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)

Hepatocyte monolayer cultures from two preruminating and two ruminating calves were used to study the effects of triglyceride accumulation on induction of ureagenesis by glucagon plus dexamethasone. Whether hepatocytes from preruminating and ruminating calves respond similarly to triglyceride accumulation and hormonal treatment was also determined. Hepatocyte monolayer cultures were incubated from 24 to 48 h with a physiological mixture of nonesterified fatty acids (NEFA, 0 or 1.5 mM) and a hormone mixture containing glucagon plus dexamethasone (0 or 100 nM of both) added as a 2 x 2 factorial (NEFA x hormones). Ureagenesis was measured at 0, .25, and 5 mM NH4Cl from 48 to 51 h and activities of ornithine transcarbamylase (OTC) and arginase were measured at 48 h. There was no significant age-related interaction for any of the measurements. Therefore, monolayer culture of hepatocytes from preruminating calves provides a reasonable model for studying the effects of glucagon, dexamethasone, and triglyceride accumulation on ureagenesis in the ruminating bovine. Intracellular triglyceride was increased by NEFA (2.3 vs 15.6 +/- 1.9 microg TG/microg DNA, P < .001). Triglyceride-engorged cells exhibited decreased ureagenesis (1.04 vs .87 +/- .135 nmol/(microg DNA x h), P < .05) but had unaltered OTC and arginase activity. Hormone addition did not affect triglyceride accumulation but increased ureagenesis (.70 vs 1.21 +/- .135 nmol/(microg DNA x h), P < .0001). There was no interaction between hormone addition and triglyceride accumulation on ureagenesis. To separate the effects of dexamethasone from that of glucagon on ureagenesis, hepatocyte monolayer cultures from one ruminating and three preruminating calves were used. Hepatocyte monolayer cultures were incubated from 24 to 48 h with glucagon (0 or 100 nM) and dexamethasone (0 or 100 nM) added as a 2 x 2 factorial. Ureagenesis was measured at 0, .25, and 5 mM NH4Cl from 48 to 51 h. Glucagon increased ureagenesis (.77 vs 1.24 +/- .11 nmol/(microg DNA x h), P < .0001). Dexamethasone did not affect ureagenesis, nor was there any interaction between glucagon and dexamethasone. Therefore, glucagon alone was responsible for the induction observed with the mixture of glucagon and dexamethasone. In conclusion, glucagon is able to increase ureagenesis in bovine hepatocytes, and triglyceride accumulation does not interfere with the induction.
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PMID:Effects of triglyceride accumulation on induction of urea synthesis by glucagon and dexamethasone in monolayer cultures of bovine hepatocytes. 1087 50

Two experiments were conducted to evaluate L-carnitine supplementation to cattle fed grain-based diets. In Exp. 1, seven Angus-cross steers (216 kg) were used in a 7 x 4 incomplete Latin square experiment to evaluate the effects of supplemental L-carnitine on N balance and blood metabolites. Steers were fed a corn-based diet (17.5% CP) at 2.5% of BW. Treatments were 0, 0.25, 0.5, 1.0, 1.5, 2.0, and 3.0 g/d of supplemental carnitine. The 18-d periods included 13 d for adaptation and 5 d for collection of feces and urine. Blood was collected before feeding and 3 and 6 h after feeding on d 18 of each period. Dry matter intakes tended to be highest when 1.5 g/d of carnitine was supplied, but N retention was not affected by carnitine and averaged 29.3 g/d. Plasma carnitine concentrations and urinary excretion increased with increasing carnitine supply, indicating that at least some of the carnitine escaped ruminal degradation and was absorbed by the steers. Plasma concentrations of NEFA demonstrated a treatment x time interaction; they decreased linearly in response to carnitine before feeding but increased linearly in response to carnitine at 6 h after feeding. Serum insulin and plasma glucagon, IGF-I, cholesterol, triglyceride, and amino acids were not affected by carnitine. Plasma concentrations of glucose, glycerol, urea, and beta-hydroxybutyrate all were increased by some of the levels of carnitine supplementation, but results for these measurements did not follow easily described patterns and seemed to be related to differences in DMI. In Exp. 2, 95 crossbred steers (357 kg initial BW) were fed finishing diets (14.5% CP) for 129 d. Diets were based on steam-flaked corn and contained 6% alfalfa and 4% tallow. Feed intakes, gains, and feed efficiencies were not affected by supplementation with 2 g/d L-carnitine. However, steers receiving L-carnitine tended to have fatter carcasses, as indicated by tendencies (P < 0.2) for thicker backfat, higher marbling scores, and higher yield grades. In conclusion, carnitine supplementation did not alter lean deposition in growing steers but it did alter plasma NEFA concentrations of growing steers fed a corn-based diet and also seemed to increase fat deposition in finishing cattle.
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PMID:Effects of L-carnitine on nitrogen retention and blood metabolites of growing steers and performance of finishing steers. 1120 8

