The relationship between glucose production and plasma glucose concentration in children with falciparum malaria

To test the hypothesis that cortisol secretion plays a counterregulatory role in hypoglycemia in humans, four studies were performed in eight normal subjects. In all studies, insulin (15 mU.m-2.min-1) was infused subcutaneously (plasma insulin 27 +/- 1 microU/ml). In study 1, plasma glucose concentration and glucose fluxes [( 3-3H]glucose), substrate, and counterregulatory hormone concentrations were simply monitored, and plasma glucose decreased from 89 +/- 2 to 52 +/- 2 mg/dl for 12 h. In study 2, (pituitary-adrenal-pancreatic clamp), insulin and counterregulatory hormone secretion (except for catecholamines) was prevented by somatostatin (0.5 mg/h, iv) and metyrapone (0.5 g/4 h, per os), and glucagon, cortisol, and growth hormone were infused to reproduce the concentrations of study 1. In study 3 (lack of cortisol increase), the pituitary-adrenal-pancreatic clamp was performed with maintenance of plasma cortisol at basal levels, and glucose was infused, whenever needed, to reproduce plasma glucose concentration of study 2. Study 4 was identical to study 3, but exogenous glucose was not infused. Isolated lack of cortisol increase caused a approximately 22% decrease in hepatic glucose production (P less than 0.01) and a approximately 15% increase in peripheral glucose utilization (P less than 0.01), which resulted in greater hypoglycemia (37 +/- 2 vs. 52 +/- 2 mg/dl, P less than 0.01) despite compensatory increases in plasma epinephrine. Lack of cortisol response also reduced plasma free fatty acid, beta-hydroxybutyrate, and glycerol concentrations approximately 50%. We conclude that cortisol normally plays an important counterregulatory role during hypoglycemia by augmenting glucose production, decreasing glucose utilization, and accelerating lipolysis.

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Relationship Between Hepatic Glucose Production and Fasting Plasma Glucose Concentration in Patients With NIDDM

Diabetes ◽

10.2337/diab.43.12.1440 ◽

1994 ◽

Vol 43 (12) ◽

pp. 1440-1444 ◽

Cited By ~ 55

Author(s):

C.-Y. Jeng ◽

W. H.-H. Sheu ◽

M. M.-T. Fuh ◽

Y.-D. I. Chen ◽

G. M. Reaven

Keyword(s):

Plasma Glucose ◽

Fasting Plasma Glucose ◽

Glucose Concentration ◽

Hepatic Glucose Production ◽

Glucose Production ◽

Plasma Glucose Concentration ◽

Fasting Plasma ◽

Hepatic Glucose ◽

Fasting Plasma Glucose Concentration

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Maintenance of the postabsorptive plasma glucose concentration: insulin or insulin plus glucagon?

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00460.2004 ◽

2005 ◽

Vol 289 (2) ◽

pp. E181-E186 ◽

Cited By ~ 26

Author(s):

Bharathi Raju ◽

Philip E. Cryer

Keyword(s):

Insulin Secretion ◽

Plasma Glucose ◽

Glucose Concentration ◽

Glucose Production ◽

Glucagon Secretion ◽

Endogenous Glucose Production ◽

Plasma Glucose Concentration ◽

Alternative View ◽

Physiological Range ◽

Healthy Humans

The prevalent view is that the postabsorptive plasma glucose concentration is maintained within the physiological range by the interplay of the glucose-lowering action of insulin and the glucose-raising action of glucagon. It is supported by a body of evidence derived from studies of suppression of glucagon (and insulin, among other effects) with somatostatin in animals and humans, immunoneutralization of glucagon, defective glucagon synthesis, diverse mutations, and absent or reduced glucagon receptors in animals and glucagon antagonists in cells, animals, and humans. Many of these studies are open to alternative interpretations, and some lead to seemingly contradictory conclusions. For example, immunoneutralization of glucagon lowered plasma glucose concentrations in rabbits, but administration of a glucagon antagonist did not lower plasma glucose concentrations in healthy humans. Evidence that the glycemic threshold for glucagon secretion, unlike that for insulin secretion, lies below the physiological range, and the finding that selective suppression of insulin secretion without stimulation of glucagon secretion raises fasting plasma glucose concentrations in humans underscore the primacy of insulin in the regulation of the postabsorptive plasma glucose concentration and challenge the prevalent view. The alternative view is that the postabsorptive plasma glucose concentration is maintained within the physiological range by insulin alone, specifically regulated increments and decrements in insulin, and the resulting decrements and increments in endogenous glucose production, respectively, and glucagon becomes relevant only when glucose levels drift below the physiological range. Although the balance of evidence suggests that glucagon is involved in the maintenance of euglycemia, more definitive evidence is needed, particularly in humans.

