A role for insulin in cephalic phase of postprandial thermogenesis in dogs

1988 ◽  
Vol 254 (5) ◽  
pp. E625-E632 ◽  
Author(s):  
P. Diamond ◽  
J. LeBlanc
Keyword(s):  
Causal Relationship ◽  
Insulin Release ◽  
Respiratory Quotient ◽  
Plasma Insulin ◽  
Control Experiment ◽  
Second Phase ◽  
O2 Consumption ◽  
Cephalic Phase ◽  
Postprandial Thermogenesis ◽  
Peak Increase

The influence of insulin in the cephalic phase of postprandial thermogenesis was investigated in dogs. O2 consumption (VO2) and respiratory quotient (RQ) were continuously monitored 1 h before and 2 h after a 1,015-kcal meal during a control, an atropine, or a pancreatic-denervation experiment. A first phase (cephalic phase) in VO2 increase, lasting at least 50 min, followed by a second phase (digestive phase) were found in the control experiment. During both the atropine and pancreatic-denervation experiment, the first phase of VO2 was inhibited by 52%. The second phase was completely abolished with atropine, whereas it remained comparable to the control in the case of pancreatic denervation. A peak increase for insulin (70 microU/ml over 0 time) was observed 2 min after the onset of feeding in control. It was followed after 25 min by a second increase related to changes in glycemia. Maximal rises of norepinephrine (NE) and epinephrine corresponded to 215 and 120 pg/ml above basal values at 2 min in control experiment. During both atropine and pancreatic denervation the cephalic phase of insulin release was suppressed and the NE increase was inhibited by congruent to 65%. During the digestive phase pancreatic denervation caused an increase in plasma insulin comparable to that of the control, whereas atropine produced no such effect. It is suggested that the cephalic phase of postprandial thermogenesis is mediated through a causal relationship between insulin and NE release.

Role of autonomic nervous system in postprandial thermogenesis in dogs

1987 ◽  
Vol 252 (6) ◽  
pp. E719-E726 ◽  
Author(s):  
P. Diamond ◽  
J. LeBlanc
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Control Experiment ◽  
Autonomic Nervous ◽  
Cephalic Phase ◽  
Two Phases ◽  
Postprandial Thermogenesis ◽  
Initial Peak ◽  
Peak Value

Two phases in postprandial thermogenesis have been recently identified in dogs; an initial cephalic phase lasting 45 min and a subsequent digestive phase occurring after 45 min. The objective of this study was to determine the role of the autonomic nervous system during these two phases in dogs. O2 uptake (VO2) as well as respiratory quotient (RQ) were monitored at least 1 h before and 2 h after a meal of 1,034 kcal under the following infusion conditions: saline, propranolol, atropine, propranolol plus atropine, phenoxybenzamine, and propranolol plus phenoxybenzamine. The initial peak value for VO2 increase was 100% in the cephalic phase and 40% in the digestive phase during the saline infusion. The VO2 response during the initial phase was 58 and 56% less with propranolol and atropine, respectively, compared with the control experiment. A 36% decrease in the VO2 response was found during the digestive phase with propranolol, whereas it was abolished by atropine. Propranolol and atropine given together decreased the VO2 response during the cephalic phase by 27% and abolished it completely in the digestive phase. Phenoxybenzamine did not affect the VO2 or RQ responses during the whole period and when given in combination with propranolol the same result as propranolol alone was found. These findings indicate that both the parasympathetic and sympathetic nervous system participate in the control of postprandial thermogenesis during both the cephalic and digestive phases.

