size by 17--36%, but did not affect the normal postprandial behavioral satiety sequence or elicit any behavioral signs of toxicity. Latency to rest and intermeal interval were not affected. Glucagon decreased meal size by specifically inhibiting feeding during the terminal phase of the meal without affecting feeding earlier in the meal. This was also the case when glucagon was injected 4 min prior to meal onset. This range of glucagon doses did not affect water intake in water deprived rats consuming fluid volumes comparable to the milk intakes. They also did not affect body temperature. Finally, injection of 400 micrograms/kg glucagon after the initial exposure to a novel drinking fluid was not sufficient to form a conditioned taste aversion in a two bottle preference test. These data, together with reports that circulating pancreatic glucagon levels increase during meals, strongly suggest that pancreatic glucagon is involved in the production of postprandial satiety.

Animals↗
PubMed1982

Blood metabolites and feeding during postinsulin hypophagia.

Physiological changes accompanying a period of voluntary hypophagia in male Sprague-Dawley rats after insulin-induced hyperphagia and body weight gain were investigated. Postinsulin hypophagia was manifested as a reduction in meal duration diurnally and nocturnally (Geary et al., Behav. Neural Biol. 31: 435-442, 1981). Gastrointestinal transit of 14C-labeled nutrients was unchanged in hypophagic rats, suggesting a postabsorptive mechanism controlled the hypophagia. Basal blood glucose and plasma nonesterified fatty acids, 3-hydroxybutyrate, glycerol, and some amino acids were elevated during hypophagia, while liver glycogen content was reduced. Hypophagic rats' arteriovenous blood glucose differences and glucose oxidation rates, however, were not different from controls. After nutrient repletion blood glucose and plasma glycerol remained elevated in hypophagic rats in comparison to controls, while differences in other plasma metabolites were reduced. Liver glycogen accumulated faster in hypophagic rats. These data were related to the lipostatic and other hypotheses how energy balance status affects hunger and satiety.

3-Hydroxybutyric Acid↗
PubMed1982

Liver glycogen content decreases during meals in rats.

The effects of feeding on liver glycogen content and blood glucose in the hepatic and hepatic portal veins were investigated in rats. Liver glycogen content decreased about 25% during meals both in rats refed after 12 h food deprivation (23 +/- 1 to 17 +/- 1 mg glycogen/g liver) and in ad libitum-fed rats taking fully spontaneous meals (44 +/- 2 to 32 +/- 2 mg/g). Liver glycogen began to increase within 30 min after meals in ad libitum-fed rats. Hepatic vein blood glucose levels at meal onset (118 +/- 4 mg/dl in the food-deprived rats, 127 +/- 4 in ad libitum-fed rats) and at meal end (155 +/- 3 and 166 +/- 5 mg/dl, respectively) were similar in the two groups. Portal vein blood glucose increased during meals in the previously food-deprived rats (83 +/- 4 to 116 +/- 6 mg/dl) but not in the ad libitum-fed rats (127 +/- 5 to 132 +/- 3 mg/dl). Mechanisms that may elicit prandial glycogenolysis and the possible role of this effect in the production of meal ending satiety are discussed.

Animals↗
PubMed1981

Metabolic concomitants of glucagon-induced suppression of feeding in the rat.

The suppression of food intake elicited in rats by injection of pancreatic glucagon and the accompanying changes in energy metabolite flux were investigated. Glucagon injections, 120-360 micrograms ip, were made as rats began the first meal of the dark phase after food deprivation during the light phase. Glucagon-injected rats terminated their meals sooner and ate smaller meals than vehicle-injected rats. For metabolic assays, rats were identically treated and killed just at meal onset or 15 min later. Portal vein blood glucose increased similarly in all rats allowed to feed, whereas plasma nonesterified fatty acid and D-(-)-3-hydroxybutyrate levels decreased during feeding. In contrast, hepatic vein and aorta blood glucose levels increased more after glucagon than after vehicle injections. Liver glycogen content decreased after glucagon injections. The highest glucagon dose only had slight lipolytic and ketogenic effects. It was concluded the glycogenolytic and hyperglycemic action of glucagon may generate a satiety signal sufficient to cause premature termination of meals. Changes in ketone and lipid fluxes do not appear necessary for this behavioral effect.

Animals↗
PubMed1977

Intragastric cannulation procedures and rats' food intake and body weight maintenance.

Effects upon food and water intakes and body weight maintenance of two procedures for preparing rats with chronic intragastric cannulae were examined. A transient aphagia and rapid weight loss followed installation of the classic nasopharyngeal cannula. Growth was resumed after about a week, but subsequent food and water intakes were chronically depressed in comparison to sham operated animals of the same age. Body weight was also chronically subnormal. The response of these animals to caloric dilution of the diet was, however, normal. In contrast to the nasopharyngeal procedure, a method involving direct cannulation of the stomach wall did not lead to either behavioral or weight regulatory deficits and is therefore recommended.

Animals↗
PubMedDate not supplied

Failure of pulsatile infusion to increase glucagon's satiating potency.

Intraportal infusions of glucagon elicit a dose-related reduction in the size of rats' spontaneous meals. The glucagon doses required to reduce meal size, however, appear large in comparison to plasma glucagon concentrations during meals. Because prandial glucagon secretion may be pulsatile, however, pulsatile glucagon infusions may reduce meal size more potently than continuous infusions. To test that hypothesis, I compared the effects of a single 2-min infusion of 6.8 micrograms/min glucagon and two 1-min pulses of the same glucagon concentration separated by 1 min. Glucagon was infused via the hepatic portal vein during male rats' first spontaneous meal of the last quarter of the dark phase, and meal patterns were recorded by a computer. The results did not support the hypothesis. Meal size was reduced comparably in each infusion condition (from approximately 3.1 g in the control conditions to approximately 2.3 g after continuous glucagon infusion and approximately 2.2 g after pulsatile infusion). This result is discussed in relation to tests of glucagon antibody administration that indicate endogenous glucagon is a physiological control of meal size in rats. Additionally, in contrast to previous reports, glucagon infusion during late dark spontaneous meals decreased the length of the subsequent intermeal intervals, suggesting that glucagon's satiating effect was transient.

Animals↗