Correction factor for the estimation of plasma glucose synthesis from the transfer of 14C-atoms from labelled substrate in vivo: A preliminary report

1979 ◽  
Vol 57 (7) ◽  
pp. 767-770 ◽  
Author(s):  
G. Hetenyi Jr.

Based on a previously designed method for the estimation of the contribution of C-atoms by acetylcoenzyme A to the hepatic oxaloacetate pool, the loss of 14C-atoms on their way from a precursor to plasma glucose due to 'metabolic exchange' was estimated in normal and diabetic dogs and in normal rats. Due to this loss of 14C-atoms, the rates of gluconeogenesis when calculated from the transfer of 14C-atoms from precursors (other than glycerol) are underestimated by a factor of 2.2 ± 0.07 in normal, 1.8 ± 0.05 in diabetic dogs, and by 1.55 ± 0.04 in normal rats.

1980 ◽  
Vol 33 (4) ◽  
pp. 457 ◽  
Author(s):  
Ronald P Brockman ◽  
Cindy Greer

This study examined the effects of hypoglucagonaemia and hyperglucagonaemia on the incorporation of 14C from [2-14C]propionate into plasma glucose of sheep in vivo. The sheep were adult ewes fed a maintenance diet of lucerne pellets delivered in equal aliquots hourly. The irreversible loss of glucose was determined by the continuous infusion of [6-3H]glucose. During the control period (the hour immediately preceding infusion of hormones) 63 �2 % of the propionate was converted to glucose, accounting for 30�2 % of glucose production. Glucagon deficiency, induced by infusion of somatostatin (100 J1g/h), did not affect gluconeogenesis and the irreversible loss of glucose significantly. However, glucagon infusion at 11 �5 �O� 6 J1g/h significantly increased the irreversible loss of glucose, with the greatest increase occurring in the first 15 min of infusion. The 14C specific radioactivity of glucose and the fraction of glucose derived from propionate decreased significantly during glucagon infusion. The data are consistent with glucagon having a marked glycogenolytic effect initially, but little or no selective effect in promoting the utilization of propionate for glucose synthesis in vivo in sheep.


1974 ◽  
Vol 142 (1) ◽  
pp. 171-183 ◽  
Author(s):  
Joseph Katz ◽  
Arnold Dunn ◽  
Maymie Chenoweth ◽  
Sybil Golden

1. Glucose labelled with 3H in position 2 and uniformly with 14C was administered simultaneously to rabbits and rats either as a single injection or by continuous infusion. Plasma glucose specific radioactivity and the yield of 3H in the plasma water were monitored. 2. The rates of synthesis, recycling of carbon and total body mass of glucose were calculated, without assuming a multicompartmental model and without fitting data by exponential expressions. 3. The rate of synthesis of glucose in starved-overnight rabbits was 4mg/min per kg (range 3–4.5mg/min per kg) and 25–35% of the glucose carbon was recycled. The mass of total body glucose in starved rabbits was 290mg/kg (range 220–390mg/kg). About one-third of the total body glucose equilibrates nearly instantaneously with plasma glucose. 4. In rats starved overnight, glucose synthesis was about 10mg/min per kg and recycling of carbon ranged from 30–40%. Total body mass (per kg body weight) is similar to that in rabbits. 5. The activity in plasma water after injection of [2-3H]glucose was determined. The initial rate of 3H2O formation is rapid, indicating that the major site of glucose catabolism is in the rapidly mixing pool. The curve of total body glucose radioactivity was obtained from the 3H2O yield, and total mass of glucose was calculated. This agrees with that obtained from the 3H specific-radioactivity curve.


1982 ◽  
Vol 47 (1) ◽  
pp. 87-94 ◽  
Author(s):  
N. Chaiyabutr ◽  
Anne Faulkner ◽  
M. Peaker

1. Glucose turnover (i.e. glucose entry and utilization rates) in fed and 48 h starved goats during pregnancy and lactation was determined using a continuous infusion of [U-14C]- and [3-3H]glucose.2. Glucose synthesis and utilization increased during pregnancy and lactation in fed but not in starved goats.3. Recycling of giucosc-C was approximately 10% in fed animals and 15–20% in starved animals and was unaffected by the stage of pregnancy or lactation.4. Plasma glucose concentrations were maintained during pregnancy and lactation in fed goats but decreased during 48 h starvation in pregnant goats. Little change was seen in the plasma concentration of lipids and their metabolites during pregnancy and lactation in fed goats, but increases were observed after 48 h starvation.5. The control of glucose metabolism in ruminants during pregnancy and lactation is discussed.


