Adrenergic blockade prevents endotoxin-induced increases in glucose metabolism

1988 ◽  
Vol 255 (5) ◽  
pp. E629-E635 ◽  
Author(s):  
D. M. Hargrove ◽  
G. J. Bagby ◽  
C. H. Lang ◽  
J. J. Spitzer
Keyword(s):  
Plasma Insulin ◽  
Lactate Concentration ◽  
Insulin Concentration ◽  
Adrenergic Blockade ◽  
Plasma Lactate ◽  
Glucose Kinetics ◽  
Plasma Insulin Concentration ◽  
Beta Adrenergic ◽  
Plasma Lactate Concentration ◽  
Adrenergic Antagonists

Combined alpha- and beta-adrenergic blockade was used to investigate the role of catecholamines in endotoxin-induced elevations in glucose kinetics. Glucose kinetics were measured before and for 4 h after the injection of endotoxin [100 micrograms/100 g body wt iv, 30% lethal dose (LD30) at 24 h]. Adrenergic blockade was achieved by the bolus injection of phentolamine and propranolol followed by their continuous infusion. Endotoxin-treated rats exhibited a transient hyperglycemia and sustained (greater than 4 h) increase in plasma lactate concentration, as well as elevated rates of glucose appearance (Ra, 83%), disappearance (Rd, 58%), recycling (160%), and metabolic clearance (23%). Adrenergic blockade prevented endotoxin-induced increases in plasma glucose concentration, Ra, Rd, and recycling but not glucose clearance. The increase in plasma lactate concentration was blunted by 35%. After 2 h, endotoxic animals infused with adrenergic antagonists developed hypoglycemia, which may have resulted from an increased plasma insulin concentration. The attenuation of elevated glucose turnover by adrenergic blockade in the endotoxin-treated animals was not due to a reduction in plasma glucagon level or differences in plasma insulin concentration. Administration of the alpha- or beta-adrenergic antagonists separately blunted but did not prevent endotoxin-induced changes in glucose kinetics, and therefore the efficacy of the adrenergic blockade could not be assigned to a single receptor class. These results indicate that catecholamines are important contributory factors to many of the early alterations in carbohydrate metabolism observed during endotoxemia.

Effect of beta-adrenergic blockade on plasma lactate concentration during exercise at high altitude

1991 ◽  
Vol 63 (5) ◽  
pp. 315-322 ◽  
Author(s):  
Andrew J. Young ◽  
Patricia M. Young ◽  
Robert E. McCullough ◽  
Lorna G. Moore ◽  
Allen Cymerman ◽  
...  
Keyword(s):  
High Altitude ◽  
Lactate Concentration ◽  
Adrenergic Blockade ◽  
Plasma Lactate ◽  
Beta Adrenergic ◽  
Plasma Lactate Concentration

Adrenergic blockade does not abolish elevated glucose turnover during bacterial infection

1988 ◽  
Vol 254 (1) ◽  
pp. E16-E22 ◽  
Author(s):  
D. M. Hargrove ◽  
G. J. Bagby ◽  
C. H. Lang ◽  
J. J. Spitzer
Keyword(s):  
Lactate Concentration ◽  
Glucose Turnover ◽  
Adrenergic System ◽  
Plasma Catecholamine ◽  
Adrenergic Blockade ◽  
Plasma Lactate ◽  
Glucose Kinetics ◽  
Elevated Glucose ◽  
Adrenergic Antagonists ◽  
Plasma Catecholamine Concentrations

Infusions of adrenergic antagonists were used to investigate the role of catecholamines in infection-induced elevations of glucose kinetics. Infection was produced in conscious catheterized rats by repeated subcutaneous injections of live Escherichia coli over 24 h. Glucose kinetics were measured by the constant intravenous infusion of [6-3H]- and [U-14C]glucose. Compared with noninfected rats, infected animals were hyperthermic (+1.4 degrees C) and showed increased rates of glucose appearance (45%), clearance (43%), and recycling (140%) as well as mild hyperlacticacidemia. Plasma catecholamine concentrations were increased by 50-70% in the infected rats, but there were no differences in plasma glucagon, corticosterone, and insulin levels. Adrenergic blockade was produced by primed constant infusion of both propranolol (beta-blocker) and phentolamine (alpha-blocker). A 2-h administration of adrenergic antagonists did not attenuate the elevated glucose kinetics or plasma lactate concentration in the infected rats, although it abolished the hyperthermia. In a second experiment, animals were infused with propranolol and phentolamine beginning 1 h before the first injection of E. coli and throughout the course of infection. Continuous adrenergic blockade failed to attenuate infection-induced elevations in glucose kinetics and plasma lactate. These results indicate that the adrenergic system does not mediate the elevated glucose metabolism observed in this mild model of infection.

