Short communication: Glucose infusion into early postpartum cows defines an upper physiological set point for blood glucose and causes rapid and reversible changes in blood hormones and metabolites

The use of2H2O in estimating gluconeogenesis’ contribution to glucose production (%GNG) was examined during progressive fasting in three groups of healthy subjects. One group ( n = 3) ingested2H2O to a body water enrichment of ≈0.35% 5 h into the fast. %GNG was determined at 2-h intervals from the ratio of the enrichments of the hydrogens at C-5 and C-2 of blood glucose, assayed in hexamethylenetetramine. %GNG increased from 40 ± 8% at 10 h to 93 ± 6% at 42 h. Another group ingested2H2O over 2.25 h, beginning at 11 h ( n = 7) and 19 h ( n = 7) to achieve ≈0.5% water enrichment. Enrichment in plasma water and at C-2 reached steady state ≈1 h after completion of2H2O ingestion. The C-5-to-C-2 ratio reached steady state by the completion of 2H2O ingestion. %GNG was 54 ± 2% at 14 h and 64 ± 2% at 22 h. A 3-h [6,6-2H2]glucose infusion was also begun to estimate glucose production from enrichments at C-6, again in hexamethylenetetramine. Glucose produced by gluconeogenesis was 0.99 ± 0.06 mg ⋅ kg−1 ⋅ min−1at both 14 and 22 h. In a third group ( n = 3) %GNG reached steady state ≈2 h after2H2O ingestion to only ≈0.25% enrichment. In conclusion, %GNG by 2 h after2H2O ingestion and glucose production using [6,6-2H2]glucose infusion, begun together, can be determined from hydrogen enrichments at blood glucose C-2, C-5, and C-6. %GNG increases gradually from the postabsorptive state to 42 h of fasting, without apparent change in the quantity of glucose produced by gluconeogenesis at 14 and 22 h.

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POTENTIATION OF INSULIN RELEASE BY GLUCOSE IN MAN

Acta Endocrinologica ◽

10.1530/acta.0.0790511 ◽

1975 ◽

Vol 79 (3) ◽

pp. 511-534 ◽

Cited By ~ 29

Author(s):

Erol Cerasi

Keyword(s):

Blood Glucose ◽

Insulin Release ◽

Dose Response ◽

Pancreatic Beta Cell ◽

Insulin Response ◽

Initial Response ◽

Normal Glucose Tolerance ◽

Glucose Infusion ◽

Clear Cut ◽

The Right

ABSTRACT Glucose-induced potentiation of glucose-induced insulin release was quantitatively evaluated in 14 non-obese subjects with normal glucose tolerance but decreased insulin response, and in six non-obese patients with mild, adult-onset diabetes, by measuring the insulin responses to two consecutive glucose infusion tests, administered with 40 or 70 min interval. Enhancement of the second insulin response occurred in both groups. In low insulin responders, the dose-response relationship between blood glucose and plasma insulin was flatter and shifted to the right when compared to the control. Pretreatment with glucose increased strikingly the slope of this relationship, the responses now being within the normal range. The enhancement induced by glucose seems to be of multiplicative type. In mildly diabetic subjects, insulin response to glucose infusion was low and sluggish, only a minor initial response being observed. Pretreatment with glucose modified the profile of the insulin response, a clear-cut initial response of greater magnitude being obtained at least in some of the patients. The sensitivity of the islet to the potentiating action of glucose was higher in low insulin responders than in controls, the minimal glucose concentration needed to induce potentiation of the forthcoming response being much lower. The dose-response curve for the relationship between the blood glucose level of the preinfusion period and the percentual enhancement of the insulin response obtained at the second stimulation was, in low insulin responders, higher than and shifted to the left of the curve of the control subjects. In the group of diabetics, sensitivity for potentiation by glucose seemed not different from the controls. These studies indicate that the ability of glucose to initiate insulin release and its ability to generate time-bound potentiation in the islet correspond to two distinct functions. In the early stages of the diabetic syndrome, only the recognition of glucose as the initiator of an insulinogenic signal is impaired. The pancreatic beta-cell in these subjects seems to recognize normally glucose as the promotor of the potentiation.

