Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of metabolic acidosis (MA) on amino acid and keto acid metabolism was studied in fourteen patients with chronic renal failure (CRF) under the low protein diet (0.6-0.8 g/kgBW). The comparative study of five patients with renal tubular acidosis was carried out. Each patient was investigated before [MA(+)period] and after correction with sodium bicarbonate administration lasting 10 days [MA(-)period]. The correction of MA improved nitrogen balance and elevated plasma branched-chain amino acids (BCAA), keto acids (BCKA), glutamine and alanine concentrations. No effect was however, observed in change of plasma insulin and glucagon. Oral administration of the keto-analogues of BCKA [0.1 g/kgBW of alpha-ketoisovalerates (KIV) and alpha-keto-isocaproic acid (KIC)] is made for the purpose of investigating the change in the metabolic conversion rate to amino acids. As a result, MA (+) suppressed an increase in plasma KIV and KIC concentrations. Moreover, an increase in plasma valine and leucine concentrations were suppressed by MA (+). These results suggested that MA stimulates BCKA oxidation and suppresses the protein sparing effect of leucine and KIC, and accelerates the catabolism in CRF under the low protein diet. The correction of MA is ineffective in severe renal failure (serum creatinine above 10.0 mg/dl), because the other uremic factors appear to be affecting protein and amino acid metabolism. Therefore, it might be concluded that MA should be corrected at an earlier stage of CRF.
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PMID:[The effect of metabolic acidosis on amino acid and keto acid metabolism in chronic renal failure]. 205 49

We examined the level of plasma amino acids, glucose, immunoreactive insulin (IRI) and immunoreactive glucagon (IRG) of patients in the fasted state with acute hepatitis in the actual acute stage (AHa), acute hepatitis in the convalescent stage (AHc), chronic active hepatitis (CAH), chronic persistent hepatitis (CPH) and liver cirrhosis (LC). In AHa patients, the plasma glucose (FPG), plasma alanine (Ala), tryptophan (Trp) and histidine (His) levels were significantly lower and plasma cystine (Cys) level significantly higher than the control levels. This however, was not the case in the other patients. The glutamic acid (Glu) concentration was significantly higher in AHa (p less than 0.02), CAH (p less than 0.001) and CPH (p less than 0.001) and the tyrosine (Tyr) concentration was significantly higher in AHa (p less than 0.02), CPH (p less than 0.001), CAH (p less than 0.001) and LC (p less than 0.001) than they were in the controls. The lysine (Lys) concentration was significantly raised in the AHa (p less than 0.02) and CPH (p less than 0.05) cases. The IRG level was significantly higher in AHa (p less than 0.001), in AHc (p less than 0.01) and LC (p less than 0.01). Valine (Val) showed a significant decrease in concentration in AHa (p less than 0.01) and LC (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Profiles of plasma amino acids in fasted patients with various liver diseases. 208 40

The control of protein and RNA degradation by amino acids, insulin, and glucagon was investigated in perfused livers from normal fed rats. Rates of breakdown were determined from the release of valine and cytidine after isotopic labelling in vivo. Stringent amino acid deprivation induced comparable increases (approximately 3.2% h-1) in the degradation of both macromolecular classes, and insulin inhibited them equally. By contrast, glucagon evoked the same proteolytic response at normal plasma concentrations but failed to stimulate RNA breakdown significantly. These and associated electron microscopic findings indicate the existence of two concentration-dependent modes of macroautophagy, one which sequesters both RNA and protein at low amino acid levels and a second which selectively takes up protein at normal concentrations. Control of macroautophagy is accomplished by seven regulatory amino acids and the permissive action of alanine. Alanine is required for effective inhibition by the regulatory group at normal concentrations; in its absence protein degradation accelerates sharply. This response, like that following the administration of glucagon, is mediated by the second mode.
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PMID:Mechanism and control of protein and RNA degradation in the rat hepatocyte: two modes of autophagic sequestration. 248 18