Beta-adrenergic contribution to glucagon-induced glucose production and insulin secretion in uremia

1986 ◽  
Vol 251 (3) ◽  
pp. E322-E327
Author(s):  
P. Baylor ◽  
S. Shilo ◽  
J. Zonszein ◽  
H. Shamoon
Keyword(s):  
Plasma Insulin ◽  
Insulin Response ◽  
Glucose Production ◽  
Adrenergic Blockade ◽  
Glucose Kinetics ◽  
Beta Adrenergic ◽  
Adrenergic Regulation ◽  
Insulin Secretory Response ◽  
Plasma Insulin Response ◽  
Normal Controls

Spontaneous or propranolol-induced hypoglycemia can occur in uremic humans. We studied glucose kinetics (using [3-3H]glucose) in five uremic humans 24 h after hemodialysis and in seven normal controls. The effect of glucagon infusion at rates of 3, 6, 12, and 18 ng X kg-1 X min-1 at 60-min intervals was compared with either saline or beta-adrenergic blockade (propranolol infusion). In uremics, plasma glucose increased by 20-25% and by 40-50% at the 3 and 6 ng X kg-1 X min-1 glucagon doses, respectively, with no further increases at higher infusion rates. Glucose production increased transiently and in tandem with glucose uptake at each glucagon increment (P less than 0.0001). During beta-adrenergic blockade, the effect of glucagon in stimulating glucose production was blunted by 14-24% at the 6-18 ng X kg-1 X min-1 doses (P less than 0.05). During saline infusion, plasma insulin concentrations increased progressively to peak levels fourfold above basal at the 18 ng X kg-1 X min-1 dose. This increase in plasma insulin was virtually abolished by concomitant beta-adrenergic blockade (P = 0.0002). In contrast to uremic subjects, normal controls exhibited lesser degrees of hyperglycemia and hyperinsulinemia at all glucagon infusion rates. Propranolol infusion had no effect on the increments in glucose production and uptake nor on the plasma insulin response. These results suggest that in uremic humans propranolol independently reduces the hepatic response to glucagon and the insulin secretory response to hyperglycemia and/or hyperglucagonemia. These observations provide a possible mechanism for the adrenergic regulation of glucose homeostasis in uremia.

Influence of Glucose Kinetics on Plasma Lactate Concentration and Energy Expenditure in Severely Burned Patients

2000 ◽  
Vol 49 (4) ◽  
pp. 673-678 ◽  
Author(s):  
Dennis C. Gore ◽  
Arny Ferrando ◽  
Joseph Barnett ◽  
Steven E. Wolf ◽  
Manubhai Desai ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Lactate Concentration ◽  
Plasma Lactate ◽  
Glucose Kinetics ◽  
Plasma Lactate Concentration

INHIBITORY EFFECT OF SOMATOSTATIN ON INSULIN SECRETION DURING α-ADRENERGIC BLOCKADE IN THREE DIFFERENT SPECIES

1979 ◽  
Vol 92 (1) ◽  
pp. 166-173 ◽  
Author(s):  
Johannes Järhult ◽  
Bo Ahrén ◽  
Ingmar Lundquist
Keyword(s):  
Insulin Secretion ◽  
B Cell ◽  
Insulin Release ◽  
Plasma Insulin ◽  
Inhibitory Effect ◽  
Insulin Concentration ◽  
Adrenergic Blockade ◽  
Plasma Insulin Concentration ◽  
Basal Plasma ◽  
Stimulation Of

