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)

Addition of the cyclic AMP phosphodiesterase inhibitors theophylline (10- minus 2 M) or papaverine (10- minus 4 M) leads to a complete inhibition of lactose synthesis in incubated guinea pig mammary gland slices. Addition of 10- minus 5 M cyclic AMP or dibutyryl cyclic AMP results in 1 30-40% inhibition of the synthesis, which effect is not increased by applying higher concentrations of these compounds. A 30-40% inhibition can also be obtained with epinephrine (5 - 10- minus 5 M), or isoproterenol (10- minus 4 M), but the polypeptide hormones glucagon (10- minus 7 M), insulin (1 munit/ml) and relaxin (10 mug/ml) do not significantly affect lactose synthesis. Cytochalasin B (5 mug/ml) inhibits lactose production by 58and colchicine (10- minus 5 M) by 25%. These experiments suggest that an increase in the intracellular level of cyclic AMP either through its addition, through hormonal stimulation of its synthesis, or through inhibition of its intracellular breakdown, leads to an inhibition of lactose production in lactating mammary gland. This effect of cyclic AMP is similar to that of progesterone, which is known to inhibit lactation in vivo and the withdrawal of which at parturition has been postulated to initiate lactogenesis.
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PMID:Inhibition by cyclic AMP of lactose production in lactating guinea pig mammary gland slices. 16 55

This study examined the effects of clofibrate therapy on basal plasma substrate and hormone concentrations in ketosis-prone insulin-dependent diabetic man. A double-blind crossover design was utilized during a 3-mo period in which clofibrate treatment (1 g b.i.d.) was compared to that of a lactose placebo (1 g b.i.d.). Our results demonstrate that clofibrate treatment resulted in a significant reduction in the concentration of plasma glucose, ketone bodies, free fatty acids, triglyceride, and cholesterol in diabetic man. These beneficial effects were observed without demonstrable changes in circulating concentrations of insulin and glucagon. These observations suggest that in ketosis-prone diabetic man, clofibrate therapy may provide an adjunct to exogenous insulin administration.
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PMID:Metabolic effects of clofibrate in insulin-dependent ketosis-prone diabetic man. 41 22

Previous findings that 2.5 mM quinolinic acid inhibits gluconeogenesis more strongly from alanine than from lactate have been confirmed. 15 mM quinolinic acid completely inhibited gluconeogenesis from lactate as well as from alanine whereas the formation of glucose from fructose and the production of urea from ammonia and lactose were not affected. The pattern of the gluconeogenic intermediates was the same in the presence of 15 mM quinolinic acid as with 2.5 mM of the inhibitor. It is concluded that high as well as low concentrations of quinolinic acid inhibit gluconeogenesis at the step between oxaloacetate and phosphoenolpyruvate. Furthermore, 5-methoxyindole-2-carboxylic acid, an inhibitor of mitochondrial pyruvate metabolism, also completely blocked gluconeogenesis from lactate whereas glycerol conversion to glucose was only weakly inhibited. All these results do not support the concept of an alternate pathway of gluconeogenesis from lactate proposed by others. 2.5 mM quinolinic acid also partially blocked the formation of urea from alanine. It is suggested that quinolinic acid may have a second site of action causing an inhibition of the glutamate-pyruvate transamination owing to lack of 2-oxoglutarate in the cytosol. In the presence of quinolinic acid, glucagon caused about the same increase in aspartate and malate tissue levels in the absence of added substrates as in the presence of added lactate or alanine. Therefore, no additional effect of glucagon on gluconeogenesis from lactate or alanine prior to the block by quinolinic acid could be demonstrated.
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PMID:Effects of quinolinic acid and glucagon on gluconeogenesis in the perfused rat liver. 69 6

Given the potential use of a low-calorie sweetener during weight reduction, a toxicity study of chronic aspartame ingestion was conducted. Particular attention was given to possible long-term effects of aspartame on the fuel hormonal alterations characteristically caused by weight reduction. As a group mean age was 19.3 yr, body weight was 164.6 lb, and mean height was 65.4 in. Subjects were an average of 33% in excess of ideal body weight. The aspartame dose was 2.7 g/day and was compared on a double-blind randomized basis with a lactose placebo. Both materials were given in gelatin capsules. An average of 6.9 +/- 1.5 lb was lost by the aspartame group during the 13-wk study on a calculated 1,000-calorie diet. The placebo group lost 4.5 +/- 1.2 lb (no significant difference between the two groups). After an overnight fast, reductions in glucose and immunoreactive insulin were seen in both groups, while rising trends in immunoreactive glucagon were observed. These changes are all characteristic of calorie restriction. In no instance was there a detectable effect of the ingested aspartame. No meaningful effect of weight reduction or aspartame was seen on plasma triglyceride and cholesterol, nor on any other parameter of hematologic, hepatic, or renal function that was measured. Similarly, side effects were equally distributed between asparatame and placebo.
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PMID:Effects of aspartame in young persons during weight reduction. 79 76

