Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effects of increasing glucose intake on nitrogen balance, energy expenditure and fuel utilization were measured in 12 malnourished adult patients receiving parenteral nutrition with constant, very high nitrogen intake (500 mg of N/kg), high (105 kJ/kg) or low (30 kJ/kg) glucose intake and constant fat intake (7 kJ/kg). Each patient received each diet for 8-day periods in random order. 2. Energy balance and nitrogen balance were determined daily. Blood samples, taken at admission, during 5% (w/v) dextrose (D-glucose) infusion and at the end of days 7 and 8 of each diet, were analysed for urea, glucose, lactate, triacylglycerols, fatty acids, glycerol, 3-hydroxybutyrate, insulin and glucagon. 3. The effect of increasing glucose intake was to increase nitrogen balance by 0.60 +/- 0.25 (SEM) mg/kJ. At zero energy balance, nitrogen balance was 48 mg day-1 kg-1. This confirms findings of previous studies: that the effects of glucose on nitrogen balance are greater at high than at low nitrogen intakes, and that, in malnourished patients, unlike in normal adults, markedly positive nitrogen balance can be achieved at zero or negative energy balances. 4. Changes in nitrogen balance were due almost entirely to changes in urea excretion. 5. The high nitrogen intake markedly increased plasma insulin and glucagon concentrations and reduced glycerol, fatty acid and 3-hydroxybutyrate concentrations, independent of any glucose effect. Glucagon concentrations were significantly decreased by added glucose intake, an effect not previously seen at low nitrogen intakes. At this high nitrogen intake, the effects of added glucose appear to be mediated by both insulin and glucagon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of glucose on nitrogen balance during high nitrogen intake in malnourished patients. 215 47

Regulation of urea transport by vasopressin in inner medullary collecting duct (IMCD) cells is thought to be important for the urinary concentrating mechanism. Isolated tubule perfusion studies suggest the existence of a saturable urea carrier. We have measured 14C-urea efflux in IMCD cells which were freshly isolated and grown in primary culture. Cells were isolated from rat papilla by collagenase digestion and hypotonic shock. In suspended cells, 14C-urea efflux (Jurea) from loaded cells was exponential with time constant 59 +/- 3 sec (SEM, n = 6, 23 degrees C). Jurea had an activation energy of 4.1 kcal/mole and was inhibited 42 +/- 7% by 0.25 mM phloretin and 30-40% by the high affinity urea analogues dimethylurea and phenylurea. Jurea was increased 40-60% by addition of vasopressin (10(-8) M) or 8-bromo-cAMP (1 mM); stimulated Jurea was inhibited 55 +/- 8% by the kinase A inhibitor H-8. Phorbol esters and epidermal growth factor did not alter Jurea. IMCD cells grown in primary culture were homogeneous in appearance with greater than fivefold stimulation of cAMP by vasopressin. The exponential time constant for urea efflux was 610 +/- 20 sec (n = 3). Jurea was not altered by vasopressin, cAMP or phloretin. Another function of in vivo IMCD cells, vasopressin-dependent formation of endosomes containing water channels, was absent in the cultured cells. These results demonstrate presence of a urea transporter on suspended IMCD cells which is activated by cAMP and inhibited by phloretin and urea analogues. The urea transporter and its regulation by cAMP, and cAMP-dependent apical membrane endocytosis, are lost after growth in primary culture.
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PMID:Urea transport in freshly isolated and cultured cells from rat inner medullary collecting duct. 217 46