The aim of this study was to compare the metabolic effects of a single equimolar subcutaneous injection of hepatic directed vesicle-insulin (HDV-insulin) and regular insulin on glucose levels and intermediary metabolism during a 75-g oral glucose tolerance test (OGTT). Nine Type 1 diabetic patients underwent two experiments separated by 4 weeks. Each experimental protocol consisted of an identical evening meal followed by overnight euglycemic control achieved by a continuous low-dose insulin infusion. The next morning a subcutaneous injection (0.1 U/kg) of HDV-insulin or regular insulin was administered 30 min before a 75-g OGTT. The overnight basal insulin infusion was maintained unaltered throughout the 150-min OGTT. Plasma glucose, glucoregulatory hormones (insulin, glucagon, cortisol), and intermediary metabolites (lactate, alanine, glycerol, NEFA, beta-hydroxybutyrate) were measured to assess the metabolic effects of the two insulin preparations. Compared to regular insulin, an equivalent subcutaneous dose of HDV-insulin significantly lowered glucose levels during OGTT (mean reduction 2.2+/-0.4 mmol/l; P<.005). Plasma levels of insulin and glucagon were equivalent during both series of experiments. Blood lactate, glycerol and plasma NEFA levels were not different during OGTT indicating similar peripheral action of the insulins. beta-Hydroxybutyrate levels were significantly reduced (P<.05) following HDV-insulin supporting a preferential hepatic action of the preparation. We conclude that HDV-insulin can significantly lower plasma glucose excursions compared to an equivalent dose of regular insulin during an OGTT in Type 1 diabetic patients. The metabolic profile of equivalent peripheral insulin, glucagon and glycerol levels but reduced beta-hydroxybutyrate values support a hepatospecific effect of HDV-insulin.
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PMID:The effects of HDV-insulin on carbohydrate metabolism in Type 1 diabetic patients. 1152 95

The aim of this study was to determine whether 2,4-thiazolidinedione (2,4-TZD) influences the effects of peripheral insulin action in steers given recombinant bovine tumor necrosis factor (TNF) alpha (rbTNF). Steers were treated once daily for 9 d (d0 - d8) with either s.c. injection of rbTNF (2.5 microg/kg), rbTNF + i.v. injection of 2,4-TZD (2.0 mg/kg), or s.c. injection of saline (control). The plasma glucose, NEFA, and insulin concentrations in the rbTNF-treated group increased compared to those in the control and rbTNF + 2,4-TZD groups, whereas glucagon concentration decreased. A single i.v. injection of insulin (0.2 U/kg), glucose (112.5 mg/kg), or growth hormone (GH)-releasing hormone (GHRH) (0.25 microg/kg) was performed on d4, d6, and d8, respectively. In the insulin challenge, the net area under the glucose curve (AUC) was smaller in the rbTNF group than in the control and rbTNF + 2,4-TZD groups. In the glucose challenge, the net insulin AUC was smaller in rbTNF + 2,4-TZD group than in rbTNF group. In the GHRH challenge, there was no difference in GH responses to GHRH between the rbTNF and rbTNF + 2,4-TZD groups, respectively. We conclude that 2,4-TZD treatment partially reverses the impairment of peripheral insulin action caused by rbTNF injection in steers.
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PMID:Insulin resistance induced in dairy steers by tumor necrosis factor alpha is partially reversed by 2,4-thiazolidinedione. 1152 72

The mammalian insulin gene is exclusively expressed in the beta cells of the endocrine pancreas. Two decades of intensive physiological and biochemical studies have led to the identification of regulatory sequence motifs along the insulin promoter and to the isolation of transcription factors which interact to activate gene transcription. The majority of the islet-restricted (BETA2, PDX-1, RIP3b1-Act/C1) and ubiquitous (E2A, HEB) insulin-binding proteins have been characterized. Transcriptional regulation results not only from specific combinations of these activators through DNA-protein and protein-protein interactions, but also from their relative nuclear concentrations, generating a cooperativity and transcriptional synergism unique to the insulin gene. Their DNA binding activity and their transactivating potency can be modified in response to nutrients (glucose, NEFA) or hormonal stimuli (insulin, leptin, glucagon like peptide-1, growth hormone, prolactin) through kinase-dependent signalling pathways (PI3-K, p38MAPK, PKA, CaMK) modulating their affinities for DNA and/or for each other. From the overview of the research presented, it is clear that much more study is required to fully comprehend the mechanisms involved in the regulated-expression of the insulin gene in the beta cell to prevent its impairment in diabetes.
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PMID:Regulation of insulin gene transcription. 1191 36