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Gluconeogenesis and the Cori cycle in 12-, 20-, and 40-h-fasted humans

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1998.275.3.e537 ◽

1998 ◽

Vol 275 (3) ◽

pp. E537-E542 ◽

Cited By ~ 21

Author(s):

Joseph Katz ◽

John A. Tayek

Keyword(s):

Blood Glucose ◽

Plasma Glucose ◽

Glucose Concentration ◽

Glucose Production ◽

Plasma Glucose Concentration ◽

Prolonged Fasting ◽

Cori Cycle ◽

Isotopomer Analysis ◽

Mass Isotopomer

Six subjects were infused with [U-13C]glucose (0.03–0.05 mg ⋅ kg−1 ⋅ min−1) starting 8–9 h after a meal, and the production of glucose, the recycling of glucose (the Cori cycle), the dilution of glucose by unlabeled carbon into the hepatic lactate-pyruvate pool, and gluconeogenesis were determined in these fasted volunteers by use of mass isotopomer analysis and equations previously described [J. A. Tayek and J. Katz. Am. J. Physiol.272 ( Endocrinol. Metab. 35): E476–E484, 1997]. A primed continuous 11-h infusion was started at 6:00 AM, and the above parameters were calculated after 3 h (for the 12-h fast) and at the end of the infusion (for the 20-h fast). Another group of five subjects was fasted for 40 h, and the above parameters were calculated as before. At 12, 20, and 40 h of fasting, respectively, blood glucose was 93 ± 2, 83 ± 2, and 71 ± 2 (SE) mg/dl; glucose production was 2.3, 1.8, and 1.77 mg ⋅ kg−1 ⋅ min−1; the recycling of labeled carbon was 8, 15, and 15%, and that of glucose molecules (Cori cycle) was 18, 35, and 36%; the contribution of gluconeogenesis to glucose production was 41, 71, and 92% or 0.96, 1.29, and 1.64 mg ⋅ kg−1 ⋅ min−1; and the contribution of other sources to glucose production was 1.37, 0.53, and 0.15 mg ⋅ kg−1 ⋅ min−1. The recycling of glucose is important in prolonged fasting for the maintenance of plasma glucose concentration. We demonstrate here that gluconeogenesis can be easily measured and that it accounts for ∼90% of glucose production after a 40-h fast.

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Hypovolaemia after glucose/insulin infusions in volunteers

Clinical Science ◽

10.1042/cs20080032 ◽

2008 ◽

Vol 115 (12) ◽

pp. 371-378 ◽

Cited By ~ 7

Author(s):

Dan Berndtson ◽

Joel Olsson ◽

Robert G. Hahn

Keyword(s):

Body Weight ◽

Linear Relationship ◽

Plasma Glucose ◽

Glucose Concentration ◽

Plasma Glucose Concentration ◽

High Dose ◽

Acting Insulin ◽

Insulin Solution ◽

The Relationship

High-dose intravenous infusion of 5% glucose promotes rebound hypoglycaemia and hypovolaemia in healthy volunteers. To study whether such effects occur in response to glucose/insulin, 12 healthy firemen (mean age, 39 years) received three infusions over 1–2 h that contained 20 ml of 2.5% glucose/kg of body weight, 5 ml of 10% glucose/kg of body weight with 0.05 unit of rapid-acting insulin/kg of body weight, and 4 ml of 50% glucose/kg of body weight with 1 unit of insulin/kg of body weight. The plasma glucose concentration and plasma dilution were compared at 5–10 min intervals over 4 h. Regardless of the amount of administered fluid and whether insulin was given, the plasma glucose concentration decreased to hypoglycaemic levels within 30 min of the infusion ending. The plasma dilution closely mirrored plasma glucose and became negative by approx. 5%, which indicates a reduction in the plasma volume. These alterations were only partially restored during the follow-up period. A linear relationship between plasma glucose and plasma dilution was most apparent when the infused glucose had been dissolved in only a small amount of fluid. For the strongest glucose/insulin solution, this linear relationship had a correlation coefficient of 0.77 (n=386, P<0.0001). The findings of the present study indicate that a redistribution of water due to the osmotic strength of the glucose is the chief mechanism accounting for the hypovolaemia. It is concluded that infusions of 2.5%, 10% and 50% glucose, with and without insulin, in well-trained men were consistently followed by long-standing hypoglycaemia and also by hypovolaemia, which averaged 5%. These results emphasize the relationship between metabolism and fluid balance.

