Dependence of the Circadian Rhythm of Body and Liver Protein, Lipid and Glycogen on the Hours of Protein Intake

Author(s):  
M. Markova ◽  
K. Angelova
1989 ◽  
Vol 9 (4) ◽  
pp. 257-260 ◽  
Author(s):  
Prakash R. Keshaviah ◽  
Karl D. Nolph ◽  
John C. Van Stone

The KTIV urea index ( K, clearance; T, treatment time; V, volume of urea distribution) has become an established index of hemodialysis (HD) adequacy, values of KTIV < 0.8 being associated with overt uremic toxicity. For the typical continuous ambulatory peritoneal dialysis (CAPD) regimen of 4 X 2 L exchanges/day, the equivalent KT/V -0.6. Paradoxically, overt uremic toxicity is not commonly observed in CAPD patients with this typical therapy prescription. Application of the urea kinetic model demonstrates that HD and CAPD have the same time-averaged urea concentration at the same KTIV. However, as HD is an intermittent therapy, the urea concentration in HD exceeds the time-averaged concentration for about half the hours in the week. If uremic toxicity is related to the peak rather than the time-averaged urea concentration, a higher KT/V would be required in HD to achieve a peak concentration at or below the steady state CAPD concentration. This peak concent ration hypothesis predicts, based on the results of the National Cooperative Dialysis Study, that underdialysis with CAPD would occur at KT/V < 0.4 for a protein intake of 1.1 gmlkglday.


1968 ◽  
Vol 109 (1) ◽  
pp. 69-74 ◽  
Author(s):  
A. S. Levi ◽  
S. Geller ◽  
D. M. Root ◽  
G. Wolf

1. ATP sulphurylase was assayed in various organs from vitamin A-deficient and pair-fed control rats at different stages of deficiency. Activity decreased slightly in the liver and markedly in the adrenal gland. Striking differences in liver activity were observed between pair-fed control and ad libitum-fed animals. This observation suggested that diet (apart from vitamin A) strongly influenced the activity of ATP sulphurylase. 2. Total starvation caused a severe decrease in activity in liver within 48hr. This was due to a lack of protein intake. 3. By feeding groups of vitamin A-deficient and pair-fed control rats on a diet containing 80% protein, the specific activity of the liver ATP sulphurylase was maintained in the pair-fed control group at the normal level of an ad libitum-fed rat, whereas it decreased by 25% (statistically significant at P<0·01) in the deficient rat. On a 20%-protein diet, there were no significant differences between vitamin A-deficient and pair-fed control rats. These relationships held also for enzyme activity expressed per g. of liver, per total liver and per g. of DNA. There were no differences in liver protein or DNA concentration between vitamin A-deficient and control rats on either protein intake. 4. Control rats on a 20%-protein diet had liver specific enzyme activities about one-half of those in control rats on an 80%-protein diet, as well as lower liver protein concentrations. 5. It is concluded that, when the effect of protein deprivation on ATP sulphurylase is separated from the effect of vitamin A deficiency, a lowering of the enzyme activity caused by the vitamin deficiency is demonstrable.


1959 ◽  
Vol 197 (1) ◽  
pp. 71-74 ◽  
Author(s):  
Samuel R. Tipton ◽  
C. W. Majors ◽  
J. L. Smothers

Propylthiouracil depressed and thyroxine elevated the succinoxidase activity of rat liver after 4 days of regeneration. Protein-depleted animals had a significant decrease in activity of succinic dehydrogenase and cytochrome oxidase, rate of restoration of liver mass, enzyme activity and new protein. Thyroxine increased the rate of regeneration and the enzyme activity even in protein-depleted animals. Adrenalectomized rats on low protein intake had a very low rate of regeneration and protein replacement and low amounts of new enzyme activity and new protein after partial hepatectomy. Increasing the dietary protein to 36% increased all of these factors significantly, but administration of cortisone or adrenal cortical extract, had little effect on enzyme activity even though its effect on protein restoration was about as good as that of the high protein intake. Apparently under certain conditions, these hormones can produce changes in specific enzyme proteins that are independent of changes in total cell protein.


2018 ◽  
Author(s):  
Sandra Kirsch Heibel ◽  
Peter J McGuire ◽  
Nantaporn Haskins ◽  
Himani Datta Majumdar ◽  
Sree Rayavarapu ◽  
...  

AbstractAbundance of urea cycle enzymes in the liver is regulated by the dietary protein intake. Although urea cycle enzyme levels rise in response to a high protein diet, signaling networks that sense dietary protein intake and trigger changes in expression of urea cycle genes have not been identified. The aim of this study was to identify signaling pathway(s) that respond to changes in protein intake and regulate expression of urea cycle genes in mice and human hepatocytes. Mice were adapted to either control or high (HP) protein diets followed by isolation of liver protein and mRNA and integrated analysis of the proteomic and transcriptome profiles. HP diet led to increased expression of mRNA and enzymes in amino acid degradation pathways, and decreased expression of mRNA and enzymes in carbohydrate and fat metabolism, which implicated AMPK as a possible regulator. Primary human hepatocytes, treated with AICAR an activator of AMPK, were used to test whether AMPK regulates expression of urea cycle genes. The abundance of CPS1 and OTC mRNA increased in hepatocytes treated with AICAR, which supports a role for AMPK signaling in regulation of the urea cycle. Because AMPK is either a target of drugs used to treat type-2 diabetes, these drugs might increase the expression of urea cycle enzymes in patients with urea cycle disorders, which could be the basis of a new therapeutic approach.Author summaryIntegrated analysis of transcriptional and proteomic profiles of the liver tissue from mice fed different protein content diets revealed that AMPK signaling pathway regulates expression of urea cycle enzymes.


