Effect of low temperatures on glucose-induced insulin secretion and glucose metabolism in isolated pancreatic islets of the rat

1990 ◽  
Vol 125 (1) ◽  
pp. 45-51 ◽  
Author(s):  
J. C. Escolar ◽  
R. Hoo-Paris ◽  
Ch. Castex ◽  
B. Ch. J. Sutter
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Glucose Oxidation ◽  
Glucose Utilization ◽  
Pentose Phosphate ◽  
Experimental Conditions ◽  
Isolated Pancreatic Islets ◽  
Acid Cycle ◽  
The Difference ◽  
Pentose Pathway

ABSTRACT The direct effect of hypothermia on the inhibition of insulin secretion may result from inhibition of the availability of energetic substrates and/or the lack of metabolic signals. In order to verify this hypothesis, the insulin secretion and the main metabolic glucose pathways were measured during the incubation of rat islets. In the presence of 16·7 mmol glucose/l and at 37 °C, insulin secretion was 925 ± 119 μU/2 h per ten islets. With the same experimental conditions, glucose utilization, determined as the formation of 3H2O from [5-3H]glucose was 2225 ±184 pmol/2 h per ten islets, glucose oxidation measured as the formation of 14CO2 from [U-14C]glucose was 673 ± 51 pmol/2 h per ten islets, pentose cycle determined as the formation of 14CO2 from either [1-14C]glucose or [6-14C]glucose was 37 ± 5 pmol/2 h per ten islets; glucose oxidation by the tricarboxilic acid cycle, calculated to be the difference between glucose oxidation and pentose cycle values, was 636 pmol/2 h per ten islets. Hypothermia highly inhibited glucose-induced insulin secretion and glucose utilization. Inhibition of insulin secretion was partial at 27 °C since it was 2·5 times lower than that at 37 °C, and it was complete at 17 °C. Glucose oxidation in the tricarboxilic acid cycle was markedly inhibited by hypothermia since the inhibition coefficient (Q10) between 37 and 27 °C was 5. In contrast, glucose oxidation in the pentose phosphate shunt was enhanced at 27 °C, reaching 92 ± 17 pmol/2 h per ten islets, and it was inhibited relatively little at 17 °C. These results suggest that hypothermia markedly inhibits glucose metabolism with the exception of the pentose pathway which could play an important role by inducing the insulin secretion at 27 °C. Journal of Endocrinology (1990) 125, 45–51

scholarly journals Glucose metabolism and its regulation in pieces of perirenal adipose tissue from foetal lambs

1983 ◽  
Vol 210 (3) ◽  
pp. 677-683 ◽  
Author(s):  
J P Robertson ◽  
A Faulkner ◽  
R G Vernon
Keyword(s):  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Pyruvate Dehydrogenase ◽  
Glucose Utilization ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Pentose Phosphate ◽  
Acid Cycle ◽  
Near Term ◽  
Glucose 6 Phosphate Dehydrogenase

1. The following were measured in pieces of perirenal adipose tissue obtained from foetal lambs at about 120 days of gestation or within 3 days of term, and 9-month-old sheep: the rates of synthesis from glucose of fatty acids, acylglycerol glycerol, pyruvate and lactate; the rate of glucose oxidation to CO2 and the proportions contributed by the pentose phosphate cycle, pyruvate dehydrogenase and the tricarboxylic acid cycle; the activities of hexokinase, glucose 6-phosphate dehydrogenase, phosphofructokinase, pyruvate kinase and pyruvate dehydrogenase. 2. The total rate of glucose utilization was lower in pieces of adipose tissue from near-term lambs than 120-day foetal lambs and the pattern of glucose metabolism differed, with, for example, a much smaller proportion of glucose carbon being used for fatty acid synthesis, whereas a greater proportion of glucose oxidation occurred via the tricarboxylic acid cycle in the near-term lambs. In general, these differences in glucose metabolism were not associated with differences in the activities of the various enzymes listed above. 3. The rates of glucose utilization per fat-cell by 120-day foetal lambs and 9-month-old sheep were very similar but, again, the proportions metabolized to the various products differed. In particular, there was a smaller proportion of glucose oxidized via the pentose phosphate cycle and a greater proportion oxidized via pyruvate dehydrogenase and the tricarboxylic acid cycle in adipose tissue from foetal lambs. These differences were matched by a lower activity of glucose 6-phosphate dehydrogenase and a higher pyruvate dehydrogenase activity in fat-cells from the foetal lambs.

