Priming Effect Of Glucose Research Articles

Long-term nitrogen deposition inhibits soil priming effects by enhancing phosphorus limitation in a subtropical forest.

It is widely accepted that phosphorus (P) limits microbial metabolic processes and thus soil organic carbon (SOC) decomposition in tropical forests. Global change factors like elevated atmospheric nitrogen (N) deposition can enhance P limitation, raising concerns about the fate of SOC. However, how elevated N deposition affects the soil priming effect (PE) (i.e., fresh C inputs induced changes in SOC decomposition) in tropical forests remains unclear. We incubated soils exposed to 9 years of experimental N deposition in a subtropical evergreen broadleaved forest with two types of 13 C-labeled substrates of contrasting bioavailability (glucose and cellulose) with and without P amendments. We found that N deposition decreased soil total P and microbial biomass P, suggesting enhanced P limitation. In P unamended soils, N deposition significantly inhibited the PE. In contrast, adding P significantly increased the PE under N deposition and by a larger extent for the PE of cellulose (PEcellu ) than the PE of glucose (PEglu ). Relative to adding glucose or cellulose solely, adding P with glucose alleviated the suppression of soil microbial biomass and C-acquiring enzymes induced by N deposition, whereas adding P with cellulose attenuated the stimulation of acid phosphatase (AP) induced by N deposition. Across treatments, the PEglu increased as C-acquiring enzyme activity increased, whereas the PEcellu increased as AP activity decreased. This suggests that P limitation, enhanced by N deposition, inhibits the soil PE through varying mechanisms depending on substrate bioavailability; that is, P limitation regulates the PEglu by affecting soil microbial growth and investment in C acquisition, whereas regulates the PEcellu by affecting microbial investment in P acquisition. These findings provide new insights for tropical forests impacted by N loading, suggesting that expected changes in C quality and P limitation can affect the long-term regulation of the soil PE.

Use of Carbon Isotope Composition for Characterization of Microbial Activity in Arable Soils

The effect of glucose on microbial mineralization of soil organic matter (SOM) was studied in arable soil specimens. The flows of carbon dioxide generated during this degradation were deduced from differences in the carbon isotope ratios of glucose (delta13C = -11.4 per mil) and SOM (delta13C = -27.01 per mil). The priming effect of glucose and respiratory quotient (RQ) were taken as indices of activation of SOM-consuming microbiota. The data on microbial mineralization of organic matter in soil, obtained in this study, show that addition of a readily consumable substance (glucose) to soil favors SOM degradation and increases the release of carbon dioxide from soil to atmosphere.

Altered insulin secretory responses to glucose in diabetic and nondiabetic subjects with mutations in the diabetes susceptibility gene MODY3 on chromosome 12.

One form of maturity-onset diabetes of the young (MODY) results from mutations in a gene, designated MODY3, located on chromosome 12 in band q24. The present study was undertaken to define the interactions between glucose and insulin secretion rate (ISR) in subjects with mutations in MODY3. Of the 13 MODY3 subjects, six subjects with normal fasting glucose and glycosylated hemoglobin and seven overtly diabetic subjects were studied as were six nondiabetic control subjects. Each subject received graded intravenous glucose infusions on two occasions separated by a 42-h continuous intravenous glucose infusion designed to prime the beta-cell to secrete more insulin in response to glucose. ISRs were derived by deconvolution of peripheral C-peptide levels. Basal glucose levels were higher and insulin levels were lower in MODY3 subjects with diabetes compared with nondiabetic subjects or with normal healthy control subjects. In response to the graded glucose infusion, ISRs were significantly lower in the diabetic subjects over a broad range of glucose concentrations. ISRs in the nondiabetic MODY3 subjects were not significantly different from those of the control subjects at plasma glucose levels <8 mmol/l. As glucose rose above this level, however, the increase in insulin secretion in these subjects was significantly reduced. Administration of glucose by intravenous infusion for 42 h resulted in a significant increase in the amount of insulin secreted over the 5-9 mmol/l glucose concentration range in the control subjects and nondiabetic MODY3 subjects (by 38 and 35%, respectively), but no significant change was observed in the diabetic MODY3 subjects. In conclusion, in nondiabetic MODY3 subjects insulin secretion demonstrates a diminished ability to respond when blood glucose exceeds 8 mmol/l. The priming effect of glucose on insulin secretion is preserved. Thus, beta-cell dysfunction is present before the onset of overt hyperglycemia in this form of MODY. The defect in insulin secretion in the nondiabetic MODY3 subjects differs from that reported previously in nondiabetic MODY1 or mildly diabetic MODY2 subjects.

