Glucose biokinetics in normal and ketotic cows

1959 ◽  
Vol 14 (6) ◽  
pp. 1026-1028 ◽  
Author(s):  
D. S. Kronfeld ◽  
E. G. Tombropoulos ◽  
Max Kleiber
Keyword(s):  
Transfer Rate ◽  
Extracellular Volume ◽  
Turnover Time ◽  
Intracellular Compartment

The size, turnover time and transfer rate of the glucose pool were estimated with glucose–C14 in normal and ketotic cows. The size and turnover time of the pool were both about 1/5 greater in the ketotic than in the normal cows, so that the transfer rate remained similar, being about 1 gm/min. The hypoglycemia which is characteristic of the disease appeared to be associated with an expansion of the glucose space, which in the normal cows approximated the extracellular volume, into the intracellular compartment of the ketotic cows. These results do not favor theories of bovine ketosis which presume a shortage of body glucose. Submitted on June 25, 1959

Glucose metabolism in lactating reindeer

1976 ◽  
Vol 54 (1) ◽  
pp. 55-64 ◽  
Author(s):  
R. G. White ◽  
J. R. Luick
Keyword(s):  
Plasma Glucose ◽  
Transfer Rate ◽  
Turnover Time ◽  
Pool Size ◽  
Glucose Turnover ◽  
Irreversible Loss ◽  
Domestic Species ◽  
Glucose Transfer ◽  
Glucose Synthesis ◽  
Lactation Cycle

Changes in glucose synthesis during the lactation cycle were estimated in pen-fed and grazing reindeer. The pool size, space, transfer rate, and irreversible loss of glucose were determined using simultaneous injections of [2-3H]glucose and primed infusions of [U-14C]glucose in reindeer lactating for 1–2, 4–5, 8–9, and 12–16 weeks. Glucose transfer rate and irreversible loss were higher during early to midlactation than at other times of the year; maximum estimates were at 8–9 weeks postpartum (July), and a decline was noted at 12–16 weeks (August). During the first 1–2 weeks in pen-fed and 4–5 weeks in grazing reindeer, glucose transfer rate and irreversible loss were almost twice the values reported for reindeer at maintenance. No difference in the irreversible loss of glucose was noted between lactating and non-lactating reindeer at 18–20 weeks postpartum (September), and there is evidence that this may occur as early as 12–16 weeks postpartum. No significant trend was noted in the glucose space throughout lactation; however, a significant increase in plasma glucose concentration and pool size was noted when glucose synthesis was highest (8–9 weeks postpartum). Glucose turnover time was consistently faster (78–88 min) in lactating than in non-lactating reindeer (107–140 min). Reindeer used a smaller proportion of plasma glucose-C for lactose synthesis than did other domestic species. This probably results from the low lactose content of reindeer milk and the relatively low rate of milk secretion.

scholarly journals Seasonal variations in glucose metabolism of reindeer (Rangifer tarandus L.) estimated with [U-14C]glucose and [3-3H]glucose

1973 ◽  
Vol 29 (2) ◽  
pp. 245-259 ◽  
Author(s):  
J. R. Luick ◽  
S. J. Person ◽  
R. D. Cameron ◽  
R. G. White
Keyword(s):  
Glucose Metabolism ◽  
Transfer Rate ◽  
Rangifer Tarandus ◽  
Extracellular Fluid ◽  
Late Pregnancy ◽  
Subjective Assessment ◽  
Turnover Time ◽  
Pool Size ◽  
Irreversible Loss ◽  
Glucose Transfer

1. The pool size, space and rate of irreversible loss of glucose were estimated with primed infusions of [U-14C]glucose in reindeer cows within 6 h of being taken from outdoor pens or from free grazing in the field.2. In conjunction with primed infusions of [U-14C]glucose, single injections of [3-3H]glucose were also used to estimate pool size, space, transfer rate, and turnover time of glucose.3. Except in a period of severe undernutrition, the concentration of glucose in plasma was higher (range 0·76–1·40 mg/ml) than that recorded for other ruminants.4. The size of the glucose pool (range 8–35 g) varied in parallel with plasma glucose concentration and was generally distributed in a space in excess of the extracellular fluid volume.5. The lowest rates of irreversible loss of glucose (approximately 1·7 mg/min per kg0·75) were measured when cows were in mid pregnancy and when available food was scarce; the highest rate (5·5 mg/min per kg0·75) was found in cows during mid summer.6. Changes in irreversible loss and transfer rate of glucose are interpreted in relation to changes in body composition (estimated in a parallel study), subjective assessment of available food and factors known to control glucose metabolism in other ruminants.7. The difference between glucose transfer rate and rate of irreversible loss of glucose was used as an index of the rate of resynthesis of glucose from products of glucose catabolism. The rates of glucose resynthesis were highest during a period of rapid growth (4·52 mg/min per kg0·75 or 45% of the glucose transfer rate) and in mid and late pregnancy (respectively 4·14 and 4·28 mg/min per kg0·75 or 71 and 59% of the transfer rate).