1982 ◽  
Vol 60 (12) ◽  
pp. 1603-1609 ◽  
Author(s):  
G. Hetenyi Jr. ◽  
B. Lussier ◽  
C. Ferrarotto ◽  
J. Radziuk

The rate of gluconeogenesis in vivo may be estimated by the incorporation of 14C atoms from a labelled precursor into plasma glucose or by introducing 14C atoms into the pathway of gluconeogenesis at known stages by metabolites which in themselves do not contribute to the net synthesis of glucose (e.g., bicarbonate or acetate). The purpose of the investigation was to examine some of the assumptions involved in the calculation of gluconeogenic flux by the second approach. [2- 14C]acetate or NaH 14CO3 was infused to dogs, and the specific activity (SA) of glucose, bicarbonate CO2, urea, and lactate in the plasma was followed. The incorporation of 14C atoms from [2- 14C]acetate into glucose allows the calculation of the degree of underestimation of glucose formation due to "metabolic exchange" in the hepatic oxaloacetate pool. The possible error introduced into this calculation by the incorporation of 14C atoms from 14CO2 (a product of acetate oxidation) was found to be negligible, but the heavy labelling of plasma lactate may possibly affect the estimate of metabolic exchange. It is proposed that in the calculation of the rate of gluconeogenesis from infused NaHCO3 the SA of hepatocellular and not of plasma bicarbonate CO2 should be related to that of plasma glucose. This latter is expected to equal the SA of plasma urea, since the sole precursor of its C atom is hepatocellular CO2. The rate of gluconeogenesis estimated from the SA(glucose)/SA(urea) ratio and a previously estimated correction factor for metabolic exchange was 51% of the glucose production in the postabsorptive state. The nearly identical SA(urea)/SA(CO2) ratios, irrespective of the tracer infused, indicated that plasma CO2 is a major precursor of urea C and that a large fraction of injected acetate is oxidized by extrahepatic tissues.


1946 ◽  
Vol Original Series, Volume 27 (3-4) ◽  
pp. 248-256
Author(s):  
H. Berggren

2002 ◽  
Vol 35 (7) ◽  
pp. 590-593 ◽  
Author(s):  
F. Grimberg ◽  
G. Banegas ◽  
L. Chiacchio ◽  
O. Zmener

2004 ◽  
Vol 286 (4) ◽  
pp. G627-G634 ◽  
Author(s):  
Chang An Chu ◽  
Yuka Fujimoto ◽  
Kayano Igawa ◽  
Joseph Grimsby ◽  
Joseph F. Grippo ◽  
...  

The rate of liver glucokinase (GK) translocation from the nucleus to the cytoplasm in response to intraduodenal glucose infusion and the effect of physiological rises of plasma glucose and/or insulin on GK translocation were examined in 6-h-fasted conscious rats. Intraduodenal glucose infusion (28 mg·kg-1·min-1 after a priming dose at 500 mg/kg) elevated blood glucose levels (mg/dl) in the artery and portal vein from 90 ± 3 and 87 ± 3 to 154 ± 4 and 185 ± 4, respectively, at 10 min. At 120 min, the levels had decreased to 133 ± 6 and 156 ± 5, respectively. Plasma insulin levels (ng/ml) in the artery and the portal vein rose from 0.7 ± 0.1 and 1.8 ± 0.3 to 11.8 ± 1.5 and 20.2 ± 2.0 at 10 min, respectively, and 12.4 ± 3.1 and 18.0 ± 4.8 at 30 min, respectively. GK was rapidly exported from the nucleus as determined by measuring the ratio of the nuclear to the cytoplasmic immunofluorescence (N/C) of GK (2.9 ± 0.3 at 0 min to 1.7 ± 0.2 at 10 min, 1.5 ± 0.1 at 20 min, 1.3 ± 0.1 at 30 min, and 1.3 ± 0.1 at 120 min). When plasma glucose (arterial; mg/dl) and insulin (arterial; ng/ml) levels were clamped for 30 min at 93 ± 7 and 0.7 ± 0.1, 81 ± 5 and 8.9 ± 1.3, 175 ± 5 and 0.7 ± 0.1, or 162 ± 5 and 9.2 ± 1.5, the N/C of GK was 3.0 ± 0.5, 1.8 ± 0.1, 1.5 ± 0.1, and 1.2 ± 0.1, respectively. The N/C of GK regulatory protein (GKRP) did not change in response to the intraduodenal glucose infusion or the rise in plasma glucose and/or insulin levels. The results suggest that GK but not GKRP translocates rapidly in a manner that corresponds with changes in the hepatic glucose balance in response to glucose ingestion in vivo. Additionally, the translocation of GK is induced by the postprandial rise in plasma glucose and insulin.