Priming effect of substrate addition in soil-based biodegradation tests

To test whether substrate addition changes background CO2 evolution of soil, we measured both 14CO2 and net CO2 evolution from various test compounds. Glucose caused a priming effect, defined as substrate-stimulated soil organic matter mineralization. Formate, benzoate, n-hexadecane, and bis(2-ethylhexyl)phthalate caused no priming, and phenol caused only a transient one. The priming effect of glucose appears to be unusual and does not require a general rejection of net CO2 evolution measurements in biodegradability testing.

Altered Insulin Secretory Responses to Glucose in Subjects with a Mutation in the MODY1 Gene on Chromosome 20

This study was undertaken to test the hypothesis that the diabetes susceptibility gene on chromosome 20q12 responsible for maturity-onset diabetes of the young (MODY) in a large kindred, the RW family, results in characteristic alterations in the dose-response relationships between plasma glucose concentration and insulin secretion rate (ISR) that differentiate this form of MODY from MODY in subjects with glucokinase mutations. Ten marker-positive subjects and six matched nondiabetic marker-negative subjects from the RW family received graded intravenous glucose infusions on two occasions separated by a 42-h continuous intravenous glucose infusion designed to prime the beta-cell to secrete more insulin in response to glucose. ISR was derived by deconvolution of peripheral C-peptide levels. Basal glucose and insulin levels were similar in marker-negative and marker-positive groups (5.3 +/- 0.2 vs. 5.0 +/- 0.2 mmol/l, P > 0.2, and 86.1 +/- 3.9 vs. 63.7 +/- 12.1 pmol/l, P > 0.1, respectively). However, the marker-positive subjects had defective insulin secretory responses to an increase in plasma glucose concentrations. Thus, as the glucose concentration was raised above 7 mmol/l, the slope of the curve relating glucose and ISR was significantly blunted in the marker-positive subjects (13 +/- 4 vs. 68 +/- 8 pmol.min-1.mmol-1 x 1, P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Possible involvement of diacylglycerol-activated, Ca2+-dependent protein kinase in glucose memory of the rat pancreatic B-cell.

Exposure to high concentrations of glucose potentiates insulin release from the pancreatic B-cell stimulated by various secretagogues after an interval under basal condition. We studied the role of diacylglycerol-activated, Ca2+-dependent protein kinase (protein kinase C) in this priming effect of glucose in rat pancreatic islets, using 12-O-tetradecanoyl phorbol-13-acetate (TPA), 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7),N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA-1004) and forskolin. The priming effect of glucose was mimicked by 10 nmol/l of TPA, an activator of protein kinase C, but not by 5 mumol/l of forskolin, which increases cAMP via activating adenylate cyclase. When pancreatic islets were exposed to glucose (10 mmol/l) together with 50 mumol/l of H-7, an inhibitor of protein kinase C, the secretory response to glucose (10 mmol/l) after a 30-min interval was significantly reduced compared with that in the islets previously exposed to 10 mmol/l glucose alone. In contrast, this was not the case for HA-1004, its inhibitory activity against protein kinase C being less potent than H-7. These findings suggest that protein kinase C may play an important role in the priming effect of glucose on the pancreatic B-cell.

The priming effect of glucose on the gastric inhibitory polypeptide-induced insulin release.

Six healthy subjects were given a 15-min intravenous infusion of gastric inhibitory polypeptide (GIP) in a dose of 1.0 microgram X kg-1 X h-1 at a mean blood glucose level of 4.9 mmol/l after a priming infusion with glucose. A significant insulin release was seen during the GIP infusion, an effect that could not be demonstrated without the priming glucose infusion.

Influence of thiol groups, calcium, and glucose metabolism on cholinergic-induced insulin release and on methylscopolamine binding to muscarinic receptors in pancreatic islets of the rat

Short-term regulation of [3H]methylscopolamine binding to muscarinic receptors and acetylcholine-induced stimulation of insulin release was investigated in pancreatic islets of the rat. Binding of methylscopolamine was reversible; 47% of label was displaced 10 min and 70% 30 min after addition of unlabelled substance. 0.1 mM chloromercuribenzoic acid, when present during binding incubations, inhibited binding by 54%, whereas acetylcholine-induced insulin release was unaffected by the presence of the thiol reactant. Pre-incubation for 60 min in a calcium-deprived medium or in the presence of 50 microM trifluoroperazine likewise inhibited binding. Pre-incubation with 1.0 mM 3-isobutyl-l-methylxanthine or 16.7 M glucose failed to influence subsequent binding although acetylcholine-induced insulin release was 4-fold enhanced by priming with glucose. We conclude that 1) binding to muscarinic receptors is influenced by thiol interaction, 2) short-term alterations in calcium fluxes influence binding, whereas short-term changes in cyclic AMP (cAMP) or glucose metabolism do not, 3) a priming effect of glucose on insulin secretion is not mediated by changes in receptor binding.

The priming effect of glucose on insulin secretion from isolated islets of Langerhans.

