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

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.
 ...
PMID:Effects of L-carnitine on nitrogen retention and blood metabolites of growing steers and performance of finishing steers. 1120 8

An experiment was conducted to test the hypothesis that incubator temperature may affect circulating insulin-like growth factors (IGF-I and IGF-II). In prior studies, growth of turkey embryos was altered by increasing incubator temperatures. Interestingly, the embryonic growth of a growth-selected line (F) was reduced, whereas embryos from an egg-production-selected line (E) did not alter embryonic growth but altered organogenesis. Growth of the F and E lines was altered experimentally in the current study by increasing incubator temperature from 36.8 to 37.2 C during the last 3 d of incubation. Embryonic blood samples were taken and analyzed for glucose, glucagon, IGF-I, and IGF-II concentrations. Increased incubator temperature elevated embryonic plasma glucose concentrations of all treatments compared to controls, which was accompanied by increased plasma glucagon concentration only in the E line embryos. Line and treatment interacted to affect IGF-I and IGF-II concentrations of embryo and hatchlings. Line E embryos increased IGF-I in response to the higher temperature, but controls did not; F embryos altered IGF-II in response to treatment, but controls did not. Alterations in IGF-I in E corresponded to growth responses, whereas IGF-II in F corresponded to metabolic responses. We concluded that changes in turkey embryo growth rates to incubator temperature involved changes in IGF-I. Additionally, IGF-II and glucagon are involved in intermediary metabolism during higher temperature exposure.
 ...
PMID:Incubation temperature affects plasma insulin-like growth factors in embryos from selected lines of turkeys. 1146 60

Pycnodysostosis is a rare hereditary bone abnormality with an autosomal recessive mode of inheritance. We report the clinical, radiologic, and endocrine status of 8 children with this rare disease. All patients had the characteristic phenotype of the disorder including short stature (8 of 8), increased bone density (7 of 8), separated cranial sutures (8 of 8), large fontanel with delayed closure (8 of 8), obtuse mandibular angle (8 of 8), delayed teeth eruption (8 of 8), enamel hypoplasia (7 of 8), dysplastic acromial ends of the clavicles (6 of 8), frontal bossing (6 of 8), ocular proptosis (8 of 8), and dysplastic nails (8 of 8). Developmental evaluation according to the revised Denever developmental screening showed normal motor, fine motor-adaptive language, and personal social abilities in all the children. All had normal hepatic and renal functions. Serum calcium and phosphorus concentrations were normal. Two children had low serum alkaline phosphatase concentration. Short stature is a characteristic feature of pycnodysostosis. Seven of the 8 children were born short (length standard deviation score [SDS] = -3 to -1.5). Deceleration of linear growth was significant during the first 3 years of life. All the children had height SDS below -3 at the end of their third year of life. Although short stature is a feature of this genetic disorder, defective growth hormone (GH) secretion in response to provocation with clonidine and glucagon was found in 4 of the 8 patients. These 4 patients had pituitary hypoplasia on the magnetic resonance imaging (MRI) of their brain. In addition, 3 of these 4 patients had demyelination of the cerebrum. Patients with pycnodysostosis (n = 8) had low circulating concentrations of insulin-like growth factor-1 (IGF-1) compared with normal age-matched short children with constitutional short stature (CSS). IGF-I increased significantly after injecting GH for 3 days in these patients. Physiologic replacement with GH (18 U/m(2)/week) divided in daily evening doses subcutaneously increased IGF-1 concentration and improved linear growth velocity and height standard deviation scores (HtSDS) in the 4 children with GH deficiency. These data ruled out GH resistance and proved the usefulness of GH therapy in the management of short stature in these patients. In summary, some patients with pycnodysostosis have partial GH deficiency and low IGF-1 concentration. GH therapy markedly increases IGF-I secretion and improves their linear growth. MRI study of the brain including the hypothalamic-pituitary area is recommended in these children because of the high incidence of pituitary hypoplasia and cerebral demyelination.
 ...
PMID:Pycnodysostosis: clinical, radiologic, and endocrine evaluation and linear growth after growth hormone therapy. 1147 77

Body weight gain and severe hypoglycemia are the major adverse effects of insulin therapy in type 2 diabetic patients. Metformin has been shown to prevent insulin therapy-induced body weight gain when used in combination with insulin. However, the effects of metformin on hormonal and symptomatic responses to hypoglycemia mediating hypoglycemia awareness have not been assessed to date. Fifteen young healthy men were treated with 850 mg metformin and placebo twice daily for a 16-d period in a double blind, cross-over design. On the last 2 d of the treatment period, the subjects underwent three hypoglycemic clamp experiments, with the first and the last performed with identical patterns of plasma glucose decrease. Differences between the effects of metformin and placebo (effect of metformin) as well as between first and last hypoglycemic clamps (effect of antecedent hypoglycemia) were assessed. Antecedent hypoglycemia significantly reduced epinephrine, ACTH, cortisol, glucagon, GH, and symptomatic responses to hypoglycemia (P < 0.05 for all variables). There was no detectable effect of metformin on epinephrine, norepinephrine, ACTH, cortisol, glucagon, or autonomic symptomatic response to hypoglycemia (P > 0.05 for all comparisons), except that metformin slightly increased the response of GH to hypoglycemia (P = 0.039). The latter finding may be due to an IGF-I-reducing effect of metformin, as after 14 d of metformin treatment baseline levels of IGF-I were significantly lower than in the placebo condition (236.9 +/- 13.9 vs. 263.2 +/- 14.4 microg/liter; P = 0.015). The data indicate that metformin does not adversely affect hormonal and symptomatic responses to hypoglycemia. This finding appears to be relevant with regard to the safety of the combination of metformin with insulin therapy.
 ...
PMID:Metformin does not adversely affect hormonal and symptomatic responses to recurrent hypoglycemia. 1154 48