The structure-activity relationship of sugars inducing secretion of glucagon-like peptide-1 from the gut was examined using intestinal loops prepared from the terminal portion of the ileum of dogs. The plasma glucagon-like peptide-1 concentration in a mesenteric vein draining only the looped region of the intestine was increased after infusion of 139 mmol/l solutions of D-glucose, D-galactose, D-glucuronic acid, 3-0-methyl-D-glucose, maltose, sucrose or maltitol into the intestinal lumen, but not after infusion of solutions of D-fructose, D-fucose, D-mannose, D-xylose or lactose. The increases in plasma glucagon-like peptide-1 concentration correlated with the corresponding increases in glucagon-like immunoreactivity induced by these sugars. The plasma glucose level of the regional mesenteric vein increased significantly from the basal level after instillation of D-glucose, but not after instillation of other sugars. It is suggested that cells of the gut have a glucose sensor for release of products of the glucagon gene and that this sensor has specific steric requirements. The sugars that induced glucagon-like peptide-1 release share the molecular features of electron density near C(6), an equatorial hydroxyl at C(2), and an axial hydroxyl at C(1), which could account for their recognition by the glucose sensor to initiate the releases of glucagon-like peptide-1 and glucagon-like immunoreactivity.
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PMID:Relationship between molecular structures of sugars and their ability to stimulate the release of glucagon-like peptide-1 from canine ileal loops. 223 92

Eight Holstein cows were utilized to examine the effect of prolactin on lactational performance prior to peak milk production (day 21-34 postpartum) and after peak milk production (day 60-73 postpartum). During each 14 day period, cows received daily intramuscular injections of pituitary-derived bovine prolactin (120 mg; 13.0 IU/mg protein) or excipient. Cows were housed in a controlled environment at 18.1C, 47.8% relative humidity and a 15 hr light: 9 hr dark cycle. In cows administered exogenous prolactin, circulating prolactin concentrations increased within one-half hr post injection, peaked within 2 to 6 hours and declined through the remainder of the day. Average prolactin concentration in the plasma was increased 2 to 5 fold over the 24 hr period in response to prolactin treatment. Yields of milk and milk components (fat, lactose and protein) were not affected by prolactin treatment in either period but the concentration of alpha-lactalbumin in milk was significantly increased (P less than .10) in both periods. Circulating concentrations of somatotropin, triiodothyronine, thyroxine, glucagon, nonesterified fatty acids and glucose were not altered. In prolactin-treated cows, the milking-stimulated prolactin release was decreased at both the PM milking, when circulating concentrations of prolactin were high, and the AM milking, when prolactin concentrations had returned to baseline. Concentration of prolactin in milk tended to increase but was not significantly altered by administration of exogenous prolactin. However, prolactin concentrations in plasma were correlated (r = .56) with milk concentrations. It is clear that postpartum administration of exogenous prolactin during the period of lactation prior to peak milk yield or after peak milk yield does not alter lactational performance in high producing dairy cows.
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PMID:Effect of exogenous prolactin administration on lactational performance of dairy cows. 350 96

We have shown previously that short-term nutritional deprivation causes a tissue-specific loss of liver ornithine decarboxylase (ODC) induction after isoproterenol, phenylephrine, or glucagon administration in rat pups. To examine the role of nutrition in the regulation of hepatic ODC, we tested the ability of intragastric nutrient administration to reverse nutritionally related deficits in the ODC response to hormonal challenge. Intragastric whole milk was effective in restoring ODC induction and accumulation of its immediate product, putrescine, in response to isoproterenol administration. Glucose was shown to mediate this effect by the ability of intragastric skimmed milk, lactose, galactose, or D-glucose to return ODC induction, and the inability of casein, sucrose, fructose, L-glucose, or pyruvate plus lactate to do so. D-Glucose also reestablished ODC induction by phenylephrine and glucagon. Parenteral administration of D-glucose produced results comparable to those obtained after intragastric administration. Isoproterenol induction of ODC was prevented when hepatic glucose uptake was blocked by phlorizin but not by blockade of central nervous system glucose uptake with 2-deoxyglucose. We conclude that intrahepatic glucose is an absolute requirement for hepatic ODC induction by isoproterenol, phenylephrine, or glucagon in preweanling rats.
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PMID:Intrahepatic glucose: a requirement for neonatal ODC induction by specific hormones. 638 Mar 9