1. The effect of uraemia on the rates of protein synthesis and protein degradation in liver, heart and vastus lateralis muscle were examined in the rat. Uraemia was induced by a five-sixths nephrectomy and the rates of protein turnover were compared with pair-fed sham-operated littermate controls. 2. The procedure produced plasma concentrations (means +/- SEM) of urea of 7.3 +/- 0.4 mmol/l in control and 39 +/- 2 mmol/l in uraemic rats, and of creatinine of 41 +/- 1 mumol/l in control and 133 +/- 7 mumol/l in uraemic rats. 3. Uraemia reduced the rates of protein synthesis in liver, heart and muscle by 35 +/- 5, 4.0 +/- 1.2 and 4.0 +/- 0.6%/day, respectively, compared with control rats (P less than 0.01). Since the reductions in tissue growth rate were too small to be accounted for by the reduction seen in protein synthesis alone, this implied that protein degradation was also reduced. Uraemia also caused an 18% reduction in the rate of growth as measured by the increase in tail length (P less than 0.01). 4. Uraemia reduced both protein synthesis and protein degradation. Protein synthesis exceeded protein degradation in all tissues. This would cause a reduced rate of protein accumulation in the uraemic compared with the control rats, and hence a reduced rate of growth.
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PMID:Protein turnover in uraemia in the rat. 217 24

Recombinant human insulin-like growth factor I (IGF-I) was administered subcutaneously to each of 5 normal human subjects at doses of 0 mg/kg (control), 0.06 mg/kg, or 0.12 mg/kg successively at one week intervals. After 0.06 mg/kg or 0.12 mg/kg IGF-I injections, plasma IGF-I levels increased from 185 +/- 17 ng/ml (mean +/- SEM) to maximal levels of 396 +/- 21 ng/ml at 3 hours and from 169 +/- 14 ng/ml to 480 +/- 27 ng/ml at 4 hours, respectively. These two peak values were statistically different (p less than 0.05). After 0.06 mg/kg and 0.12 mg/kg IGF-I administration, blood glucose levels decreased from 85 +/- 2 mg/dl to minimal levels of 73 +/- 3 mg/dl at 3 hours and from 83 +/- 1 mg/dl to 50 +/- 4 mg/dl at 2 hours, respectively. These two minimal values were statistically different (p less than 0.001). Serum insulin and C-peptide levels were decreased in a dose dependent manner after IGF-I administration. There were no changes between blood urea nitrogen levels before and 4 hours after IGF-I administration. The urinary GH concentration decreased after 0.06 mg/kg IGF-I administration, but increased and maintained normal values after 0.12 mg/kg IGF-I administration.
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PMID:Effects of sc administration of recombinant human insulin-like growth factor I (IGF-I) on normal human subjects. 222 47

Since carnitine deficiency has been reported in some patients undergoing maintenance hemodialysis, we studied the effects of intravenous infusion of L-carnitine or placebo at the end of each dialysis treatment. The trial, which lasted seven months (one month baseline, 6 months treatment) was multicenter, double blind, placebo controlled, and randomized. Eighty-two long-term hemodialysis patients, who were given either carnitine (N = 38) or placebo (N = 44), completed this study. In each group, clinical and biochemical parameters during treatment were compared with baseline values. Intra-dialytic hypotension and muscle cramps were reduced only in the carnitine treated group, while improvement in post-dialysis asthenia was noticed in both carnitine and placebo groups. Maximal oxygen consumption, measured during a progressive work exercise test, improved significantly in the carnitine group (111 +/- 50 ml/min. P less than 0.03) and was unchanged in the placebo group. L-carnitine treatment was associated with a significant drop in pre-dialysis concentrations of serum urea nitrogen, creatinine and phosphorus (means +/- SEM, 101 +/- 4.5 to 84 +/- 3.9, 16.7 +/- 0.67 to 14.7 +/- 0.64, and 6.4 +/- 0.3 to 5.5 +/- 0.4 mg/dl, respectively, P less than 0.004). No significant changes in any of these variables were noticed in the placebo group. Mid-arm circumference and triceps skinfold thickness were measured in 11 carnitine and 13 placebo treated patients. Calculated mid-arm muscle area increased in the carnitine patients (41.37 +/- 2.68 to 45.6 +/- 2.82 cm2, P = 0.05) and remained unchanged in the placebo patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Multicenter trial of L-carnitine in maintenance hemodialysis patients. II. Clinical and biochemical effects. 226 75