Biphasic insulin secretion from perifused rat islets of Langerhans was enhanced if islets had previously been stimulated with glucose 16.6 mmol/l. The priming effect of glucose was reduced if mannoheptulose (16.6 mmol/l), deuterium oxide (D2O; 98% v/v) or adrenaline 10 mumol/l) was included in the medium during the initial stimulation period, or if Calcium was omitted. Glyceraldehyde (16.6 mmol/l) but not theophylline (5 mmol/l) could substitute for glucose during the initial stimulation and make islets more responsive to subsequent stimulation. The results suggest that the priming effect of glucose on insulin secretion may be related to 1) glucose metabolism and 2) Ca fluxes in the B cell and the consequent activation of the microtubular system. Neither the generation of intracellular cyclic AMP nor the release of insulin per se appears to be involved in the priming process.

Time and dose dependencies for priming effect of glucose on insulin secretion.

Short-term exposure to glucose increases insulin secretion during subsequent stimulation. This priming effect of glucose was further investigated in the perfused rat pancreas. A 5-min pulse of 27.7 mM glucose enhanced the response to a second pulse of the sugar after a 5- or 30-min period of 3.9 mM glucose. With a 10-min pulse of 27.7 mM glucose, the priming effect tended to persist also after a 60-min but not after a 90-min rest period. The priming effects of glucose were also evaluated from enhancement of stimulation 15 min later with 3-isobutyl-l-methylxanthine (IBMX). A 10-min pulse of 8.3 and 27.7, but not 5.6 mM glucose enhanced IBMX-induced insulin secretion. Cycloheximide did not abolish the priming effect of glucose on IBMX-induced insulin secretion. Conclusions are 1) priming is rapidly induced; 2) it persists longer than the time of induction; 3) threshold concentrations of glucose that induce priming are similar to those that initiate insulin secretions; and 4) mechanisms causing priming may not involve protein synthesis.

The priming effect of glucose in soil sterilized by gamma-radiation and reinoculated with Cellulomonas sp.

Mineralization of native organic matter and U-14C-glucose was followed by measuring the formation of CO2 and its radioactivity in chernozem soil presterilized by gamma-radiation and inoculated with a washed suspension of Cellulomonas sp. cells. The introduced bacteria mineralized the soil organic component to a higher extent in variants enriched with glucose. This so-called priming effect of glucose was observed also in the presence of chloramphenicol, inhibiting the growth of the bacteria. The increased mineralization of the native soil organic fraction was also detected in samples that were not enriched with glucose when the bacterial suspension was first disintegrated ultrasonically and the material then used for the inoculation. Possible participation of phenomena of the type of cometabolism and activation of cell membrane transport mechanisms on the occurrence of the priming effect of glucose in the soil is discussed.

Effects of priming with D-glucose on insulin secretion from rat pancreatic islets: increased responsiveness to other secretagogues.

Short term exposure to a high concentration of glucose enhances the insulin response to a second stimulation with the sugar. This priming effect of glucose has been further investigated by comparing the insulin-releasing effects of various secretagogues in the perfused rat pancreas before and after previous exposure to 27.7 mM glucose. Priming markedly increased the insulin release to agents whether metabolizable (leucine) or nonmetabolizable (tolbutamide, Ba++, 3-isobutyl-lmethylxanthine, and alloxan). The priming effect was seen both in cases where secretagogues were administered in the complete absence of metabolic substrate and when tested in the simultaneous presence of a low nonstimulatory glucose concentration (3.9 mM). The insulinotropic effects of tolbutamide were examined at concentrations of 50, 200, and 400 μg/ml of the drug, with and without priming. In the absence of priming, 200 and 400 μg/ml were maximally effective. Previous exposure to 27.7 mM glucose enhanced the secretory responses to ...

DECOMPOSITION OF GLUCOSE CONTINUOUSLY ADDED TO SOIL.

The continuous flow method was used to study the decomposition of uniformly tagged glucose in soil with different inorganic nitrogen and phosphorus levels. It was found that the amount of glucose carbon mineralized to carbon dioxide was higher if nitrogen and phosphorus were added together with the glucose. Some of the labelled carbon escaped from the soil and the amount of leached-out carbon was in inverse proportion to the amount of nitrogen and phosphorus in the soil. The level of mineral nutrient elements stimulated the rate of glucose mineralization in the initial phase of the continuous process. The rate of glucose mineralization in the steady state was stimulated in soil continuously enriched with glucose together with nitrogen and phosphorus. The quantitative relationship between the assimilation and oxidation of glucose carbon depended on the nitrogen and phosphorus concentration and was in inverse proportion to the mineral element level. The continuous addition of glucose stimulated decomposition of the native soil organic matter. The resultant priming effect was balanced, however, by the retention of glucose carbon in the soil, with the result that the carbon balance remained positive. The rate of glucose oxidation, the amount of carbon retained in the soil and the priming effect of glucose were strongly influenced by the flow rate.