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Tissue Pco2 in Brain Ischemia Related to Lactate Content in Normo- and Hypercapnic Rats

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1992.37 ◽

1992 ◽

Vol 12 (2) ◽

pp. 270-280 ◽

Cited By ~ 27

Author(s):

Kenichiro Katsura ◽

Anders Ekholm ◽

Bo K. Siesjö

Keyword(s):

Linear Relationship ◽

Glial Cells ◽

Brain Ischemia ◽

Plasma Glucose ◽

Glucose Concentration ◽

Plasma Glucose Concentration ◽

Buffer System ◽

Equilibration Time ◽

Tissue Pco2 ◽

The Relationship

The amount of lactate formed during ischemia determines the rise in tissue Pco2 (Ptco2). Conflicting results exist on the relationship between lactate and Ptco2. The objective of this study was to settle this issue. We varied the preischemic plasma glucose concentration of normo- and hypercapnic rats, assessed tissue lactate and total CO2 contents, and determined the Pco2/lactate relationship over the lactate range 2–40 mmol kg−1. The results showed that whatever the equilibration time, the Pco2/lactate relationship was linear. The results obtained could be reproduced by a theoretical buffer system that mimics the buffering behavior of intracellular fluid. Our results bear on the question of whether compartmentation of H+ occurs during ischemia, with glial cells becoming more acid than neurons. A discontinuous Pco2/lactate relationship, with a constant Pco2 above a certain lactate content, would support this contention. Since our results demonstrate a linear relationship between lactate and Pco2 over the lactate range 2–40 mmol kg−1, they considerably weaken any argument for gross compartmentation of H+.

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Effect of Streptozotocin-Diabetes on the Local and General Responses to Injury in the Rat

Clinical Science ◽

10.1042/cs0540431 ◽

1978 ◽

Vol 54 (4) ◽

pp. 431-437 ◽

Cited By ~ 4

Author(s):

E. A. Elebute ◽

R. A. Little

Keyword(s):

Plasma Glucose ◽

Glucose Concentration ◽

Hind Limb ◽

Plasma Osmolality ◽

Streptozotocin Diabetes ◽

Significant Negative Correlation ◽

Diabetic Rats ◽

Plasma Glucose Concentration ◽

Limb Ischaemia ◽

The Relationship

1. The effects of streptozotocin-diabetes on the local and general responses to a 4 h period of bilateral hind-limb ischaemia in the rat have been investigated. The rats were injured 48 h after the intravenous injection of the streptozotocin. 2. Less fluid was lost from the circulation into the injured limbs after injury in the diabetic rats and this was directly related to the severity of the diabetes, but could not be explained by dehydration. However, when the diabetic and non-diabetic injured rats were considered together there was a significant negative correlation between either plasma osmolality or plasma glucose concentration and water content in the injured hind limb. 3. The relationship between plasma glucose concentration and plasma osmolality was changed by injury such that, particularly in the injured diabetic rats, plasma osmolality at a given glucose concentration was higher than that predicted from the relationship between these variables in the uninjured rat.

