Liver fructose 2,6-bisphosphate in rats running at different treadmill speeds

1988 ◽  
Vol 255 (1) ◽  
pp. R38-R41
Author(s):  
W. W. Winder ◽  
H. T. Yang ◽  
J. Arogyasami

To determine the effect of work rate on liver fructose 2,6-bisphosphate (fructose 2,6-P2), rats were run for 5 min on a treadmill up a 15% grade at 16, 21, 26, 31, and 36 m/min. The liver content of fructose 2,6-P2 decreased 25, 42, 50, 62, and 71% from resting values after 5 min of running at these work rates. The time course of the decline in liver fructose 2,6-P2 was also studied in rats run at 16 m/min for times ranging from 5 to 100 min, at 23 m/min for times ranging from 5 to 60 min, and at 31 m/min for times of 5, 10, and 20 min. The hepatic content of fructose 2,6-P2 declined significantly after 5 min in all three groups of rats. The rate of decline was greatest in rats run at 31 m/min. After 100 min of running, fructose 2,6-P2 in livers of rats running at 16 m/min declined to levels seen in rats run at 31 m/min for 20 min. Changes in fructose 2,6-P2 occurred before a detectable decline in liver glycogen and in the absence of any significant change in blood glucose. Liver adenosine 3',5'-cyclic monophosphate (cAMP) was elevated after 5 min of exercise in rats running at 23 and 31 m/min but not in rats running at 16 m/min. By the end of exercise, hepatic cAMP was elevated in rats running at all speeds. The rapid decline in fructose 2,6-P2 probably plays a role in decreasing hepatic glycolysis, thereby ensuring that glucose 6-phosphate derived from glycogenolysis is diverted to blood glucose.

1983 ◽  
Vol 245 (3) ◽  
pp. R353-R356
Author(s):  
W. W. Winder ◽  
M. A. Beattie ◽  
E. O. Fuller

The purposes of this study were to determine the effect of different work rates on the rate of liver glycogenolysis and to determine the relationship between liver adenosine 3',5'-cyclic monophosphate (cAMP) levels and the glycogenolytic rate. Rats were run at treadmill speeds ranging from 10 to 34 m/min up a 15% grade for either 30 or 60 min. Both the magnitude of the decrease in liver glycogen and the increase in hepatic cAMP were dependent on the running speed and the duration of running. At the highest work rate a disproportionate acceleration in the liver glycogenolytic rate was observed compared with that at lower work loads, thus resulting in a curvilinear relationship between work rate and liver glycogenolytic rate. A high degree of correlation was found between the liver glycogenolytic rate and hepatic cAMP concentration (r = 0.98). This observation is consistent with the idea that hepatic glycogenolytic rates are determined by cAMP-mediated mechanisms.


1961 ◽  
Vol 200 (2) ◽  
pp. 269-273 ◽  
Author(s):  
H. Hift ◽  
J. G. Strawitz

Various time course studies were conducted in dogs subjected to a modified Wiggers procedure in an effort to ascertain whether the first reinfusion demand (the earliest overt sign of cardiovascular instability) could be associated with any other measurable biological change. The biphasic blood glucose pattern characteristic of irreversible hemorrhagic shock was thus shown generally to reach its hyperglycemic peak shortly before or at the time of first reinfusion, typically preceded by or coinciding with the earliest morphological changes in liver mitochondria (phase contrast, electron micrographs) and followed by progressive lengthening of the prothrombin time. The declining phase in blood glucose concentration was apparently not associated with any critical liver glycogen level or with any unusual rises in blood lactate, etc. The suggestion is therefore made that the sugar is used metabolically because of a liver shutdown induced by some extrahepatic agent(s) and that these events may, in turn, elicit malfunction elsewhere, e.g. the heart.


1990 ◽  
Vol 69 (2) ◽  
pp. 686-693 ◽  
Author(s):  
J. Arogyasami ◽  
R. K. Conlee ◽  
C. L. Booth ◽  
R. Diaz ◽  
T. Gregory ◽  
...  

The purpose of this study was to determine the effect of exercise on the rate of onset of hypoglycemia induced by infusion of excess insulin (0.8 mU.min-1.100 g-1). Rats were either fasted overnight (FS) or fed ad libitum (FD). FS rats were killed after 5, 10, or 15 min of infusion at rest or after running on the treadmill at 21 m/min and 15% grade. FD rats were killed after 10, 20, or 40 min of infusion at rest or after exercise. Rats were also killed 15 min postexercise for FS and 60 or 120 min postexercise for FD with continued insulin infusion. The progressive decline in blood glucose was not altered by exercise in the FS rats. FD rats showed a significant difference due to exercise only after 40 min (rest 4.2 +/- 0.3 mM, exercise 3.2 +/- 0.2 mM). A significant postexercise repletion of glycogen was observed in red vastus and soleus muscles of FD rats despite the decreasing blood glucose values. These data indicate that exercise accelerates the rate of development of hypoglycemia in FD rats. In the FS rats, where the rate of decline in blood glucose was greater, exercise had no effect on the time course of development of hypoglycemia.


1964 ◽  
Vol 207 (2) ◽  
pp. 411-414 ◽  
Author(s):  
Jiro Oyama ◽  
William T. Platt

Unrestrained mice were centrifuged for varying periods ranging from 0.5 to 10 hr at 2.5, 5, and 10 x gravity. Liver glycogen and blood glucose levels increased significantly depending on the g load and exposure time. Adrenalectomy completely abolished the glycogen deposition response. The glycogen response was a critical function of the age of mice; unweaned mice did not respond. Blood corticosterone increased significantly prior to the deposition of glycogen. Centrifuged fed mice deposited three times the amount of glycogen of fasted mice. There was no significant difference in the amount of glycogen deposited in centrifuged mice previously starved for 1, 2, or 3 days. It is concluded that the increased glycogen deposited following centrifugation is effected by an increased elaboration of adrenal corticosterone.