scholarly journals Effects in vitro of alloxan on the glucose metabolism of mouse pancreatic B-cells

1979 ◽  
Vol 182 (3) ◽  
pp. 797-802 ◽  
Author(s):  
L. A. Håkan Borg ◽  
Susan J. Eide ◽  
Arne Andersson ◽  
Claes Hellerström
Keyword(s):  
Glucose Metabolism ◽  
Glucose Oxidation ◽  
Glucose Utilization ◽  
Essential Feature ◽  
Inhibitory Effect ◽  
Endogenous Respiration ◽  
Cytotoxic Action ◽  
Dependent Manner ◽  
Isolated Pancreatic Islets

To facilitate detailed studies of the B-cytotoxic action of alloxan we developed a model using isolated pancreatic islets of normal mice. An essential feature of this model is the low temperature employed during exposure to alloxan, which minimizes the degradation of the drug. The islets were incubated with alloxan for 30min at 4°C and subsequently various aspects of their metabolism were studied. The O2 consumption was measured by the Cartesian-diver technique. Islets exposed to 2mm-alloxan and control islets had the same endogenous respiration, whereas the O2 uptake of the alloxan-treated islets was inhibited and that of the control islets stimulated when they were incubated with 28mm-glucose as an exogenous substrate. The islet glucose oxidation was estimated by measurement of the formation of 14CO2 from [U-14C]glucose at 37°C. Compared with the controls, alloxan-treated islets showed a decrease in the glucose-oxidation rate in a dose-dependent manner. Pretreatment of the islets with 28mm-glucose for 30min at 37°C completely protected against this effect, whereas preincubations at glucose concentrations below 16.7mm failed to exert any protective effect. The glucose utilization was estimated as the formation of 3H2O from [5-3H]glucose. Alloxan (2mm) failed to affect islet glucoseutilization rate in the presence of either 2.8 or 28mm-glucose. In contrast, islets exposed to 5 or 10mm-alloxan exhibited lowered glucose utilization. It is concluded that in vitro alloxan has an acute inhibitory effect on the islet glucose metabolism, and that this action can be prevented by previous exposure to a high glucose concentration. The results are consistent with the idea that the B-cytotoxicity of alloxan reflects an interaction with intracellular sites involved in the oxidative metabolism of the B-cell.

scholarly journals The effect of starvation on insulin secretion and glucose metabolism in mouse pancreatic islets

1974 ◽  
Vol 140 (3) ◽  
pp. 423-433 ◽  
Author(s):  
Carl J. Hedeskov ◽  
Kirsten Capito
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Pancreatic Islets ◽  
Glucose Utilization ◽  
Secretory Response ◽  
Secretory Process ◽  
Fed State ◽  
Lactate Output ◽  
Extracellular Glucose ◽  
Km Value