This study was performed to investigate blood metabolite, tumor necrosis factor-alpha, and hormone responses to intravenous administration of lipopolysaccharides (2 microg of endotoxin of Escherichia coli 026:B6/kg body weight at times of feeding) in veal calves orally supplemented with arginine (0.25 g/kg of body weight twice daily for 4 d; group GrA) compared with calves not supplemented with arginine (group GrC). Arginine supplementation alone caused a significant rise of plasma arginine, urea, and insulin concentrations, whereas glucagon concentrations tended to increase, but there were no significant group differences. Concentrations of triglycerides, NEFA, glucose, protein, albumin, growth hormone, insulin-like growth factor-I, 3.5.3'-triiodothyronine, and thyroxine were not affected by arginine supplementation. Lipopolysaccharide administration alone caused a rise of tumor necrosis-factor-a, lactate, and cortisol concentrations and concentrations of tumor necrosis-factor-a after 1 h, and of triglycerides and urea after 6 h were higher, whereas of glucose after 3 h were lower in GrA than in GrC. Concentrations of NEFA, glucose, protein, albumin, insulin, growth hormone, insulin-like growth factor-I, 3.5.3'-triiodothyronine, and thyroxine were not affected by lipopolysaccharide administration. In conclusion, arginine supplementation had selective effects on plasma metabolites and hormones, but barely modified lipopolysaccharide effects. Effects of lipopolysaccharides in the postprandial state were different from what is usually seen in the fasted state.
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PMID:Metabolic and endocrine changes in response to endotoxin administration with or without oral arginine supplementation. 1221 85

The bi-guanide metformin is used to treat noninsulin dependent diabetes in obese patients. In addition to having antihyperglycemic effects, metformin is also anorectic and reduces BW. These studies were performed to determine if metformin possesses similar properties in chickens. Metformin-HCl was administered to 14-day-old broiler chickens at either 300 or 600 mg/kg per day in the drinking water for 10 d while monitoring BW and feed intake. No changes in water intake were observed, while feed intake and daily gains were only significantly reduced by the 600 mg/kg dose. After oral administration of a single dose of 300 mg/kg metformin-HCl, feed intake was significantly reduced by 4 h and remained suppressed for greater than 24 h relative to controls. Plasma hormones and metabolites (glucose, lactate, insulin, glucagon, uric acid, nonesterified fatty acid, and triglycerides) were monitored at 1, 2, 3, 6, and 24 h posttreatment. Significant and acute decreases in blood glucose, insulin, and triglycerides were observed at 3 h posttreatment as compared to controls. Opposing acute increases in glucagon and NEFA levels were also observed at 3 h followed by an increase in uric add 6 h posttreatment. These observations suggest that metformin induces metabolic changes in birds, similar to that observed in mammals and may act in a common manner. Metformin-HCl may be useful in glucose metabolism studies by inducing hypoglycemia, a condition rarely observed in birds.
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PMID:Hypoglycemia and reduced feed intake in broiler chickens treated with metformin. 1258 Feb 51

Continuous, intravenous infusions of glucagon improve carbohydrate status in lactating dairy cows without increasing concentrations of plasma NEFA. The objective was to test whether single subcutaneous injections and multiple subcutaneous injections of glucagon delivered at 8-h intervals over 14 d improve the carbohydrate status in lactating dairy cows without increasing concentrations of plasma BHBA and NEFA. In a single-injection experiment, four midlactation cows each were injected with 2.5 and 5 mg of glucagon 1 wk apart. In a multiple-injection experiment, nine cows, assigned randomly to three treatments, were injected subcutaneously with 0, 2.5, or 5 mg of glucagon every 8 h for 14 d, beginning at d 8 postpartum. Single subcutaneous injections of glucagon increased concentrations of plasma glucagon and single and multiple subcutaneous injections of glucagon increased concentrations of plasma glucose, with larger increases at the 5-mg dosage. Injections of 5 mg of glucagon increased concentrations of plasma insulin in both experiments, whereas the 2.5-mg dosage increased plasma insulin only in the multiple-injection experiment. The response of glucose and insulin to injections of 5 mg of glucagon persisted throughout the 14-d injection period. Concentrations of plasma NEFA decreased in the single-injection experiment, and concentrations of BHBA decreased after 5 mg of glucagon was injected in the multiple-injection experiment. These results document that both single and multiple injections of 5 mg of glucagon over 14 d consistently improve the carbohydrate status of dairy cows and decrease concentrations of plasma NEFA and BHBA.
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PMID:Metabolic responses of lactating dairy cows to single and multiple subcutaneous injections of glucagon. 1283 43