ABSTRACT It has recently been suggested from experiments in dogs that somatostatin suppresses insulin release via a stimulation of the inhibitory α-adrenoceptors of the pancreatic B-cell. The effect of somatostatin on insulin secretion during α-adrenergic blockade with phentolamine was therefore studied in three different species; the rat, the cat and the mouse. It was found that somatostatin significantly depressed insulin release during α-adrenoceptor blockade in all three species. In the rat, infusion of somatostatin at a dose of 0.3 μg/kg/min decreased basal plasma insulin concentration by 92 %. In the presence of phentolamine, the same dose of somatostatin lowered plasma insulin by 85 %. In the cat, a similar infusion of somatostatin lowered basal plasma insulin concentration by 87 %, but its depressive effect during α-adrenergic blockade was comparatively less pronounced (68 %) than in the rat. In the mouse, a single iv injection of somatostatin induced a short-lasting depression of plasma insulin concentration during α-adrenergic blockade. From these results it seems unlikely that somatostatin should inhibit insulin release simply by stimulation of α-adrenoceptors on the B-cell. It cannot be ruled out, however, that a more complex interaction exists between somatostatin and the sympatho-adrenal system with regard to the control of insulin secretion.

Comparison of thermogenic effect of fructose and glucose in normal humans

1986 ◽  
Vol 250 (6) ◽  
pp. E718-E724 ◽  
Author(s):  
L. Tappy ◽  
J. P. Randin ◽  
J. P. Felber ◽  
R. Chiolero ◽  
D. C. Simonson ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Lipid Oxidation ◽  
Plasma Insulin ◽  
Carbohydrate Oxidation ◽  
Insulin Concentration ◽  
Adrenergic Blockade ◽  
Plasma Insulin Concentration ◽  
Carbohydrate Ingestion ◽  
Glucose Ingestion ◽  
Adrenergic Nervous System

After nutrient ingestion there is an increase in energy expenditure that has been referred to as dietary-induced thermogenesis. In the present study we have employed indirect calorimetry to compare the increment in energy expenditure after the ingestion of 75 g of glucose or fructose in 17 healthy volunteers. During the 4 h after glucose ingestion the plasma insulin concentration increased by 33 +/- 4 microU/ml and this was associated with a significant increase in carbohydrate oxidation and decrement in lipid oxidation. Energy expenditure increased by 0.08 +/- 0.01 kcal/min. When fructose was ingested, the plasma insulin concentration increased by only 8 +/- 2 microU/ml vs. glucose. Nonetheless, the increments in carbohydrate oxidation and decrement in lipid oxidation were significantly greater than with glucose. The increment in energy expenditure was also greater with fructose. When the mean increment in plasma insulin concentration after fructose was reproduced using the insulin clamp technique, the increase in carbohydrate oxidation and decrement in lipid oxidation were markedly reduced compared with the fructose-ingestion study; energy expenditure failed to increase above basal levels. To examine the role of the adrenergic nervous system in fructose-induced thermogenesis, fructose ingestion was also performed during beta-adrenergic blockade with propranolol. The increase in energy expenditure during fructose plus propranolol was lower than with fructose ingestion alone. These results indicate that the stimulation of thermogenesis after carbohydrate ingestion is related to an augmentation of cellular metabolism and is not dependent on an increase in the plasma insulin concentration per se.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals 146 Nutritional Advances in Fetal and neonatal development: effect of fatty acid supplementation

2020 ◽  
Vol 98 (Supplement_3) ◽  
pp. 121-122
Author(s):  
Alejandro E Relling
Keyword(s):  
Small Intestine ◽  
Fatty Acid ◽  
Plasma Insulin ◽  
Linear Increase ◽  
Late Gestation ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
Pufa Supplementation ◽  
Epa And Dha ◽  
Offspring Growth

Abstract Data from a series of experiments demonstrates that maternal supply of polyunsaturated fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), during late gestation affects offspring growth. The increase in growth is independent on the fatty acid supplemented during the growing or finishing phase of the offspring; but it is sex dependent. Dam PUFA supplementation increases wether growth. Supplementation with EPA and DHA to pregnant ewes and to their offspring after weaning showed a treatment interaction in mRNA concentration of hypothalamic neuropeptides associated with dry matter intake (DMI) regulation. A dose increased in EPA and DHA in pregnant ewe diets shows a linear increase in growth, but a quadratic change in DMI or feed efficiency; growth was associated with a linear increase in plasma glucose concentration and a linear decrease in plasma ghrelin concentration. In lambs born from ewes supplemented with different sources of FA during a glucose tolerance test; males’ plasma insulin concentration increased as FA unsaturation degree increased in the dam diet, the opposite happened with females’ plasma insulin concentration. Recent data from our lab showed that the supplementation with EPA and DHA during the last third of gestation to pregnant ewes increased liver and small intestine global DNA methylation and small intestine transporters for amino acids in the fetus. Despite EPA and DHA during late gestation increase growth in the offspring; when EPA and DHA were supplemented in early gestation, offspring growth was lesser that lambs born from ewes supplemented a saturated and monounsaturated lipid. The reason for the difference in results it is not clear. However, more studies focusing in some aspect of the biology will help to understand what specific fatty acid needs to be supplemented at different stages of gestation to improve offspring growth.

