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)

1. The concentration and oxidoreduction state of the liver nicotinamide nucleotides of rats subjected to a number of hormonal treatments have been measured. 2. Adrenalectomy decreases the NADP(+) content by 80% but has little effect on NAD(+), NADH or NADPH. High doses of cortisone produce similar changes, but more physiological doses (5mug. daily) tend to increase the NADP(+) content. 3. Glucagon treatment of normal rats lowered the NADH and NADP(+) concentrations but did not affect the total amounts present. Growth hormone increased the concentrations and total amounts of NAD(+) and NADH but significantly decreased the concentrations and total amounts of NADP(+) and NADPH. 4. Measurements have been made of a number of enzymes in the livers of adrenalectomized and glucagon-treated rats that could affect the oxidoreduction state of NADP. The activities of glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase are not affected by adrenalectomy or treatment with cortisone or glucagon. Nor does adrenalectomy affect the activity of NADPH-cytochrome c oxidoreductase or NADPH-glutathione oxidoreductase. The hepatic content of glutathione is, however, decreased 50% by adrenalectomy. 5. Measurements of the oxidation of [1-(14)C]glucose and [6-(14)C]glucose by liver slices from adrenalectomized rats showed that glucose oxidation was substantially normal, although phenazine methosulphate caused a smaller stimulation of the oxidation of C-1 of [1-(14)C]glucose in slices from the livers of adrenalectomized rats than it did with slices from controls. The hepatic synthesis of lipids from [1-(14)C]glucose was marginally increased in adrenalectomized rats. 6. The additional NADP(+) found when liver is extracted with 0.02n-sulphuric acid-0.1m-sodium sulphate is less affected than the NADP(+) extracted with 0.1n-hydrochloric acid in adrenalectomized or glucagon-treated rats. Hooded Norway rats appear to have less of this extra form of NADP(+) than albino rats. 7. An attempt has been made to correlate the observed changes in the nicotinamide nucleotides with metabolic patterns prevailing in different hormonal conditions.
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PMID:THE EFFECT OF DIFFERENT HORMONAL CONDITIONS ON THE CONCENTRATION AND OXIDOREDUCTION STATE OF THE NICOTINAMIDE NUCLEOTIDES OF RAT LIVER. 1433 53

Growth hormone (GH) and cortisol are important to ensure energy supplies during fasting and stress. In vitro experiments have raised the question whether GH and cortisol mutually potentiate lipolysis. In the present study, combined in vivo effects of GH and cortisol on adipose and muscle tissue were explored. Seven lean males were examined four times over 510 min. Microdialysis catheters were inserted in the vastus lateralis muscle and in the subcutaneous adipose tissue of the thigh and abdomen. A pancreatic-pituitary clamp was maintained with somatostatin infusion and replacement of GH, insulin, and glucagon at baseline levels. At t = 150 min, administration was performed of NaCl (I), a 2 microg.kg(-1).min(-1) hydrocortisone infusion (II), a 200-microg bolus of GH (III), or a combination of II and III (IV). Systemic free fatty acid (FFA) turnover was estimated by [9,10-3H]palmitate appearance. Circulating levels of glucose, insulin, and glucagon were comparable in I-IV. GH levels were similar in I and II (0.50 +/- 0.08 microg/l, mean +/- SE). Peak levels during III and IV were approximately 9 microg/l. Cortisol levels rose to approximately 900 nmol/l in II and IV. Systemic (i.e., palmitate fluxes, s-FFA, s-glycerol) and regional (interstitial adipose tissue and skeletal muscle) markers of lipolysis increased in response to both II and III. In IV, they were higher and equal to the isolated additive effects of the two hormones. In conclusion, we find that GH and cortisol stimulate systemic and regional lipolysis independently and in an additive manner when coadministered. On the basis of previous studies, we speculate that the mode of action is mediated though different pathways.
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PMID:Additive effects of cortisol and growth hormone on regional and systemic lipolysis in humans. 1460 73