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Effects of supplemental chromium and heat exposure on glucose metabolism and insulin action in sheep

The Journal of Agricultural Science ◽

10.1017/s0021859699007613 ◽

2000 ◽

Vol 134 (3) ◽

pp. 319-325 ◽

Cited By ~ 2

Author(s):

H. SANO ◽

S. KONNO ◽

A. SHIGA

Keyword(s):

Blood Glucose ◽

Glucose Metabolism ◽

Infusion Rate ◽

Insulin Action ◽

Heat Exposure ◽

Glucose Infusion ◽

Glucose Infusion Rate ◽

Isotope Dilution Method ◽

Glucose Turnover ◽

Dilution Method

An isotope dilution method using [U-13C]glucose and a glucose clamp approach were applied to determine the effects of supplemental chromium (Cr) and heat exposure on blood glucose metabolism and tissue responsiveness and sensitivity to insulin in sheep. The sheep consumed diets with either 0 or 1 mg of Cr/kg (Control and +Cr diet, respectively) from high-Cr-yeast, and were exposed from a thermoneutral environment (20 °C) to a hot environment (30 °C) for 5 days. Blood glucose turnover rate did not differ between the diets, and was lower (P < 0·05) during heat exposure than in the thermoneutral environment. The maximal glucose infusion rate (tissue responsiveness to insulin) tended to be lower (P = 0·06) for the +Cr diet than for the Control diet, but did not change with heat exposure. The plasma insulin concentration at half maximal glucose infusion rate (tissue sensitivity to insulin) did not differ between the diets, and was greater (P < 0·05) during heat exposure than in the thermoneutral environment. No significant diet × environment interactions were observed. There was no significant evidence that Cr supplementation moderated heat stress in sheep from the measures of blood glucose metabolism and insulin action.

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Effect of the artificial sweetener, sucralose, on small intestinal glucose absorption in healthy human subjects

British Journal Of Nutrition ◽

10.1017/s0007114510001327 ◽

2010 ◽

Vol 104 (6) ◽

pp. 803-806 ◽

Cited By ~ 91

Author(s):

Jing Ma ◽

Jessica Chang ◽

Helen L. Checklin ◽

Richard L. Young ◽

Karen L. Jones ◽

...

Keyword(s):

Blood Glucose ◽

Human Subjects ◽

Glucose Absorption ◽

Glucose Infusion ◽

Artificial Sweetener ◽

Healthy Human ◽

Proximal Small Intestine ◽

Healthy Human Subjects ◽

Glucagon Like Peptide 1 ◽

Glucose Plasma

It has been reported that the artificial sweetener, sucralose, stimulates glucose absorption in rodents by enhancing apical availability of the transporter GLUT2. We evaluated whether exposure of the proximal small intestine to sucralose affects glucose absorption and/or the glycaemic response to an intraduodenal (ID) glucose infusion in healthy human subjects. Ten healthy subjects were studied on two separate occasions in a single-blind, randomised order. Each subject received an ID infusion of sucralose (4 mm in 0·9 % saline) or control (0·9 % saline) at 4 ml/min for 150 min (T = − 30 to 120 min). After 30 min (T = 0), glucose (25 %) and its non-metabolised analogue, 3-O-methylglucose (3-OMG; 2·5 %), were co-infused intraduodenally (T = 0–120 min; 4·2 kJ/min (1 kcal/min)). Blood was sampled at frequent intervals. Blood glucose, plasma glucagon-like peptide-1 (GLP-1) and serum 3-OMG concentrations increased during ID glucose/3-OMG infusion (P < 0·005 for each). However, there were no differences in blood glucose, plasma GLP-1 or serum 3-OMG concentrations between sucralose and control infusions. In conclusion, sucralose does not appear to modify the rate of glucose absorption or the glycaemic or incretin response to ID glucose infusion when given acutely in healthy human subjects.