Effects of different feeding frequencies on growth performance, preprandial metabolic parameters, and endocrine traits were studied in calves up to 28 d after birth and respective postprandial changes were investigated on d 3 and 7. Calves were fed with a computer-programmed automate that allowed frequent daily intakes (GrA; n = 7) or were fed twice daily by bucket (GrB; n = 7) the same daily amounts (pair-feeding) of colostrum and milk. Weight gains did not differ significantly between groups. Plasma protein was higher (P < 0.01) from d 14 to 28 in GrB than in GrA. Plasma glucose increased postprandially in GrB on d 3 and 7 but in GrA only on d 3, and there was a significant treatment x time interaction on d 3 and 7 after feed intake. For plasma triglycerides there was a significant postprandial treatment x time interaction on d 3, and triglycerides were higher (P < 0.05) in GrA than in GrB before feed intake on d 7. For insulin concentrations on d 7 the treatment x time interaction was significant and concentrations 8 h after feed intake were higher (P < 0.05) in GrA than GrB. For concentrations of growth hormone on d 7 during an 8-h period the treatment x time interaction was significant and concentrations from 320 to 340 min after feed intake were higher (P < 0.05) in GrB than in GrA. Plasma IGF-I concentrations were higher (P < 0.05) in GrA than in GrB on d 7. The hematocrit and concentrations of immunoglobulin G, albumin, urea, creatinine, L-lactate, nonesterified fatty acids, cholesterol, glucagon, and thyroxine did not differ between groups. In conclusion, feed intake at high frequency by an automate transiently changed some metabolic and endocrine traits (glucose, triglyceride, insulin, and IGF-I) but had no significant effects on growth performance during the first 4 wk of life.
 ...
PMID:Growth performance and metabolic and endocrine traits in calves pair-fed by bucket or by automate starting in the neonatal period. 1207 36

Abdominally obese individuals have reduced 24-h plasma GH concentrations. Their normal plasma IGF-I levels may reflect GH hypersensitivity. Alternatively, obesity-associated hyposomatotropism may cause less biological effect in target tissues. We therefore determined whole-body responsiveness to the anabolic effects of GH in abdominally obese (OB) and normal weight (NW) premenopausal women. A 1-h iv infusion of GH or placebo was randomly administered to six NW (body mass index, 21.1 +/- 1.9 kg/m(2)) and six OB (body mass index, 35.5 +/- 1.5 kg/m(2)) women in a cross-over design. Endogenous insulin, glucagon and GH secretion was suppressed by infusion of somatostatin. Whole-body protein turnover was measured using a 10-h infusion of [(13)C]-leucine. GH administration induced a similar plasma GH peak in NW and OB women (49.8 +/- 10.4 vs. 45.1 +/- 5.6 mU/liter). GH, compared with placebo infusion, increased nonoxidative leucine disposal, P < 0.0001) and endogenous leucine appearance (R(a), P = 0.0004) but decreased leucine oxidation (P = 0.0051). All changes were similar in both groups. Accordingly, whole-body GH responsiveness, defined as the maximum response of nonoxidative leucine disposal, leucine R(a), and oxidation per unit of GH, was not different in OB and NW women (0.25 +/- 0.18 vs. 0.19 +/- 0.17 micro mol/kg.h, 0.21 +/- 0.23 vs. 0.13 +/- 0.17 micro mol/kg.h, and -0.10 +/- 0.08 vs. -0.08 +/- 0.05 micro mol/kg.h, respectively). These results indicated that whole-body tissue responsiveness to the net anabolic effect of GH is similar in OB and NW women. Hence, we inferred that hyposomatotropism may promote amino acid oxidation and blunt protein turnover in abdominal obesity. However, hyposomatotropism cannot account for all anomalous features of protein metabolism in abdominally obese humans.
 ...
PMID:Growth hormone blunts protein oxidation and promotes protein turnover to a similar extent in abdominally obese and normal-weight women. 1246 70