The effect of fatty infiltration on liver function was studied in 29 dairy cows aged 6 +/- 0.4 (SEM) years with primary acetonaemia, secondary acetonaemia or the fat cow syndrome. The average interval from calving at diagnosis was 16.4 +/- 2.0 days and the animals had been anorexic for a mean of 5.6 +/- 0.8 days. Fatty infiltration of the liver occurred well before calving and was associated with severe clinical illness and intercurrent infections. The percentage of fatty infiltration in the liver (mean 53.1 +/- 2.8 per cent) was significantly correlated with both the degree of clinical illness (P less than 0.001) and the period of anorexia (P less than 0.05). Alterations in uptake, conjugation and excretion at the hepatocyte level were determined by measuring bromsulphthalein clearance, and plasma total bilirubin and total bile acid concentrations. Values for all three were positively correlated with the extent of fatty infiltration. Plasma albumin, urea and glucose concentrations were reliable indicators of the liver's synthetic function and together with plasma aspartate aminotransferase, iditol and glutamate dehydrogenase were correlated with the degree of hepatic lipidosis.
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PMID:Effect on liver function of acetonaemia and the fat cow syndrome in cattle. 233 29

Grey seal pups (Halichoerus grypus) were collected at the time of weaning (mid-October) and fasted for 52 days at thermoneutrality in separate cages. Body weight decreased exponentially, while metabolic rate dropped 45% from an average of 2.95 +/- 0.15 (SEM) W kg-1 at day 2 of fasting to a stable level of 1.62 +/- 0.06 (SEM) W kg-1 from day 10 to day 47 of fasting. Respiratory quotient was low, indicating extensive catabolism of triglycerides, while plasma cortisol was fairly stable at 110 +/- 8 (SEM) nmol l-1 throughout the fasting period. Daily urinary output decreased from 236 +/- 20 (SEM) ml day-1 at day 2 to a stable value of 87 +/- 6 (SEM) ml day-1 between days 8 and 50 of fasting. The urine was analysed for urea, uric acid, creatinine, ammonia, total nitrogen and osmolality. Urea was always the principal excretory end-product, amounting to between 70 and 80% of the total excreted nitrogen. The urine was moderately concentrated (range 770-1300 mosmol kg-1). Total excreted urinary nitrogen decreased by 68% from 3.7 +/- 0.7 (SEM) g day-1 to 1.2 +/- 0.4 (SEM) g day-1 between days 2 and 50. The urinary nitrogen was used to calculate the daily amount of protein being oxidized and its energy content was compared with the measured basal metabolic rate of individual animals. Approximately 6% of the energy expended by grey seal pups during the post-weaning fast is derived from oxidation of protein. It is concluded that a rapid depression of basal metabolic rate and extensive blubber catabolism enable grey seal pups to endure prolonged periods of fasting without any apparent signs of discomfort or stress.
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PMID:Depressed metabolism and low protein catabolism in fasting grey seal pups. 236 22

Normothermic ischemia tolerance is an important aspect of organ procurement and transplantation. The function of pancreas and kidney autografts was investigated in totally pancreatectomized or nephrectomized canine recipients. In 30 dogs the left limb (tail) of the pancreas was removed but left in the abdominal cavity after cessation of blood flow to produce warm ischemia for 30, 60, and 120 min (10 dogs at each time point), and then was flushed with cold Ringers' lactate and transplanted to the iliac vessels. Twenty dogs with fresh pancreatic transplants were controls. The success rate of pancreas transplants with warm ischemia of 1/2 and 1 hr was the same as that of controls (80%); however, after 1 hr normothermia 5/10 dogs had episodes of hyperglycemia for 1 week before glucose levels came back to normal. All but one graft with 2 hr warm ischemia failed. Intravenous glucose tolerance test (IVGTT) mean (+/- SEM) K values were not different in the successful groups, i.e., no warm ischemia: -1.55 +/- 0.15%; 1/2 hr warm ischemia: -1.81 +/- 0.18%; 1 hr warm ischemia: -1.64 +/- 0.09%. Amylase levels increased after transplant with maximum values at Day 2, then returned to normal, but the levels remained elevated in recipients of grafts subjected to longer normothermia with evidence of pancreatitis after 1 hr warm ischemia. Fifteen kidney grafts were treated similarly with warm ischemia exposure of 1/2 hr (n = 9) and 1 hr (n = 6) before being flushed and autotransplanted, and were compared to 16 fresh kidney transplants. After 1/2 hr warm ischemia none of the kidney grafts failed but 78% of the recipients had elevated serum creatinine and urea nitrogen levels which returned slowly to normal after 3 to 4 weeks. There was only one long-term survivor after 1 hr warm ischemia. Thus the pancreas seems to be more resistant to warm ischemia damage than is the kidney. This difference should be taken into consideration in regard to organ procurement for clinical transplantation.
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PMID:Definition of normothermic ischemia limits for kidney and pancreas grafts. 242 97