Hormonal control of postprandial thermogenesis in dogs

1987 ◽  
Vol 253 (5) ◽  
pp. E521-E529 ◽  
Author(s):  
P. Diamond ◽  
J. LeBlanc
Keyword(s):  
Plasma Catecholamines ◽  
Tube Feeding ◽  
Hormonal Control ◽  
Second Phase ◽  
Feeding Experiment ◽  
Experimental Conditions ◽  
Sham Feeding ◽  
Cephalic Phase ◽  
Postprandial Thermogenesis

The role of catecholamines, insulin, and thyroid hormones on postprandial thermogenesis was determined in dogs. O2 consumption (VO2) and respiratory quotient (RQ) were continuously monitored 1 h before and 2 h after a 1,016-kcal meal under the three following experimental conditions corresponding to 1) normal feeding, 2) sham feeding (with food deflected into an esophageal pouch), and 3) tube feeding intragastrically. A first phase (cephalic phase), lasting at least 45 min, was observed during both normal and sham feeding, whereas a second phase (digestive phase), occurred in both normal and tube feeding. Increases of 260% for norepinephrine (NE) were found during the cephalic phase in both normal and sham feeding. Epinephrine (E) increased by 425 and 600% during this early phase in normal and sham feeding, respectively. No change in plasma catecholamines was found in the tube-feeding experiment. Large increases of 75 and 39 microU/ml of insulin occurred early after the meal in both normal and sham feeding, whereas insulin increased only after 30 min in tube feeding. Thyroxine and triiodothyronine were not changed with any feeding experiment. Insulin change was positively correlated with NE and E changes rather than with glucose change during the cephalic phase after feeding. The results suggest an important role of catecholamines in the increased postprandial thermogenesis during the cephalic phase with a possible modulating effect of insulin.

Interactions between postprandial thermogenesis, sensory stimulation of feeding, and hunger

1996 ◽  
Vol 271 (4) ◽  
pp. R936-R940 ◽  
Author(s):  
J. LeBlanc ◽  
J. Soucy
Keyword(s):  
Control Experiment ◽  
Sensory Stimulation ◽  
O2 Consumption ◽  
Feeding Experiment ◽  
Sham Feeding ◽  
Preceding Experiment ◽  
The One ◽  
Postprandial Thermogenesis ◽  
Stimulation Of

An early thermogenic response has been described following the ingestion of palatable food. This study was designed to investigate the possible relationship between this so-called cephalic response, the sensory stimulation of feeding, and the declining feeling of hunger as the meal progresses. O2 consumption, carbohydrate and lipid oxidation, as well as ratings of hunger were measured in four experimental situations in which the subjects, after overnight fast, ate either two small caramel cakes at one time or the same amount of calories divided in eight portions that were eaten at 10-min intervals. The third experiment, the sham-feeding experiment, was similar to the last one except that the food was spit out instead of being swallowed after being chewed. A control experiment was added in which no food was given but during which the subject mimicked the act of chewing as was done in the preceding experiment. A small increase in O2 consumed was observed in the control experiment. After the one-meal experiment, the increase was larger for the first 90 min and declined thereafter. During the first 40 min of the sham-feeding experiment, O2 consumption increased more than when the eight meals were eaten, indicating that during this period the sensory stimulation per se is responsible for the cephalic thermic response to food. At 90 min, the ratings of hunger were diminished not only in the eight meals experiment but in the eight sham meals experiment as well, showing the role of sensory stimulation in the control of hunger. These results indicate a possible causal relationship between the cephalic thermogenesis, the control of hunger, and the prandial sensory stimulations.

Cephalic phase insulin release in normal weight males: verification and reliability

1991 ◽  
Vol 261 (4) ◽  
pp. E430-E436 ◽  
Author(s):  
K. L. Teff ◽  
R. D. Mattes ◽  
K. Engelman
Keyword(s):  
Insulin Release ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Normal Weight ◽  
Significant Decline ◽  
Plasma Glucagon ◽  
Food Ingestion ◽  
Blood Samples ◽  
Food Stimulus ◽  
Cephalic Phase