2017 ◽  
Vol 15 (2) ◽  
pp. 151-156
Author(s):  
Somrudee NAKINCHAT ◽  
Voravuth SOMSAK

The emergence and spread of antimalarial drug resistance of Plasmodium parasites, as well as hypoglycemia, during malaria infection, and subsequent death, are critical problems in malaria-endemic areas. Hence, finding new compounds, especially plant extracts having antimalarial and anti-hypoglycemic activities, are urgently needed. The present study aimed to investigate the antimalarial and anti-hypoglycemic effects of Moringa oleifera leaf extract in Plasmodium berghei infection in mice. Aqueous crude extract of M. oleifera leaves was freshly prepared and used for an efficacy test in vivo. Groups of ICR mice (5 mice in each) were infected with 1´107 infected red blood cells of P. berghei ANKA by intraperitoneal injection and given the extract orally with doses of 100, 500, and 1000 mg/kg for 4 consecutive days. Parasitemia and plasma glucose levels were subsequently measured. The results showed that M. oleifera leaf extract presented significant (p < 0.001) inhibition of parasitemia in a dose-dependent manner. Moreover, this extract exerted anti-hypoglycemia effects in infected mice in a dose-dependent manner. The highest degrees of activity were found at a dose of 1000 mg/kg of the extract. Additionally, no effect on plasma glucose was found in normal mice treated with this extract. It can be concluded that aqueous crude extract of M. oleifera leaves exerted antimalarial and anti-hypoglycemic effects in P. berghei infection in mice.


1990 ◽  
Vol 48 (5) ◽  
pp. 351-357 ◽  
Author(s):  
Christer Bessing ◽  
Margareta Molin

1955 ◽  
Vol 33 (6) ◽  
pp. 926-939 ◽  
Author(s):  
Margaret J. Henderson ◽  
Gerald A. Wrenshall ◽  
Paul Odense

An attempt to answer the question as to whether insulin acts to lower blood glucose by increasing utilization, or by decreasing production, or by both, has been made using a new experimental approach. A trace dose of radioactive glucose was injected into each of six postabsorptive depancreatized dogs which had been deprived of exogenous insulin for 66 hr. Blood samples were collected before and after the intravenous injection of insulin, and plasma glucose concentration and specific activity were measured. From these data the simultaneous rates of appearance and disappearance of plasma glucose were calculated for a sequence of time intervals, both before and after insulin, by a method which did not assume dynamic equilibrium. Previous in vivo experiments using radioactive tracers to measure rates of production and utilization of glucose have been made in animals which were in steady states, either with or without insulin, and the effects of insulin were ascertained by comparison of the state with insulin and the state without insulin. The method described in this paper has made it possible to follow the effects of insulin while it is acting in one and the same animal. Insulin was found to cause an abrupt and marked increase in the rate of disappearance of glucose, and this increased rate became less with time, reaching the preinsulin level in about 90 min. Insulin caused a slower and much smaller decrease in the rate of appearance, but the decrease became greater with time during the three hour period of observation. Thus, it appeared that insulin acted in vivo both to increase the utilization of glucose and to decrease its production, but the effects differed in magnitude and in speed of response.


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