1. Rates of insulin secretion, glucose utilization, lactate output, incorporation of glucose into glycogen, contents of glucose 6-phosphate, fructose 1,6-diphosphate and ATP, and maximally extractable enzyme activities of hexokinase, high-Km glucose-phosphorylating activity (`glucokinase'), glucose 6-phosphatase and unspecific acid phosphatase were measured in isolated pancreatic islets from fed and 48-h-starved mice. 2. In the fed state insulin secretion from isolated islets was increased five- to six-fold when the extracellular glucose concentration was raised from 2.5mm to 16.7mm; 5mm-caffeine potentiated this effect. The secretory response to glucose of islets from mice starved for 48h was diminished at all glucose concentrations from 2.5mm up to approx. 40mm. Very high glucose concentrations (60mm and above) restored the secretory response to that found in the fed state, suggesting that the Km value for the overall secretory process had been increased (approx. fourfold) by starvation. Addition of 5mm-caffeine to islets from starved mice also restored the insulin secretory response to 2.5–16.7mm-glucose to normal values. 3. Extractable hexokinase, `glucokinase', glucose 6-phosphatase and unspecific phosphatase activities were not changed by starvation. 4. Glucose utilization and glycolysis (measured as the rate of formation of 3H2O from [5-3H]glucose over a 2h period) was decreased in islets from starved mice at all glucose concentrations up to approx. 55mm. At still higher glucose concentrations up to approx. 100mm, there was no difference between the fed and starved state, suggesting that the Km value for the rate-limiting glucose phosphorylation had been increased (approx. twofold) by starvation. Preparation of islets omitting substrates (glucose, pyruvate, fumarate and glutamate) from the medium during collagenase treatment lowered the glucose utilization measured subsequently at 16.7mm-glucose by 38 and 30% in islets from fed and starved mice respectively. Also the 2h lactate output by the islets at 16.7mm extracellular glucose was diminished by starvation. Incorporation of glucose into glycogen was extremely low, but the rate of incorporation was more than doubled by starvation. 5. After incubation for 30min at 16.7mm-glucose the content of glucose 6-phosphate was unchanged by starvation, that of ATP was increased and the concentration of (fructose 1,6-diphosphate plus triose phosphates) was decreased. 6. Possible mechanisms behind the correlated impairment in insulin secretion and islet glucose metabolism during starvation are discussed.

scholarly journals Quantitative measurement of the L-type pentose phosphate cycle with [2-14C]glucose and [5-14C]glucose in isolated hepatocytes

1980 ◽  
Vol 188 (3) ◽  
pp. 859-865 ◽  
Author(s):  
J P Longenecker ◽  
J F Williams
Keyword(s):  
Glucose Metabolism ◽  
Exchange Reaction ◽  
Quantitative Measurement ◽  
Distribution Patterns ◽  
Isolated Hepatocytes ◽  
Pentose Phosphate ◽  
Triose Phosphate ◽  
Pentose Phosphate Cycle ◽  
Quantitative Contribution ◽  
Pentose Pathway

1. Investigations of the mechanism of the non-oxidative segment of the pentose phosphate cycle in isolatd hepatocytes by prediction-labelling studies following the metabolism of [2-14C]-, [5-14C]- and [4,5,6-14C]glucose are reported. The 14C distribution patterns in glucose 6-phosphate show that the reactions of the L-type pentose pathway in hepatocytes. 2. Estimates of the quantitative contribution of the L-type pentose cycle are the exclusive form of the pentose cycle to glucose metabolism have been made. The contribution of the L-type pentose cycle to the metabolism of glucose lies between 22 and 30% in isolated hepatocytes. 3. The distribution of 14C in the carbon atoms of glucose 6-phosphate following the metabolism of [4,5,6-14C]- and [2-14C]glucose indicate that gluconeogenesis from triose phosphate and non-oxidative formation of pentose 5-phosphate do not contribute significantly to randomization of 14C in isolated hepatocytes. The transaldolase exchange reaction between fructose 6-phosphate and glyceraldehyde 3-phosphate is very active in these cells.

Local cerebral glucose utilization in systemic acidosis

1984 ◽  
Vol 247 (4) ◽  
pp. R639-R645
Author(s):  
D. Van Nimmen ◽  
J. Weyne ◽  
G. Demeester ◽  
I. Leusen
Keyword(s):  
Metabolic Acidosis ◽  
Glucose Metabolism ◽  
Gray Matter ◽  
Glucose Utilization ◽  
Local Level ◽  
Hypercapnic Acidosis ◽  
Local Cerebral Glucose Utilization ◽  
Experimental Conditions ◽  
Cerebral Glucose Utilization ◽  
Neuronal Regulation

Cerebral glucose metabolism (CMRglu) is decreased during acute and prolonged hypercapnic acidosis and during prolonged metabolic (HCl) acidosis; it is increased in acute (hypocapnic) metabolic acidosis and is not changed in acute isocapnic metabolic acidosis. The alteration in CMRglu can be explained by the changes occurring in intracerebral pH under these experimental conditions. In pontine gray matter, n. tractus solitarii, and n. ambiguus, three structures participating in the neuronal regulation of ventilation, local CMRglu is increased in all acidotic groups, suggesting coupling of function and metabolism at the local level during acidosis-induced hyperventilation.