Diagnosis of glucose status requires knowledge of the homeostatic mechanisms that maintain the blood glucose concentration between the narrow range of 2.5 and 7.5 mmol/l during periods of eating or fasting. Hypoglycaemia occurring within the first few hours after eating is suggestive of hyperinsulinism. Most glucose is subsequently converted into glycogen in the liver, and hypoglycaemia occurring during this phase is suggestive of glycogenosis. During fasting, gluconeogenesis progressively replaces glycogen as the major source of blood glucose, and hypoglycaemia occurring during this period is suggestive of impaired gluconeogenesis or fatty acid disorders. Growth hormone, glucagon, cortisol and insulin-like growth factor 1 deficiencies may also play a role. Other causes of hypoglycaemia have also been identified recently, namely glucose transporter disorders, respiratory chain disorders and congenital disorders of glycosylation.
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PMID:Neonatal hypoglycaemia: aetiologies. 1501 75

Poor growth is a common finding in patients with organic acidemias. Growth hormone (GH) therapy has been considered in the management of these disorders as a mode to enhance anabolism and lower the high levels of methylmalonic acid. We report two patients with methylmalonic acidemia (mut(o)) and GH deficiency. Both patients had persistently elevated serum concentrations of methylmalonic acid, which failed to respond to conventional therapy. In anticipation of using GH therapy to reduce high methylmalonic acid concentrations, the first patient underwent GH testing utilizing a provocative glucagon stimulation test and was found to be deficient. He was subsequently treated with GH and demonstrated improved growth, but his methylmalonic acid concentrations remain elevated. The second patient was also found to be GH deficient. These findings suggest that GH deficiency may be an etiologic factor in the poor growth seen in patients with organic acidemia.
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PMID:Growth hormone deficiency associated with methylmalonic acidemia. 1505 62

Growth hormone and prolactin are important growth factors for pancreatic beta-cells. The effects exerted by these hormones on proliferation and on insulin synthesis and secretion in beta-cells are largely mediated through the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway. Suppressors of cytokine signaling (SOCS) proteins are specific inhibitors of the JAK/STAT pathway acting through a negative-feedback loop. To investigate in vivo effects of SOCS-3 in growth hormone (GH)/prolactin signaling in beta-cells we generated transgenic mice with beta-cell-specific overexpression of SOCS-3. The relative beta-cell proliferation and volume in the mice were measured by morphometry. Beta-cell volume of transgenic female mice was reduced by over 30% compared with beta-cell volume in wild-type female mice. Stimulation of transgenic islets in vitro with GH showed a reduced tyrosine phosphorylation of STAT-5 when compared with wild-type islets. Transduction of primary islet cultures with adenoviruses expressing various SOCS proteins followed by stimulation with GH or glucagon-like peptide-1 (GLP-1) revealed that SOCS-3 inhibited GH- but not GLP-1-mediated islet cell proliferation, indicating that the decreased beta-cell volume observed in female transgenic mice could be caused by an inhibition of GH-induced beta-cell proliferation by SOCS-3. In spite of the reduced beta-cell volume the transgenic female mice exhibited enhanced glucose tolerance compared with wild-type littermates following an oral glucose-tolerance test. Together these data suggest that SOCS-3 modulates cytokine signaling in pancreatic beta-cells and therefore potentially could be a candidate target for development of new treatment strategies for diabetes.
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PMID:Regulation of pancreatic beta-cell mass and proliferation by SOCS-3. 1621 5