Bovine growth hormone (51.5 IU/day) and placebo injections were administered for 10 days to four Holstein cows in early lactation (wk 12) and again in late lactation (wk 35). Milk productions in the last 5 days of each period were compared. In early lactation, growth hormone increased milk yield by 15%, fat yield by 17%, protein yield by 14%, and lactose yield by 21%. In late lactation the respective increases were 31, 42, 18, and 35%. For responses of early and late lactation to growth hormone on a quantitative basis, increases for milk yield (4.3 versus 3.9 kg/day) and milk energy secretion (3.3 versus 3.4 Mcal/day) were similar. Concurrent with these increased milk yields, ad libitum intakes of a complete mixed diet declined during the period of growth hormone treatment by 3% in early lactation and 16% in late lactation. During the 6 h immediately following injections of growth hormone, blood plasma concentrations of growth hormone were elevated about 400% in early lactation and 700% in late lactation. Concentrations in plasma of free fatty acids were also higher during growth hormone treatment in late lactation but not in early lactation. Treatments did not affect plasma concentrations of glucose, insulin, glucagon, prolactin, tri-iodothyronine, thyroxine, or cortisol in either early or late lactation. Daily administration of growth hormone in early or late lactation resulted in similar and substantial increases of milk yield and efficiency of milk production.
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PMID:Effect of exogenous growth hormone in early and late lactation on lactational performance of dairy cows. 685 99

Galactose usually is ingested as lactose, which is composed of equimolar amounts of glucose and galactose. The contribution of galactose to the increase in glucose and insulin levels following ingestion of equimolar amounts of galactose and glucose, or lactose, has not been reported in people with non-insulin-dependent diabetes mellitus (NIDDM). Therefore, we studied the effects of galactose ingestion alone, as well as with glucose either independently or in the form of lactose, in subjects with untreated NIDDM. Eight male subjects with untreated NIDDM ingested 25 g glucose, 25 g galactose with or without 25 g glucose, or 50 g lactose as a breakfast meal in random sequence. They also received 50 g glucose on two occasions as a reference. Water only was given as a control meal. Plasma galactose, glucose, glucagon, alpha-amino nitrogen (AAN), nonesterified fatty acids (NEFA), and serum insulin and C-peptide concentrations were determined over a 5-hour period. The integrated area responses were quantified over the 5-hour period using the water control as a baseline. Following ingestion of 25 g galactose, the maximal increase in plasma galactose concentration was 1 mmol/L. The mean maximal increases in plasma galactose concentration following ingestion of 25 g galactose + 25 g glucose or following 50-g lactose meals were similar and were only 12% of that following ingestion of galactose alone (P < .05). The mean galactose area response over the water control for the 25-g galactose meal was 0.95 +/- 0.31 mmol.h/L.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of glucose, galactose, and lactose ingestion on the plasma glucose and insulin response in persons with non-insulin-dependent diabetes mellitus. 824 70

Hydrolyzed soy protein (SH) could be used as a protein source in formulas for infants with intolerance to cow's milk protein and may be preferable to intact soy protein (SI). However, metabolic responses to SH are poorly defined. Because of their partially hydrolyzed nature, nonphysiological elevations in either plasma amino acids or regulatory hormones may occur. Therefore, we evaluated effects of SH on plasma nutrient and pancreatic hormone (insulin, glucagon) concentrations. In Experiment 1, 24 newborn pigs were fitted with umbilical arterial and portal catheters, fed formula for 36 h and food deprived for 12 h. Pigs were then fed formula including either SH or SI with glucose polymers or casein-whey proteins (CW) containing lactose, and serial blood samples were taken for 2 h postprandially. Peak portal exceeded peak arterial amino acid concentrations within each treatment, and peak amino acid concentrations in CW-fed pigs exceeded those of SH- and SI-fed pigs. However, only SH formula-fed piglets had higher postprandial portal minus arterial amino acid concentrations (P < 0.05) throughout Experiment 1, suggesting that SH was well digested and absorbed. In Experiment 2, arterial catheters were inserted in 24 piglets. Previous procedures were followed except dietary carbohydrate was standardized to glucose polymers for all three diets, and sampling was extended to 3 h. Overall, portal or arterial nutrient and hormone concentrations were not different in the SI and SH groups (P > 0.05), indicating that hydrolyzed soy protein did not cause abnormal plasma concentrations. In conclusion, hydrolyzed soy protein did not result in elevated nutrient concentrations or hormone responses compared with intact soy or cow's milk protein.
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PMID:Short-term metabolic responses do not differ between neonatal piglets fed formulas containing hydrolyzed or intact soy proteins. 861 95


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