Strahlenwirkung am Normalgewebe

2010 ◽  
Vol 49 (S 01) ◽  
pp. S53-S58 ◽  
Author(s):  
W. Dörr
Keyword(s):  
Radiation Exposure ◽  
Normal Tissue ◽  
Radiation Effects ◽  
A Priori ◽  
Cell Loss ◽  
Turnover Time ◽  
Complete Healing ◽  
Internal Radiotherapy ◽  
Normal Tissues ◽  
Chronic Radiation

SummaryThe curative effectivity of external or internal radiotherapy necessitates exposure of normal tissues with significant radiation doses, and hence must be associated with an accepted rate of side effects. These complications can not a priori be considered as an indication of a too aggressive therapy. Based on the time of first diagnosis, early (acute) and late (chronic) radiation sequelae in normal tissues can be distinguished. Early reactions per definition occur within 90 days after onset of the radiation exposure. They are based on impairment of cell production in turnover tissues, which in face of ongoing cell loss results in hypoplasia and eventually a complete loss of functional cells. The latent time is largely independent of dose and is defined by tissue biology (turnover time). Usually, complete healing of early reactions is observed. Late radiation effects can occur after symptom-free latent times of months to many years, with an inverse dependence of latency on dose. Late normal tissue changes are progressive and usually irreversible. They are based on a complex interaction of damage to various cell populations (organ parenchyma, connective tissue, capillaries), with a contribution from macrophages. Late effects are sensitive for a reduction in dose rate (recovery effects).A number of biologically based strategies for protection of normal tissues or for amelioration of radiation effects was and still is tested in experimental systems, yet, only a small fraction of these approaches has so far been introduced into clinical studies. One advantage of most of the methods is that they may be effective even if the treatment starts way after the end of radiation exposure. For a clinical exploitation, hence, the availability of early indicators for the progression of subclinical damage in the individual patient would be desirable. Moreover, there is need to further investigate the molecular pathogenesis of normal tissue effects in more detail, in order to optimise biology based preventive strategies, as well as to identify the precise mechanisms of already tested approaches (e. g. stem cells).

THE DEPENDENCE OF URINARY CALCIUM AND OTHER ELECTROLYTES ON ADRENAL FUNCTION DURING ACUTE SODIUM DEPLETION AND LOADING

1970 ◽  
Vol 64 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Lars Runeberg ◽  
B.-A. Lamberg ◽  
P. Reissell ◽  
H. Adlercreutz
Keyword(s):  
Sodium Excretion ◽  
Extracellular Volume ◽  
Normal Subjects ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Minor Importance ◽  
Sodium Depletion ◽  
Sodium Loading ◽  
Urinary Potassium ◽  
Normal Controls

ABSTRACT The time course of the renal excretion of calcium, magnesium, sodium, and potassium during sodium depletion and the rapid correction of the extracellular volume deficit was studied in normal subjects and in patients with Addison's disease (AD). The decrease in body weight was similar in the two groups, but the haematocrit value increased more in the patients with AD. Sodium depletion suppressed sodium excretion much more efficiently in normal controls than in the AD patients. Calcium excretion was roughly equally depressed in two groups. During sodium loading there was an immediate increase in renal sodium excretion in the patients with AD, whereas the sodium-retaining state generally continued for about one day in the normal controls. Urinary potassium decreased gradually during the first day of sodium loading in the normal controls but not in the AD patients. In the normal subjects calcium excretion remained low during the first day and increased on the second day of sodium loading. In the AD patients there was a gradual increase in urinary calcium during the first day of sodium loading, which did not, however, parallel the changes in urinary sodium content in individual urine samples. Urinary magnesium did not change significantly. It is concluded that the effect of adrenal steroids on renal calcium excretion is of minor importance. They may, however, to some extent induce calcium retention.

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