In children with type 1 diabetes (T1DM), altered adaptive responses to exercise (secretion of growth factors, inflammatory cytokines, and glucoregulatory mediators) may have potential implications in growth and development, early onset of disease complications, and incidence of hypoglycemia. We therefore measured a broad spectrum of exercise responses in 12 children with T1DM (seven males and five females) and 12 controls (six males / six females) aged 11-15 yr, during a 30-min exercise challenge @ 80% VO(2)max. Euglycemia was strictly controlled during exercise, and in diabetic patients a basal rate of i.v. insulin was allowed to maintain baseline insulin concentrations. Throughout the experiment, interleukin-6 (IL-6) concentrations (pg/mL) were markedly higher in T1DM vs. controls (preexercise: 5.0+/-1.3 vs. 1.9+/-0.6, p<0.02; end-exercise 5.3+/-1.2 vs. 2.7+/-1.0, p<0.05; 30-min postexercise: 8.2+/-2.2 vs. 3.9+/-0.8, p<0.05). A similar pattern was also observed with norepinephrine. Growth hormone (GH) concentration was similar in both groups at baseline and end-exercise, but in T1DM the exercise-induced GH remained significantly elevated 30 min after exercise (9.2+/-2.2 vs. 3.1+/-0.9 ng/L, p<0.01). The exercise-induced increase in glucagon elicited by exercise in controls was similar to that previously observed in healthy adults (10+/-3 pg/mL); however, it was significantly blunted in T1DM children (2+/-2 pg/mL, p<0.05). In conclusion, T1DM children displayed significant alterations in multiple aspects of their adaptive response to intense exercise.
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PMID:Inflammatory cytokine, growth factor and counterregulatory responses to exercise in children with type 1 diabetes and healthy controls. 1648 70

To date, the hormonal factors used in the treatment of patients with short-bowel syndrome have been growth hormone and glucagon-like peptide (GLP)-2. In high-dose growth hormone studies, the effects on wet-weight absorption of approximately 0.7 kg/day have mainly been described in short-bowel syndrome patients with a preserved colon who also received oral rehydration solutions. Treatment with high doses of growth hormone is associated with severe adverse effects in the majority of patients. Low-dose growth hormone increased energy absorption by approximately 1.8 MJ/day in a group of 12 short-bowel syndrome patients (9 with a preserved colon), but it did not affect wet-weight absorption. Growth hormone does not seem to affect either wet-weight or energy absorption in patients with a jejunostomy. GLP-2 and the analogue teduglutide mainly affect wet-weight absorption, resulting in a mean increase in wet-weight absorption of 0.4-0.7 kg/day. The effects on energy absorption are minor at 0.4-0.8 MJ/day. However, these effects are seen in all short-bowel syndrome patients, regardless of anatomy, and the adverse effects are minor. In all studies employing growth hormone or GLP-2, the effects are transient, disappearing when treatments are discontinued. With the need for long-term treatment, adverse effects and safety issues become important. Therefore, it is recommended that treatment is initiated in research settings only and that close monitoring of the long-term effects is a part of the protocol.
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PMID:The use of hormonal growth factors in the treatment of patients with short-bowel syndrome. 1662 Jan 38

This study hypothesized that increased feeding frequency (FF) decreases problems with glucose homeostasis seen at high feeding levels (FL) in heavy veal calves. Effects of FF and FL on hormone and metabolite concentrations were studied in 15 heavy veal calves fed once (FF1; at 12:00), twice (FF2; at 12:00 and 24:00) or four times daily (FF4; at 06:00, 12:00, 18:00 and 24:00). In period 1, all calves were fed at a low FL (FL(low); 1.5 x metabolizable energy requirements for maintenance, ME(m)). In period 2, FF2 and FF4 calves were fed at high FL (FL(high); 2.5 x ME(m)), whereas FF1 calves were still fed at FL(low). Blood was sampled every 30 min from 12:00 to 18:00 and postprandial integrated plasma hormone and metabolite concentrations (AUC(12-18 h)) were calculated. Glucose AUC(12-18 h) increased with increasing FL, but decreased with increasing FF, urea AUC(12-18 h) increased with increasing FL, whereas non-esterified fatty acid AUC(12-18 h) were unaffected by FL and FF. Insulin AUC(12-18 h) decreased with increasing FF and decreasing FL. Glucagon AUC(12-18 h) increased with increasing FL and FF. Growth hormone AUC(12-18 h) decreased, whereas insulin-like growth factor-1 and leptin AUC(12-18 h) increased with increasing FL. Mean thyroxine and 3,5,3'-triiodothyronine concentrations were modified by FF and FL. There were no FF x FL interactions, except for plasma glucose. In conclusion, postprandial hormone and metabolite responses were differentially affected by FF and (or) FL. Glucose and insulin concentrations were maximally increased at high FL and low FF. Hyperglycemia, glucosuria and excessive insulinemia were prevented by increasing FF and decreasing FL.
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PMID:Postprandial blood hormone and metabolite concentrations influenced by feeding frequency and feeding level in veal calves. 1722 5