In recent years, short-term effects of the composition of each meal on the synthesis of brain neurotransmitters have been studied. This paper reviews studies of the influence of dietary precursors such as tryptophan and other competing amino acids on serotonin synthesis and metabolism and emphasizes the important influence of insulin. The paper then focuses on assessment of newborn state behavior, since evidence in adult humans has suggested a relationship between sleep behavior and brain serotonin levels. Several studies are then summarized. First, a study of healthy full-term newborns examining the relationship between diet and sleep behavior showed that infants fed tryptophan entered active and quiet sleep sooner than infants fed valine and low carbohydrate. Other studies designed to examine the influence of hyperinsulinemia on this system are then described. An observational study of newborns of diabetic mothers during the first weeks of life showed that they were quieter babies, with difficulties in visual orientation and motor performance. Plasma amino acid ratios studied during a glucagon-stimulation test in an infant with hyperinsulinemia showed a marked increase in parallel with changes in insulin levels. The results suggest that infant sleep behavior can be a sensitive dependent variable in studies of behavioral effects of diet and suggests that variations in serotonin levels may play a modulating role.
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PMID:Nutrients, neurotransmitters and infant behavior. 286 87

In the search for selective and long-acting analogs of somatostatin, nearly 200 compounds were synthesized by solid-phase methods, purified, and tested biologically. Among these octapeptides, some contained N-terminal (Formula: see text) were 177 times and 113 times more potent, respectively, than somatostatin in tests for inhibition of growth hormone release. These two octapeptides containing tyrosine and valine in positions 3 and 6, respectively, were more active and more selective than their Phe-3 and Thr-6 counterparts, D-Phe-Cys-Phe-D-Trp-Lys-Thr-Cys-Thr-NH2 and D-Phe-Cys-Phe-D-Trp-Lys-Thr-Cys-Trp-NH2. D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Thr-NH2 was also about 6 times more potent than its L-Trp-4 diastereoisomer. The analogs D-Phe-Cys-Tyr-Lys-Val-Cys-Thr-NH2 and D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2 showed a prolonged duration of action and were able to inhibit growth hormone release for at least 3 hr. Analogs of both Phe-3/Thr-6 and Tyr-3/Val-6 classes also suppressed the release of insulin and glucagon in rats and pentagastrin-induced secretion of gastric acid in dogs, but their potencies in these tests were much smaller than the growth-hormone-release inhibitory activity. Some of these analogs possessed antitumor activities as shown by the inhibition of growth of animal models of prostate, mammary, and ductal pancreatic tumors.
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PMID:Synthesis and biological activity of highly potent octapeptide analogs of somatostatin. 286 90

We studied the effect of an arginine vasopressin (AVP) analogue, (1-[beta-mercapto-beta, beta-cyclopentamethylenepropionic acid],2-O-ethyltyrosine, 4-valine)AVP(d[CH2]5Tyr[Et]VAVP), on the stimulation of adenylate cyclase by various hormones in the isolated nephron segments and 3H-AVP binding to renal papillary membranes from the rat. The net water flux across the renal cortical collecting tubules of the rabbit was also examined. We found that d(CH2)5Tyr(Et)VAVP significantly inhibited adenylate cyclase activation by AVP in cortical, medullary, and papillary collecting tubules and in the medullary thick ascending limb. In contrast, the AVP analogue did not alter the stimulation of adenylate cyclase by parathyroid hormone in the cortical thick ascending limb, by glucagon in the medullary thick ascending limb, and by calcitonin in cortical collecting tubules. In addition, d(CH2)5Tyr(Et)VAVP blocked [3H]AVP binding to renal papillary membranes. The enhanced net water transport induced by AVP in isolated, perfused rabbit cortical collecting tubules also was completely blocked by this AVP analogue. These results indicate that d(CH2)5Tyr(Et)VAVP specifically antagonizes the cellular action of AVP on the medullary thick ascending limb and on the cortical, medullary, and papillary collecting tubules. Evidence is also presented for competitive antagonism as the cellular mechanism of action.
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PMID:Effects of vasopressin antagonist on vasopressin binding, adenylate cyclase activation, and water flux. 299 81