2019 ◽  
Vol 104 (12) ◽  
pp. 5935-5947 ◽  
Author(s):  
R C Bhake ◽  
V Kluckner ◽  
H Stassen ◽  
G M Russell ◽  
J Leendertz ◽  
...  

Abstract Context The pituitary–adrenal axis had historically been considered a representative model for circadian rhythms. A recently developed portable collection device has provided the opportunity to evaluate free cortisol profiles using the microdialysis approach in individuals free to conduct their day-to-day activities in their own surroundings. Methods Two separate experiments were conducted in healthy male volunteers. The total and subcutaneous (SC) free cortisol levels were measured at 10-minute intervals for a 24-hour period in one experiment, and the SC free cortisol levels were measured at 20-minute interval for 72 consecutive hours in free-living individuals in the second experiment. Results The characteristic circadian rhythm was evident in both serum total and SC free cortisol, with the lowest levels achieved and maintained in the hours surrounding sleep onset and the peak levels occurring in every individual around waking. In all free-living individuals, the circadian rhythm was consistent across the 72-hour period, despite a wide range of activities. All the participants also showed increased cortisol after the consumption of lunch. The lowest levels during all 24-hour periods were observed during the hours after lights off, at the onset of sleep. Conclusions To the best of our knowledge, the present study is the first to report up to three consecutive 24-hour measurements of SC free cortisol in healthy individuals. We believe our study is a landmark study that paves the way for ambulatory monitoring of free cortisol profiles continuously for a period of 72 hours in free-living individuals performing their day-to-day activities whether healthy or with diseases involving the hypothalamic–pituitary–adrenal axis.


1978 ◽  
Vol 55 (s4) ◽  
pp. 395s-397s ◽  
Author(s):  
J. S. Floras ◽  
J. V. Jones ◽  
J. A. Johnston ◽  
D. E. Brooks ◽  
M. O. Hassan ◽  
...  

1. We have recorded ambulant intra-arterial blood pressure in five normo- and 14 hyper-tensive subjects over 24 h, particular attention being paid to the timing of arousal. 2. The data were edited beat-by-beat before storing systolic, diastolic, and mean blood pressure ± sd for every 2 min period on a computer file. 3. When pooled hourly mean data are plotted there is a rise of 52·9 mmHg systolic and 22·3 mmHg diastolic pressure from 03.00 hours to 11.00 hours in the 14 hypertensive subjects. 4. When the data are plotted in 20 min periods for the hours before and after arousal it is clear that the major rise in pressure occurs abruptly at that time. The 2 h period before arousal shows only a small rise in pressure, i.e. 6·9 mmHg systolic and 2·9 mmHg diastolic. 5. It is suggested that the apparent rapid early morning rise of blood pressure is an artifact of the method of analysis.


1998 ◽  
Vol 23 (3) ◽  
pp. 280-280 ◽  
Author(s):  
Mehanna ◽  
Robinson ◽  
Gatehouse ◽  
Mcgarry

2005 ◽  
Vol 38 (10) ◽  
pp. 19
Author(s):  
SHERRY BOSCHERT
Keyword(s):  

2008 ◽  
Vol 78 (2) ◽  
pp. 64-69 ◽  
Author(s):  
Choi ◽  
Cho

This study investigated the effect of vitamin B6 deficiency on the utilization and recuperation of stored fuel in physically trained rats. 48 rats were given either vitamin B6-deficient (B6–) diet or control (B6+) diet for 4 weeks and were trained on treadmill for 30 minutes daily. All animals were then subdivided into 3 groups: before-exercise (BE); during-exercise (DE); after-exercise (AE). The DE group was exercised on treadmill for 1 hour just before being sacrificed. Animals in the AE group were allowed to take a rest for 2 hours after being exercised like the DE group. Glucose and free fatty acids were compared in plasma. Glycogen and triglyceride were compared in liver and skeletal muscle. Protein levels were compared in plasma, liver, and skeletal muscle. Compared with the B6+ group, plasma glucose levels of the B6– group were significantly lower before and after exercise. Muscle glycogen levels of the B6– group were significantly lower than those of the B6+ group regardless of exercise. The liver glycogen level of the B6– group was also significantly lower than that of B6+ group during and after exercise. Before exercise, plasma free fatty acid levels were not significantly different between the B6+ and B6– groups, and plasma free fatty acid levels of the B6– group were significantly lower during and after exercise. The muscle triglyceride level of the B6– group was significantly lower than that of the B6+ group before exercise, and there were no differences between B6+ and B6– groups during and after exercise. Liver triglyceride levels were not significantly different between B6+ and B6– groups. Plasma protein levels of the B6– group were lower than those of B6+ before and after exercise. Muscle protein levels of the B6– group were not significantly different from those of the B6+ group. Liver protein levels of the B6– group were significantly lower than that of the B6+ group after exercise. Liver protein levels of both B6+ and B6– groups were not significantly changed, regardless of exercise. Thus, it is suggested that vitamin B6 deficiency may reduce fuel storage and utilization with exercise in physically trained rats.


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