The metabolism of critical illness is characterised by a combination of starvation and stress. There is increased production of cortisol, catecholamines, glucagon and growth hormone and increased insulin-like growth factor-binding protein-1. Phagocytic, epithelial and endothelial cells elaborate reactive oxygen and nitrogen species, chemokines, pro-inflammatory cytokines and lipid mediators, and antioxidant depletion ensues. There is hyperglycaemia, hyperinsulinaemia, hyperlactataemia, increased gluconeogenesis and decreased glycogen production. Insulin resistance, particularly in relation to the liver, is marked. The purpose of nutritional support is primarily to save life and secondarily to speed recovery by reducing neuropathy and maintaining muscle mass and function. There is debate about the optimal timing of nutritional support for the patient in the intensive care unit. It is generally agreed that the enteral route is preferable if possible, but the dangers of the parenteral route, a route of feeding that remains important in the context of critical illness, may have been over-emphasised. Control of hyperglycaemia is beneficial, and avoidance of overfeeding is emphasised. Growth hormone is harmful. The refeeding syndrome needs to be considered, although it has been little studied in the context of critical illness. Achieving energy balance may not be necessary in the early stages of critical illness, particularly in patients who are overweight or obese. Protein turnover is increased and N balance is often negative in the face of normal nutrient intake; optimal N intakes are the subject of some debate. Supplementation of particular amino acids able to support or regulate the immune response, such as glutamine, may have a role not only for their potential metabolic effect but also for their potential antioxidant role. Doubt remains in relation to arginine supplementation. High-dose mineral and vitamin antioxidant therapy may have a place.
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PMID:Nutritional interventions in critical illness. 1734 68

In previous studies, high plasma insulin was associated with earlier resumption of postpartum estrous cycles in dairy cows. The objective of this experiment was to quantify hormonal and ovarian responses to dietary starch and fat contents. Thirty cows were fed on a standard diet from calving until 40 d in milk (DIM) and then 6 cows were allocated to each of 5 isoenergetic diets containing 231, 183, 159, 135, and 87 g of starch and 39, 42, 43, 45, and 48 g of fat/kg of dry matter (DM) for diets 1 to 5, respectively, until 70 DIM. Estrus was synchronized at 60 DIM. Between 60 and 70 DIM, energy intake, milk yield, and energy balance were similar among diet groups. Plasma insulin-to-glucagon ratio increased with increasing dietary starch and decreasing dietary fat concentrations, reaching a break point at 159 g of starch, 43 g of fat/kg of DM (diets 1 to 5: mean 3.86, 3.78, 3.59, 2.98, 2.06 +/- standard error 0.22). Growth hormone, insulin-like growth factor-I, and leptin did not vary among diets. The greatest dietary starch concentration was associated with elevated plasma urea-N (diets 1 to 5: mean 3.69, 3.01, 2.94, 2.95, 2.75, +/- standard error 0.13 mmol/L, respectively) and delayed postovulatory progesterone increase (progesterone at 3 to 5 d postovulation for diets 1 to 5: mean 2.7, 5.9, 4.2, 5.6, 4.3 +/- standard error 0.9 ng/mL, respectively). The number of small (<5 mm) ovarian follicles was positively related to starch intake (r = 0.381) and plasma insulin concentration (r = 0.402). It is concluded that to maintain adequate insulin-to-glucagon ratio in cows at the start of the breeding period, dietary starch concentration should be above 160 g/kg of DM and dietary fat below 44 g/kg of DM, and this should have a positive effect on ovarian function.
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PMID:Nutrition, metabolism, and fertility in dairy cows: 1. Dietary energy source and ovarian function. 1883 3


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