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Importance of blood glucose concentration in regulating lipolysis during fasting in humans

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1990.258.1.e32 ◽

1990 ◽

Vol 258 (1) ◽

pp. E32-E39 ◽

Cited By ~ 5

Author(s):

S. Klein ◽

O. B. Holland ◽

R. R. Wolfe

Keyword(s):

Blood Glucose ◽

Plasma Glucose ◽

Glucose Concentration ◽

Plasma Insulin ◽

Blood Glucose Concentration ◽

Glucose Infusion ◽

Short Term ◽

Epinephrine Infusion ◽

Isotopic Studies ◽

Fasting Plasma Insulin

The importance of the decline in blood glucose concentration on lipolysis and the lipolytic effect of epinephrine was evaluated during short-term fasting. Lipolytic rates were determined by infusing [2H5]glycerol and [1-13C]palmitic acid. Five volunteers were studied after 12 h of fasting before and during epinephrine infusion and after 84 h of fasting, before and during glucose infusion when plasma glucose was restored to postabsorptive values, and during glucose plus epinephrine infusion. In another protocol, five volunteers were given glucose intravenously throughout fasting to maintain plasma glucose at postabsorptive levels and isotopic studies were performed after 12 and 84 h of fasting before and during epinephrine infusion. Glucose infusion after 84 h of fasting restored glucose and insulin concentrations and lipolytic rates toward 12-h fasting values. When euglycemia was maintained throughout fasting, plasma insulin still declined (P less than 0.05) and lipolytic rates still increased (P less than 0.05). Despite similar glucose concentrations, the lipolytic response to epinephrine infusion was greater after 84 h than after 12 h of fasting in both protocols (P less than 0.05). These studies demonstrate that the decline in plasma glucose contributes to, but is not required for, the increase in lipolysis during fasting. The increase in epinephrine-stimulated lipolysis that occurs during fasting is not dependent on a decrease in plasma glucose concentration.

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Inclusion of low amounts of fructose with an intraportal glucose load increases net hepatic glucose uptake in the presence of relative insulin deficiency in dog

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00391.2004 ◽

2005 ◽

Vol 288 (6) ◽

pp. E1160-E1167 ◽

Cited By ~ 6

Author(s):

Masakazu Shiota ◽

Pietro Galassetti ◽

Kayano Igawa ◽

Doss W. Neal ◽

Alan D. Cherrington

Keyword(s):

Blood Glucose ◽

Glucose Uptake ◽

Control Period ◽

Glucose Infusion ◽

Control Group ◽

Hepatic Glycogen ◽

Arterial Blood ◽

Hepatic Glucose ◽

Arterial Blood Glucose ◽

Hepatic Glucose Uptake

The effect of small amounts of fructose on net hepatic glucose uptake (NHGU) during hyperglycemia was examined in the presence of insulinopenia in conscious 42-h fasted dogs. During the study, somatostatin (0.8 μg·kg−1·min−1) was given along with basal insulin (1.8 pmol·kg−1·min−1) and glucagon (0.5 ng·kg−1·min−1). After a control period, glucose (36.1 μmol·kg−1·min−1) was continuously given intraportally for 4 h with (2.2 μmol·kg−1·min−1) or without fructose. In the fructose group, the sinusoidal blood fructose level (nmol/ml) rose from <16 to 176 ± 11. The infusion of glucose alone (the control group) elevated arterial blood glucose (μmol/ml) from 4.3 ± 0.3 to 11.2 ± 0.6 during the first 2 h after which it remained at 11.6 ± 0.8. In the presence of fructose, glucose infusion elevated arterial blood glucose (μmol/ml) from 4.3 ± 0.2 to 7.4 ± 0.6 during the first 1 h after which it decreased to 6.1 ± 0.4 by 180 min. With glucose infusion, net hepatic glucose balance (μmol·kg−1·min−1) switched from output (8.9 ± 1.7 and 13.3 ± 2.8) to uptake (12.2 ± 4.4 and 29.4 ± 6.7) in the control and fructose groups, respectively. Average NHGU (μmol·kg−1·min−1) and fractional glucose extraction (%) during last 3 h of the test period were higher in the fructose group (30.6 ± 3.3 and 14.5 ± 1.4) than in the control group (15.0 ± 4.4 and 5.9 ± 1.8). Glucose 6-phosphate and glycogen content (μmol glucose/g) in the liver and glucose incorporation into hepatic glycogen (μmol glucose/g) were higher in the fructose (218 ± 2, 283 ± 25, and 109 ± 26, respectively) than in the control group (80 ± 8, 220 ± 31, and 41 ± 5, respectively). In conclusion, small amounts of fructose can markedly reduce hyperglycemia during intraportal glucose infusion by increasing NHGU even when insulin secretion is compromised.