Critical Care ◽  
2014 ◽  
Vol 18 (Suppl 1) ◽  
pp. P440
Author(s):  
F Bass ◽  
S Bird ◽  
N Hammond ◽  
J Myburgh ◽  
S Finfer

1969 ◽  
Vol 115 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Olga Greengard

1. The administration of glucagon, cAMP [adenosine 3′,5′-(cyclic)-monophosphate], BcAMP [6-N-2′-O-dibutyryladenosine 3′,5′-(cyclic)-monophosphate] or adrenaline to foetal rats during the last 2 days of gestation evoked the appearance of tyrosine aminotransferase and enhanced the accumulation of glucose 6-phosphatase in the liver. In foetuses 1–2 days younger only BcAMP was effective. After birth liver glucose 6-phosphatase no longer responds to glucagon or BcAMP. Tyrosine aminotransferase is still inducible by these agents in 2-day-old rats, but not in 50-day-old rats. After adrenalectomy of adults glucagon or BcAMP can enhance the induction of the enzyme by hydrocortisone. The results indicate that the ability to synthesize tyrosine aminotransferase and glucose 6-phosphatase when exposed to cAMP develops sooner than the ability to respond to glucagon with an increase in the concentration of cAMP; the responsiveness of enzymes to different hormones changes with age. A scheme illustrating the sequential development of competence in regulating the level of an enzyme is presented. 2. Actinomycin inhibited the effects of glucagon and BcAMP on liver tyrosine aminotransferase and glucose 6-phosphatase in foetal rats. Growth hormone, insulin and hydrocortisone did not enhance the formation of these enzymes. 3. The time-course of accumulation of glucose 6-phosphatase in the kidney is different from that in the liver. Hormones that increase the accumulation in foetal liver do not do so in the kidney of the same foetus or in the livers of postnatal rats.


2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
J. N. Seheult ◽  
A. Pazderska ◽  
P. Gaffney ◽  
J. Fogarty ◽  
M. Sherlock ◽  
...  

Background. Poor inpatient glycaemic control has a prevalence exceeding 30% and results in increased length of stay and higher rates of hospital complications and inpatient mortality. The aim of this study was to improve inpatient glycaemic control by developing an alert system to process point-of-care blood glucose (POC-BG) results.Methods. Microsoft Excel Macros were developed for the processing of daily glucometry data downloaded from the Cobas IT database. Alerts were generated according to ward location for any value less than 4 mmol/L (hypoglycaemia) or greater than 15 mmol/L (moderate-severe hyperglycaemia). The Diabetes Team provided a weekday consult service for patients flagged on the daily reports. This system was implemented for a 60-day period.Results. There was a statistically significant 20% reduction in the percentage of hyperglycaemic patient-day weighted values >15 mmol/L compared to the preimplementation period without a significant change in the percentage of hypoglycaemic values. The time-to-next-reading after a dysglycaemic POC-BG result was reduced by 14% and the time-to-normalization of a dysglycaemic result was reduced from 10.2 hours to 8.4 hours.Conclusion. The alert system reduced the percentage of hyperglycaemic patient-day weighted glucose values and the time-to-normalization of blood glucose.


1999 ◽  
Vol 82 (6) ◽  
pp. 3030-3040 ◽  
Author(s):  
Michelle Moyer ◽  
Erik van Lunteren

Neuromuscular junction endplate potentials (EPPs) decrease quickly and to a large extent during continuous stimulation. The present study examined the hypothesis that EPP rundown recovers rapidly, thereby substantially preserving neurotransmission during intermittent compared with continuous stimulation. Studies were performed in vitro on rat diaphragm, using μ-conotoxin to allow recording of normal-sized EPPs from intact fibers. During continuous 5- to 100-Hz stimulation, EPP amplitude declined with a biphasic time course. The initial fast rate of decline was modulated substantially by stimulation frequency, whereas the subsequent slow rate of decline was relatively frequency independent. During intermittent 5- to 100-Hz stimulation (duty cycle 0.33), EPP amplitude declined rapidly during each train, but recovered substantially by the onset of the following train. The intra-train declines were substantially greater than the inter-train declines in EPP amplitude. Intra-train reductions in EPP amplitude were stimulation frequency dependent, based on both the total decline and rate constant of EPP decline. In contrast, the degree of recovery from train to train was independent of stimulation frequency, indicating low frequency dependence of inter-train rundown. The substantial recovery of EPP amplitude in between trains resulted in greater cumulative EPP size during intermittent compared with continuous stimulation. During continuous stimulation, EPP drop-out was only seen during 100-Hz stimulation; this was completed mitigated during intermittent stimulation. Miniature EPP size was unaffected by either continuous or intermittent stimulation. The pattern of rapid intra-train rundown and slow inter-train rundown of EPP size during intermittent stimulation is therefore due to rapid changes in the magnitude of neurotransmitter release rather than to axonal block or postsynaptic receptor desensitization. These findings indicate considerable rundown of EPP amplitudes within a stimulus train, with near complete recovery by the onset of the next train. This substantially attenuates the decrement in EPP amplitude during intermittent compared with continuous stimulation, thereby preserving the integrity of neurotransmission during phasic activation.


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