The effect of major operative trauma on skeletal muscle metabolism was examined in nine patients receiving a constant infusion of calories (1460 kcal/m2/day) and protein (75 gm of amino acids/m2/day) for 5 days before and 4 days after an operation. Compared with the preoperative state, 72 hours after the operation there was a significant rise in arterial levels of glucagon, cortisol, norepinephrine, and inactive triiodothyronine and a drop in concentrations of insulin, active triiodothyronine, and amino acids. Forearm blood flow increased, as well as the efflux from forearm muscle of lactate, taurine, serine, glycine, valine, methionine, isoleucine, leucine, phenylalanine, lysine, arginine, and total amino acid nitrogen (440%). This loss of muscle protein after trauma is associated with increased muscle proteolysis, as measured by increased urinary 3-methylhistidine excretion (83%), and accounts for increased nitrogen loss (54%) from the body. Increased activity of the sympathetic nervous system is manifested by increased levels of epinephrine and norepinephrine, a relative lack of insulin, and increased levels of glucagon. This hormonal milieu plays an important role in the production of hypoaminoacidemia, increased efflux of amino acids and lactate from muscle, and negative nitrogen balance observed in these traumatized patients.
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PMID:Major operative trauma increases peripheral amino acid release during the steady-state infusion of total parenteral nutrition in man. 308 29

The effects on gastrin, insulin, and glucagon release of neuromedin B (NMB), the C-fragment decapeptide of gastrin-releasing peptide-10 (GRP-10), seven analogues replacing amino acid positions 3, 6, and 9, and two C-terminal desamide analogues were examined in conscious dogs using intravenous bolus injection of these peptides study the structure-activity relationship of two bombesin-related peptides identified in mammals. The replacement from valine of position 6 of GRP-10 to threonine effectively reduced the stimulatory potency of these hormone secretions. Removal of the C-terminal amide of NMB and GRP-10 resulted in an almost complete loss of their stimulatory effect on gastrin secretion. [Leu3]GRP-10 elicited the most potent stimulatory activity on three hormone secretions among the analogues including NMB and GRP-10. These results indicate that valine in position 6 of GRP-10 and C-terminal amide of two peptides play an important role in the bioactivities of bombesin family peptides.
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PMID:Stimulation of dog gastropancreatic hormone release by neuromedin B and its analogues. 310 52

We compared the acute effects of intragastric administration of protein and carbohydrate on tryptophan and 5-hydroxytryptamine (5HT) in rat brain, pineal, intestine, and pancreas. Protein decreased and carbohydrate increased brain indoles relative to water-infused controls. These effects were due to competition between the large neutral amino acids for entry into the brain. This competition does not exist in the pineal. The macronutrients had no effect on pineal tryptophan metabolism. In the intestine, protein resulted in higher tryptophan levels as compared to controls, owing to absorption of tryptophan in the protein. However intestinal 5HT levels were influenced by factors other than precursor availability. Pancreatic indoles were affected in a similar manner to the brain indoles. Competition between the large neutral amino acids for entry into the pancreas was also indicated by the finding that valine administration lowered brain and pancreatic tryptophan, but not the levels in the intestine and pineal. It remains to be seen whether the decrease in pancreatic 5HT after a protein meal and the increase after carbohydrate modulate the release of insulin and glucagon.
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PMID:Effects of carbohydrate and protein administration on rat tryptophan and 5-hydroxytryptamine: differential effects on the brain, intestine, pineal, and pancreas. 316 82

Week-old lambs received an intravenous injection of 4.3, 8.5, 12.8 or 17.1 mmol [3H]valine/5 kg body weight, i.e., 3.6-14.4-times the whole-body free valine content. To ensure that protein synthesis measurements in lambs are reliable within a 30-min period, these large amounts of valine must account for at least around 11-times the total free pool of valine. This amounted to 12.8 mmol valine/5 kg body weight. There were no significant variations in plasma insulin and plasma glucagon levels 5, 13 and 30 min after the injection of so much valine. The fractional rates of protein synthesis were determined in tissues of animals receiving either 12.8 or 17.1 mmol valine/5 kg body weight. The rates of protein synthesis in the jejunum (87.5%/day), liver (106.6%/day) and tensor fasciae latae muscle (18.8%/day) of lambs injected with the 12.8 mmol [3H]valine flooding dose, were in the range of data obtained in immature rats. Increasing the flooding amount of valine up to 17.1 mmol/5 kg body weight did not significantly alter protein synthesis rates in the jejunum, liver or skeletal muscle. This suggested that both the flooding-dose method in itself and valine had no effect on in vivo protein synthesis.
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PMID:Assessment of in vivo protein synthesis in lamb tissues with [3H]valine flooding doses. 352 91


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