The existence and reliability of cephalic phase insulin release (CPIR) were tested in 20 normal weight males. Each subject was challenged three times with the same food stimulus over a 5-day period. Four baseline blood samples were taken at 5-min intervals before food ingestion and then every 2 min for 16 min postingestion. Significant increases in plasma insulin were found at 4 min postingestion on each trial day. CPIR was found to be highly reproducible between trials (r = 0.83; P less than 0.001). Fifty percent of the subjects exhibited a significant increase of plasma insulin above their own baseline mean on the first trial, whereas 75 and 72% exhibited increases on trials 2 and 3, respectively. Only two subjects (10%) did not demonstrate a response on any trial. A significant decline in plasma glucose was observed at 4 min postingestion on trials 2 and 3. No significant changes in plasma glucagon were found during any trial day. This study confirms a reliable CPIR in normal weight males.

GASEOUS METABOLISM IN PREMATURE INFANTS AT 32-34°C AMBIENT TEMPERATURE

PEDIATRICS ◽  
1964 ◽  
Vol 33 (1) ◽  
pp. 75-82
Author(s):  
Forrest H. Adams ◽  
Tetsuro Fujiwara ◽  
Robert Spears ◽  
Joan Hodgman
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Consumption ◽  
Premature Infants ◽  
Rectal Temperature ◽  
Respiratory Quotient ◽  
Carbon Dioxide Production ◽  
Open Circuit ◽  
Co2 Production ◽  
O2 Consumption ◽  
Rate Of Increase

Thirty-four measurements of oxygen consumption, carbon dioxide production, respiratory quotient, and rectal temperature were made on 22 premature infants with ages ranging from 2½ hours to 18 days. The studies were conducted at 32-34°C utilizing an open circuit apparatus and a specially designed climatized chamber. Oxygen consumption and carbon dioxide production were lowest in the first 12 hours and increased thereafter. The rate of increase in O2 consumption was greater than that of CO2 production, with a consequent fall in respiratory quotient during the first 76 hours of life. A reverse relation of O2 consumption and CO2 production was found following the 4th day of life with a consequent rise in respiratory quotient. There was a close correlation between O2 consumption and rectal temperature regardless of age. A respiratory quotient below the value of 0.707 for fat metabolism was observed in 7 premature infants with ages ranging from 24 to 76 hours.

Effect of galanin on glucose-, arginine-, or potassium-stimulated insulin release

1989 ◽  
Vol 256 (5) ◽  
pp. E619-E623
Author(s):  
T. Yoshimura ◽  
J. Ishizuka ◽  
G. H. Greeley ◽  
J. C. Thompson
Keyword(s):  
Insulin Release ◽  
High Glucose ◽  
Second Phase ◽  
Dependent Manner ◽  
Perfused Pancreas ◽  
Isolated Perfused Pancreas ◽  
Second Phases ◽  
High Concentrations ◽  
Dose Dependent ◽  
Stimulation Of

We have examined the effect of galanin infusion on glucose-stimulated release of insulin from the isolated perfused pancreas of the rat to better characterize the effect of galanin on the first and second phases of insulin release. The effects of galanin on insulin release stimulated by L-arginine or high concentrations of potassium were also examined. When perfusion of galanin was started 4 min before the start of perfusion of high glucose (16.7 mM), galanin (10(-8)-10(-11) M) inhibited both the first and second phases of insulin release in a dose-dependent manner. When perfusion of galanin (10(-8) or 10(-9) M) was started simultaneously with high glucose (16.7 mM), only the second phase of insulin release was suppressed (P less than 0.05). Galanin (10(-9) M) failed to inhibit insulin release stimulated by L-arginine (10 and 5 mM) or potassium (25 and 20 mM). These findings suggest that the inhibitory action of galanin on glucose-stimulated insulin release is exerted on early intracellular events that occur during the stimulation of insulin release and that are common to both phases. Because galanin does not inhibit insulin release stimulated by L-arginine or potassium, galanin may inhibit glucose-stimulated closure of potassium channels.

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