Angiotensin-converting enzyme (ACE) inhibition with captopril is accepted therapy for the treatment of symptomatic congestive heart failure. In this trial, we compared the new ACE inhibitor, lisinopril, to captopril during a 12-week randomized double-blind study. One hundred twenty-nine patients with New York Heart Association class II, III, or IV congestive heart failure were randomized to receive either lisinopril 5 mg/day (n = 64) or captopril 37.5 mg/day (n = 65) in 15 centers. Drug doses could be titrated upwards every 4 weeks. The primary measure of drug efficacy was improvement in treadmill exercise time using a modified Naughton protocol. Secondary measures of efficacy and the development of adverse effects were also examined. Lisinopril improved exercise time (following 12 weeks of therapy) more than captopril [from 500 +/- 30 to 682 +/- 34 sec (mean +/- SEM) with lisinopril versus 480 +/- 26 to 600 +/- 35 sec with captopril; difference between groups, p less than 0.05]. Adverse drug effects were unusual and similar in frequency in the two groups, although an increase in blood urea nitrogen was more common with lisinopril than with captopril (p less than 0.05). These results indicate that using the doses and treatment regimens studied, lisinopril is more effective than captopril for the treatment of symptomatic congestive heart failure. Adverse experiences with lisinopril were infrequent and similar in incidence to those observed with captopril.
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PMID:A double-blind comparison of lisinopril with captopril in patients with symptomatic congestive heart failure. 244 59

Cartilage sulfation (somatomedin) inhibitors (CSI) from rat liver produce reversible inhibition of cartilage growth. After gel filtration Sephadex G-200, CSI appear to have MW approximately 100,000 and they are urea- and trypsin-labile factors. To explore further the mechanism of CSI action, we used the chick pelvic rudiment bioassay and studied the effect of CSI on the incorporation on 35S-sulfate (proteoglycan synthesis), 14C-leucine (protein synthesis), 3H-uridine (RNA synthesis), and 3H-thymidine (DNA synthesis). Normal rat serum (NRS) significantly stimulated the incorporation of all four isotopes, as expected. After a 24-hour incubation, CSI significantly blunted cartilage stimulation by NRS regarding total isotope uptake (1), 35S-sulfate (NRS, 96 +/- 8 mcg/100 mg cartilage dry weight; NRS + CSI, 48 +/- 4, mean +/- SEM, n = 29, P less than .05); and (2) 14C-leucine (NRS, 2,089 +/- 172 cpm/mg dry weight; NRS + CSI, 1,102 +/- 141, n = 18, P less than .05); and (3) 3H-uridine (NRS, 6,711 +/- 832 cpm/mg; NRS + CSI, 3,227 +/- 425 cpm/mg, n = 18, P less than .05); but not (4) 3H-thymidine (NRS, 3,540 +/- 620 cpm/mg; NRS + CSI 3,249 +/- 285, n = 19). The inhibition of 35S-sulfate and 14C-leucine uptake by CSI was dose-dependent and reversible. For 35S-sulfate, uptake by cartilage incubated with CSI alone for 40 hours was 13 +/- 3 micrograms/100 mg; with CSI for 16 hours then fresh medium with NRS for 24 hours uptake was 39 +/- 12, P less than .05.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cartilage sulfation inhibitor from rat liver: partial characterization of properties and biologic action. 244 68


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