Glucose metabolism in rat hypothalamus

1981 ◽  
Vol 98 (4) ◽  
pp. 481-487 ◽  
Author(s):  
Pentti Lautala ◽  
Julio M. Martin
Keyword(s):  
Glucose Metabolism ◽  
Glucose Transport ◽  
Glucose Concentration ◽  
Glucose Oxidation ◽  
Glucose Utilization ◽  
Rat Hypothalamus ◽  
Extracellular Glucose Concentration ◽  
Extracellular Glucose ◽  
Phenazine Methosulphate

Abstract. In vitro glucose oxidation and glucose transport in the rat medial (MH) and lateral (LH) hypothalamic areas was measured. Glucose oxidation was calculated from the conversion of [U-14C]glucose to 14C02 and glucose transport from 14C02 produced from [114C]glucose in the presence of phenazine methosulphate and NaF. Increasing glucose in the medium from 1 him to 20 mm enhanced glucose oxidation two-fold in MH and 40% in LH. Addition of insulin, 100 (iU/ml, to the medium decreased glucose oxidation 30% both in MH and LH at both 4 mm and 20 mm glucose. Fasting did not affect glucose oxidation in either of these hypothalamic areas. Glucose transport was not affected by insulin, but was increased significantly when glucose was raised from 0.25 mm to 1.0 mm. Fasting also increased glucose transport in both hypothalamic areas. In conclusion, extracellular glucose concentration seems to be the major regulator of glucose utilization by the rat hypothalamus. Insulin, rather than increasing, seems to decrease glucose oxidation while having no effect on glucose transport.

scholarly journals Role of brown adipose tissue in glucose utilization in conscious pre-obese Zucker rats

1989 ◽  
Vol 263 (1) ◽  
pp. 305-308 ◽  
Author(s):  
S Krief ◽  
R Bazin ◽  
F Dupuy ◽  
M Lavau
Keyword(s):  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Brown Adipose Tissue ◽  
Glucose Utilization ◽  
Whole Body ◽  
Zucker Rats ◽  
Noradrenaline Content ◽  
Metabolism Rate ◽  
Brown Adipose ◽  
The Difference

In 16-day-old conscious Zucker rats, at a time when pre-obese fa/fa rats were not yet hyperinsulinaemic compared with their lean Fa/fa littermates, the whole-body glucose-metabolism rate was decreased by 10% in pre-obese compared with lean pups. The markedly decreased glucose utilization found in brown adipose tissue (BAT) of pre-obese compared with lean pups accounted for at least 70% of the difference in whole-body glucose metabolism observed between the two genotypes. In pre-obese fa/fa rats, the 20% decrease in noradrenaline content of BAT reported in this study is consistent with the diminished glucose utilization by this tissue, and further supports the hypothesis of a defect in the sympathetic-nervous-system regulation of BAT metabolism as one of the primary causes for this genetic obesity.

Glucose Metabolism in the Caecum of the Marine Borer Bankia setacea

1968 ◽  
Vol 25 (5) ◽  
pp. 853-862 ◽  
Author(s):  
D. Liu ◽  
P. M. Townsley
Keyword(s):  
Citric Acid ◽  
Glucose Metabolism ◽  
Soluble Protein ◽  
Citric Acid Cycle ◽  
Digestive Organ ◽  
Acid Cycle ◽  
Wood Borer ◽  
Pentose Pathway

The degradation of uniformly labelled glucose-C14 was followed in the caeca preparations of the marine wood borer Bankia setacea (Tryon). This digestive organ was found to contain large quantities of soluble protein. Various accumulating intermediates were isolated, indicating the presence of enzymes typical of the Embden–Meyerhof pathway, the pentose pathway, the citric acid cycle, and the non-triose pathway. The presence of wood in the caeca may be required for the synthesis of glutamic and aspartic acids within the caeca. Approximately 10% of the added glucose was found in an unidentified, unstable, electronegative compound called glucose-X. The function of this compound is unknown.