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Evaluation of the relationship between the one-hour plasma glucose concentration and beta-cell functions and cardiometabolic parameters during oral glucose tolerance test in obese children and adolescents

Journal of Pediatric Endocrinology and Metabolism ◽

10.1515/jpem-2020-0016 ◽

2020 ◽

Vol 33 (6) ◽

pp. 767-775

Author(s):

Eda Mengen ◽

Seyit Ahmet Uçaktürk

Keyword(s):

Glucose Tolerance ◽

Beta Cell ◽

Plasma Glucose ◽

Glucose Concentration ◽

Glucose Tolerance Test ◽

Tolerance Test ◽

Plasma Glucose Concentration ◽

Oral Glucose ◽

Cell Functions ◽

The Relationship

AbstractBackgroundIn this study, we aimed to evaluate the relationship between the 1-h plasma glucose (PG) level in the oral glucose tolerance test (OGTT) and conventional glycemic parameters, indices evaluating beta-cell functions, and cardiometabolic risk factors.MethodsThe records of 532 obese patients who were followed up in the Pediatric Endocrinology Polyclinic and who underwent standard OGTT were evaluated retrospectively. All patients were divided into two groups according to OGTT data as the 1-h plasma glucose concentration <155 mg/dL (n=329) and ≥155 mg/dL (n=203). Patients with normal glucose tolerance (NGT) were divided into two groups according to the 1-h PG level, as 218 patients with NGT 1 h-low (<155 mg/dL) and 53 patients with high NGT 1 h-high (≥155 mg/dL).ResultsThere was a statistically significant difference between the lipid profiles of individuals with NGT 1 h-low (<155 mg/dL) and individuals with NGT 1 h-high (≥155 mg/dL) (p<0.001). Total cholesterol, LDL cholesterol, and triglyceride levels were higher, while HDL cholesterol levels were lower in individuals with NGT 1 h-high (≥155 mg/dL). The indices evaluating beta-cell functions were significantly higher in individuals with NGT 1 h-low (<155 mg/dL).ConclusionAs a result, a plasma glucose concentration above or equal to 155 mg/dL at 1 h during an OGTT is associated with a worse clinical phenotype characterized by changes in insulin sensitivity and β-cell function. Therefore, this threshold value can predict the progression of prediabetes in obese young people with NGT.

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Glucose kinetics following administration of an intravenous fat emulsion to low-birth-weight neonates

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1992.263.5.e844 ◽

1992 ◽

Vol 263 (5) ◽

pp. E844-E849 ◽

Cited By ~ 1

Author(s):

K. A. Yunis ◽

W. Oh ◽

S. Kalhan ◽

R. M. Cowett

Keyword(s):

Birth Weight ◽

Low Birth Weight ◽

Plasma Glucose ◽

Glucose Concentration ◽

Glucose Production ◽

Plasma Glucose Concentration ◽

Glucose Kinetics ◽

Fat Emulsion ◽

Intravenous Fat Emulsion ◽

Parenteral Alimentation

To evaluate the mechanism(s) of the observed increase in plasma glucose concentration following the administration of an intravenous fat emulsion to the neonate, we measured glucose kinetics in eight low-birth-weight neonates by the prime constant rate infusion technique with D-[6,6-2H2]glucose at a rate of 0.22 +/- 0.01 mumol.kg-1 x min-1 (39.4 +/- 1.3 micrograms.kg-1 x min-1) while the neonates received 32 +/- 5 mumol.kg-1 x min-1 glucose (6.3 +/- 1.1 mg.kg-1 x min-1) plus an amino acid mixture (parenteral alimentation) alone and in combination with an intravenous fat emulsion (Intralipid). Following the latter combination, there were significant increases in plasma glucose concentration [4.07 +/- 0.11 (73 +/- 2 mg/dl) to 5.00 +/- 0.22 mmol/l (90 +/- 4 mg/dl); P < 0.01] and in plasma insulin concentration [72 +/- 14 (10 +/- 2 microU/ml) to 172 +/- 36 pmol/l (24 +/- 5 microU/ml); P < 0.05]. The parenteral alimentation and intravenous fat effusion combination did not affect the glucose production rate: 0.15 +/- 0.05 mumol.kg-1 x min-1 (0.03 +/- 0.01 mg.kg-1 x min-1) during the parenteral alimentation alone and 0.16 +/- 0.05 mumol.kg-1 x min-1 (0.03 +/- 0.01 mg.kg-1 x min-1) when parenteral alimentation was combined with an intravenous fat emulsion. We conclude that the increased plasma glucose concentration seen in association with administration of parenteral alimentation combined with an intravenous fat emulsion to the premature neonate is not due to enhanced glucose production but could be the result of alterations in glucose utilization.

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