Plasma glucose concentrations in neonates are influenced by colostrum feeding and by glucocorticoids. We have tested whether a high-glucocorticoid status after birth, as well as colostrum feeding, influences glucose metabolism in association with changes of hepatic expression and activities of gluconeogenic enzymes phosphoenolpyruvate carboxykinase (PEPCK; EC 4.1.1.32) and pyruvate carboxylase (PC; EC 6.4.1.1) in neonatal calves. Calves (n = 14 per group) were fed either colostrum or a milk-based formula with nutrient and energy contents similar to colostrum. Half the calves in each feeding group were treated with dexamethasone (DEXA; 30 microg/[kg BW x d]). Pre- and postprandial blood samples were taken on d 1, 2, 4, and 5 and liver samples were collected on d 5 of life. Dexamethasone treatment increased (P < or = 0.05) plasma concentrations of glucose, insulin, and glucagon more in colostrum-fed than in formula-fed calves but increased (P < or = 0.05) urea concentrations and decreased (P < or = 0.05) concentrations of NEFA, ACTH, and cortisol independent of colostrum vs. formula feeding. Colostrum feeding increased (P < 0.05) plasma glucose, but decreased (P < 0.05) plasma urea concentrations. Glucagon-to-insulin ratios in DEXA-treated and colostrum-fed calves were decreased (P < 0.05). Dexamethasone treatment decreased hepatic mRNA levels and activities of PC (P < 0.001 and P < 0.10) and activities of PEPCK (P < 0.001) but increased (P < 0.001) the glycogen content. Colostrum feeding increased (P < 0.05) mitochondrial PEPCK mRNA levels and PEPCK activities in calves not treated with DEXA but decreased (P < 0.1) amounts of PC mRNA. In conclusion, increased plasma glucose concentrations after DEXA treatment were not associated with a stimulation of hepatic gluconeogenic enzyme activities; however, colostrum feeding probably raised plasma glucose concentrations because of increased hepatic gluconeogenic activities.
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PMID:Dexamethasone and colostrum feeding affect hepatic gluconeogenic enzymes differently in neonatal calves. 1467 66

Glucagon-like peptide 1 (GLP-1) is a peptide hormone that is released in response to nutrient ingestion. Postprandial GLP-1 release has been reported to be attenuated in obese subjects, but reports on the effect of weight loss on GLP-1 are conflicting. The aim of the present study was to clarify the effect of a weight-loss period and a consecutive weight-maintenance period on nutrient-stimulated GLP-1 release in obese subjects. Nutrient-stimulated (standard breakfast; 1.9 MJ) GLP-1 release was investigated in thirty-two obese subjects on three occasions: before weight loss (T1) (BMI 30.0 (sd 2.5) kg/m(2)); after a 6-week very-low-energy diet (VLED) (T2) (BMI 27.6 (sd 2.3) kg/m(2)); after a 3-month weight-maintenance period (T3) (BMI 27.9 (sd 2.3) kg/m(2)). At each occasion, following a fasting blood sample the test meal was fed and blood was drawn every 30 min for 2 h relative to ingestion in order to determine plasma GLP-1, insulin, glucose and NEFA concentrations. Subjects lost 7 (sd 3.4) kg during the VLED (P<0.0001) and regained 1 (sd 3.2) kg during the weight-maintenance period (NS). The area under the curve for nutrient-stimulated plasma GLP-1 (pmol/l x h) was significantly decreased (P=0.01) at T2 (6.8 (sd 1)) compared with T1 (12.8 (sd 2.9)) and T3 (11.1 (sd 1.5)). Since we found a rebound of concentrations after a weight-maintenance period, decrease after weight loss seems to be transient and possibly due to a negative energy balance.
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PMID:Nutrient-stimulated glucagon-like peptide 1 release after body-weight loss and weight maintenance in human subjects. 1644 29


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