scholarly journals Attenuated Insulin Release and Storage in Fetal Sheep Pancreatic Islets with Intrauterine Growth Restriction

Endocrinology ◽  
2006 ◽  
Vol 147 (3) ◽  
pp. 1488-1497 ◽  
Author(s):  
Sean W. Limesand ◽  
Paul J. Rozance ◽  
Gary O. Zerbe ◽  
John C. Hutton ◽  
William W. Hay
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Intrauterine Growth Restriction ◽  
Glucose Oxidation ◽  
Placental Insufficiency ◽  
Growth Restriction ◽  
Insulin Content ◽  
Intrauterine Growth

We determined in vivo and in vitro pancreatic islet insulin secretion and glucose metabolism in fetuses with intrauterine growth restriction (IUGR) caused by chronic placental insufficiency to identify functional deficits in the fetal pancreas that might be caused by nutrient restriction. Plasma insulin concentrations in the IUGR fetuses were 69% lower at baseline and 76% lower after glucose-stimulated insulin secretion (GSIS). Similar deficits were observed with arginine-stimulated insulin secretion. Fetal islets, immunopositive for insulin and glucagon, secreted insulin in response to increasing glucose and KCl concentrations. Insulin release as a fraction of total insulin content was greater in glucose-stimulated IUGR islets, but the mass of insulin released per IUGR islet was lower because of their 82% lower insulin content. A deficiency in islet glucose metabolism was found in the rate of islet glucose oxidation at maximal stimulatory glucose concentrations (11 mmol/liter). Thus, pancreatic islets from nutritionally deprived IUGR fetuses caused by chronic placental insufficiency have impaired insulin secretion caused by reduced glucose-stimulated glucose oxidation rates, insulin biosynthesis, and insulin content. This impaired GSIS occurs despite an increased fractional rate of insulin release that results from a greater proportion of releasable insulin as a result of lower insulin stores. Because this animal model recapitulates the human pathology of chronic placental insufficiency and IUGR, the β-cell GSIS dysfunction in this model might indicate mechanisms that are developmentally adaptive for fetal survival but in later life might predispose offspring to adult-onset diabetes that has been previously associated with IUGR.

Effect of osmolality on glucose metabolism in rabbit kidney cortex and medulla in vitro

1964 ◽  
Vol 207 (2) ◽  
pp. 473-482 ◽  
Author(s):  
James B. Lee ◽  
Vernon K. Vance ◽  
George F. Cahill
Keyword(s):  
Glucose Metabolism ◽  
Glucose Oxidation ◽  
Glucose Utilization ◽  
Lactate Production ◽  
Rabbit Kidney ◽  
Kidney Cortex ◽  
Osmotic Gradient ◽  
Cortical Slice ◽  
Kidney Medulla

Slices of rabbit kidney cortex and medulla were incubated aerobically in media of varying osmotic concentrations. When medium osmolality was reduced below 280–300 mosmoles/kg H2O, by means of decreased sodium chloride and sucrose concentrations, there was an osmotically determined increase in cortical glucose utilization and oxidation, lactate production, and slice weight. Between 280 and 300 mosmoles/kg H2O maximal cortical slice weight loss and inhibition of glucose metabolism occurred, with little further change when medium osmolality was increased to 415 mosmoles/kg H2O. With urea, slice weight and relatively maximal glucose metabolism were maintained at all medium osmotic concentrations between 67 and 548 mosmoles/kg H2O. In contrast, slices of kidney medulla revealed a capacity for extensive glucose oxidation in hyperosmotic media (1,066 mosmoles/kg H2O), while maximal lactate production occurred in hypoosmotic media (67 mosmoles/kg H2O). The findings are interpreted as suggestive of responsiveness of cortical and medullary intermediary metabolism to changes in the "effective" extracellular-to-intracellular osmotic gradient.

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