scholarly journals Fetal growth, glucose tolerance and plasma insulin concentration in rats given a marginal-zinc diet in the latter stages of pregnancy

1988 ◽  
Vol 59 (2) ◽  
pp. 315-322 ◽  
Author(s):  
Susan Southon ◽  
Susan J. Fairweather-Tait ◽  
Christine M. Williams
Keyword(s):  
Blood Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Insulin Concentration ◽  
Oral Glucose ◽  
Fetal Blood ◽  
Plasma Insulin Concentration ◽  
Pregnant Rats ◽  
Zn Content ◽  
Tail Blood

1. Wistar rats were fed on a control semi-synthetic diet throughout pregnancy, or a control diet in the first 2 weeks and a marginal-zinc diet in the 3rd week of pregnancy. On day 20, after an overnight fast, half the animals in each group were given glucose by gavage and the 0–30 min rise in blood glucose measured in tail blood. After 60 min blood was taken by cardiac puncture for glucose and insulin assay. Maternal pancreases were removed and the Zn contents measured. Fetuses from each litter were combined for wet/dry weights, protein and DNA determinations.2. Plasma insulin concentration was higher, and glucose concentration and pancreatic Zn content lower, in pregnantv. non-pregnant animals of similar age, fed on the same diet. Pancreatic Zn content was lowest in the marginal-Zn group of pregnant rats. Fetuses from mothers fed on the marginal-Zn diet during the last week of pregnancy were slightly heavier than controls and had a significantly higher protein: DNA ratio. The 0–30 min rise in blood glucose was significantly greater in the marginal-Zn animals.3. In a second experiment, pregnant rats were given similar diets to those used in the first study, but the marginal-Zn diet was given for a shorter period (days 15–19 of pregnancy). On day 19 the rats were meal-fed and on day 20, after an overnight fast, an oral glucose dose was administered. Tail-blood was taken at timed intervals up to 60 min post-dosing for glucose assay. Both maternal and fetal blood glucose and insulin concentration was measured 70 min post-dosing.4. Values for maternal and fetal blood glucose and plasma insulin, measured 70 min after the administration of a glucose dose, were similar in the two groups, but the initial rise in blood glucose concentration was again significantly higher in pregnant rats given the marginal-Zn diet towards term.5. It is suggested that the change in growth and composition, observed in fetuses from rats given a marginal-Zn diet in later pregnancy, is associated with altered maternal carbohydrate metabolism.

Glucose and lactate kinetics after endotoxin administration in dogs.

1977 ◽  
Vol 232 (2) ◽  
pp. E180 ◽  
Author(s):  
R R Wolfe ◽  
D Elahi ◽  
J J Spitzer
Keyword(s):  
Lactate Concentration ◽  
Constant Infusion ◽  
Glucose Turnover ◽  
Metabolic Clearance ◽  
Plasma Lactate ◽  
Metabolic Clearance Rate ◽  
Metabolic Substrate ◽  
E Coli ◽  
Lactate Kinetics ◽  
Plasma Lactate Concentration

We studied the effects of E. coli endotoxin on the glucose and lactate kinetics in dogs by means of the primed constant infusion of [6(-3)H] glucose and Na-L-(+)-[U-14C] lactate. The infusion of endotoxin induced a transient hyperglycemic level, followed by a steady fall in plasma glucose to hypoglycemic levels. The rate of appearance (Ra) and the rate of disappearance (Rd) of glucose were both significantly elevated (P less than .05) for 150 min after endotoxin, after which neither differed from the preinfusion value. The metabolic clearance rate of glucose was significantly elevated at all times 30 min postendotoxin. By 30 min postendotoxin, Ra and Rd of lactate, plasma lactate concentration, and the percent of glucose turnover originating from lactate were significantly elevated and remained so for the duration of the experiment. We concluded that after endotoxin hypoglycemia developed because of an enhanced peripheral uptake of glucose and a failure of the liver to maintain an increased Ra of glucose. We also concluded that lactate became an important precursor for gluconeogenesis and an important metabolic substrate.

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