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Short communication: Effect of maternal heat stress in late gestation on blood hormones and metabolites of newborn calves

Journal of Dairy Science ◽

10.3168/jds.2016-11088 ◽

2016 ◽

Vol 99 (8) ◽

pp. 6804-6807 ◽

Cited By ~ 10

Author(s):

J.-R. Guo ◽

A.P.A. Monteiro ◽

X.-S. Weng ◽

B.M. Ahmed ◽

J. Laporta ◽

...

Keyword(s):

Heat Stress ◽

Short Communication ◽

Late Gestation ◽

Newborn Calves ◽

Communication Effect ◽

Blood Hormones

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Limitations in estimating gluconeogenesis and Cori cycling from mass isotopomer distributions using [U-13C6]glucose

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1998.274.5.e954 ◽

1998 ◽

Vol 274 (5) ◽

pp. E954-E961 ◽

Cited By ~ 6

Author(s):

Bernard R. Landau ◽

John Wahren ◽

Karin Ekberg ◽

Stephen F. Previs ◽

Dawei Yang ◽

...

Keyword(s):

Amino Acids ◽

Blood Glucose ◽

Isotopic Exchange ◽

Glucose Production ◽

Normal Subjects ◽

Glucose Infusion ◽

Arterial Lactate ◽

Overnight Fasting ◽

Mass Isotopomer

Tayek and Katz proposed calculating gluconeogenesis’s contributions to glucose production and Cori cycling from mass isotopomer distributions in blood glucose and lactate during [U-13C6]glucose infusion [Tayek, J. A., and J. Katz. Am. J. Physiol. 272 ( Endocrinol. Metab. 35): E476–E484, 1997]. However, isotopic exchange was not adequately differentiated from dilution, nor was condensation of labeled with unlabeled triose phosphates properly equated. We introduce and apply corrected equations to data from subjects fasted for 12 and 60 h. Impossibly low contributions of gluconeogenesis to glucose production at 60 h are obtained (23–41%). Distributions in overnight-fasted normal subjects calculate to only ∼18%. Cori cycling estimates are ∼10–15% after overnight fasting and 20% after 60 h of fasting. There are several possible reasons for the underestimates. The contribution of gluconeogenesis is underestimated because glucose production from glycerol and amino acids not metabolized via pyruvate is ascribed to glycogenolysis. Labeled oxaloacetate and α-ketoglutarate can exchange during equilibrium with circulating unlabeled aspartate, glutamate, and glutamine. Also, the assumption that isotopomer distributions in arterial lactate and hepatic pyruvate are the same may not be fulfilled.

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Considering Blood Dilution improves the Precision of Continuous Whole Blood Glucose Measurements

Journal of Diabetes Science and Technology ◽

10.1177/1932296818803621 ◽

2018 ◽

Vol 13 (4) ◽

pp. 751-755

Author(s):

Carsten Benesch ◽

Mareike Kuhlenkötter ◽

Tim Heise

Keyword(s):

Blood Glucose ◽

Retrospective Analysis ◽

Whole Blood ◽

Glucose Infusion ◽

Dilution Factor ◽

Continuous Measurements ◽

Blood Dilution ◽

And Control ◽

Blood Glucose Concentrations ◽

The Impact

Background:One major advantage of automated over manual clamps are continuous measurements of blood glucose concentrations (BG) allowing frequent adaptations in glucose infusion rates (GIR). However, BG measurements might be affected by changes in blood dilution. ClampArt®, a modern automated clamp device, corrects BG measurements for blood dilution, but the impact of this correction is unclear.Methods:The authors performed a retrospective analysis of BG during glucose clamps comparing values with a fixed dilution factor with those corrected for the actual blood dilution.Results:Clamp quality substantially improved with the consideration of blood dilution: Mean accuracy fell from 8.1% ± 2.9% to 4.1% ± 0.8%, precision improved from 9.6 ± 3.6 mg/dl to 3.7 ± 1.3 mg/dl and control deviation from −2.6 ± 4.2 mg/dl to 0.2 ± 0.2 mg/dl.Conclusions:Correcting continuous BG measurements for blood dilution significantly increases BG measurement and clamp quality.

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