Many studies have recently shown that simple computer-solved indices, based on fasting glucose and insulin levels, closely mirror the euglycemic clamp technique in studying insulin resistance or pancreatic insulin secretion. Few data are at present available on the evaluation of these novel indices in acromegalic patients, known to be GH-dependent insulin-resistant subjects, in particular during medical treatment with somatostatin analogues. Indeed, these drugs are able to inhibit not only GH and IGF-I levels, but also insulin and glucagon pancreatic secretion, with contrasting effects on glucose metabolism. In this study, insulin resistance was evaluated by the homeostasis model assessment (HOMA-IR) and insulin sensitivity by quantitative insulin check index (QUICKI) in 27 normoglycemic acromegalic patients, before and after 6-month therapy with somatostatin analogues (lanreotide-SR 30-60 mg every 7-28 days in 15 and octreotide-LAR 20-30 mg every 28 days in 12). Thirty-five age- and sex-matched healthy subjects and 17 surgically treated acromegalic patients (5 cured and 12 not cured) were studied as control groups. Before medical treatment, HOMA-IR was higher in acromegalic patients than in healthy controls (4 +/- 3 vs 1.7 +/- 0.7, p < 0.05), while QUICKI was lower (0.33 +/- 0.04 vs 0.36 +/- 0.03, p < 0.05). During medical therapy, HOMA-IR decreased to 2.4 +/- 1.6 (p < 0.05) and became similar to that recorded in both healthy subjects and surgically treated patients. However, fasting glucose was increased and fasting insulin was decreased. QUICKI did not significantly change from basal values. No differences were observed between patients who normalized or not hormonal levels. The effects of the 2 drugs, though higher glucose levels were seen in patients treated with octreotide-LAR. In conclusion, this study demonstrates that medical treatment is able to improve insulin resistance, even if only successful surgery is able to completely normalize both HOMA-IR and QUICKI.
 ...
PMID:Evaluation of insulin resistance in acromegalic patients before and after treatment with somatostatin analogues. 1295 67

The first hours of extracorporeal life support (ECLS) are commonly marked by new hemodynamic instability without a known etiology. We measured hormone and catecholamine concentrations in six ECLS primed circuits immediately before joining the patient's circulation to assess a potential role of these agents in this condition. The following hormones were significantly below the lower end of the normal range for the first week of life (data are presented as mean +/- SEM): cortisol 1.95 +/- 0.15 microg/dl (p < 0.001), aldosterone 3.73 +/- 0.74 ng/dl (p < 0.05), free thyroxine 1.2 +/- 0.1 ng/dl (p < 0.05), free triiodothyronine 0.53 +/- 0.03 pg/ml (p < 0.001), thyroid stimulating hormone 0.31 +/- 0.05 microU/ml (p < 0.001), growth hormone (GH) 0.09 +/- 0.01 ng/ml (p < 0.001), estradiol 38.3 +/- 3.72 pg/ml (p < 0.001), IGF-BP1 0.95 +/- 0.1 ng/ml (p < 0.001), glucagon 26 +/- 1.2 pg/ml (p < 0.001), epinephrine 17.3 +/- 3.7 pg/ml (p < 0.001), and norepinephrine 127 +/- 27 pg/ml (p < 0.05). No dopamine was detected. Normal hormone concentrations included IGF-I, IGF-BP3, insulin, parathyroid hormone, leptin, and testosterone. Critically low concentrations of cortisol, thyroid hormones, GH, IGF-BP1, glucagon and catecholamines were measured in the ECLS circuit even though it was primed with fresh frozen plasma. These concentrations may cause significant and precipitous dilutional reductions in the patient's circulating levels immediately after connection to the ECLS circuit and hence contribute to hemodynamic instability.
 ...
PMID:Critically low hormone and catecholamine concentrations in the primed extracorporeal life support circuit. 1476 93

Plasma ghrelin is elevated in Prader-Willi syndrome (PWS). This might contribute to obesity or GH deficiency in such patients. Visceral adiposity and insulin resistance are reduced in PWS, which might lead to hyperghrelinemia. We measured fasting plasma ghrelin in control female (n = 39), PWS female (n = 12), and PWS male (n = 6) adults. In controls and PWS, ghrelin was negatively correlated with visceral adiposity, fasting insulin, and homeostasis model insulin resistance index. There was no significant correlation with serum IGF-I in PWS. In stepwise linear regression, visceral adiposity (P < 0.02) had a stronger inverse correlation with ghrelin than sc fat depots in controls and PWS, possibly through hyperinsulinemia, as the correlations with insulin resistance were even stronger (P < 0.01). PWS females had significantly (P < 0.001) elevated ghrelin (mean +/- SD, 661 +/- 360 pg/ml), compared with both nonobese (363 +/- 163) and obese (191 +/- 66) controls. Ghrelin was increased 3.4- to 3.6-fold in PWS females adjusting for total adiposity, 3.2- to 3.4-fold adjusting for visceral adiposity, and 3.0-fold adjusting for insulin resistance. Fasting plasma glucagon-like peptide-1 was normal in PWS females. The hyperghrelinemia in PWS adults is therefore not solely explained by their reduced visceral adiposity and relative hypoinsulinemia. Its cause and consequences await further elucidation.
 ...
PMID:Elevated fasting plasma ghrelin in prader-willi syndrome adults is not solely explained by their reduced visceral adiposity and insulin resistance. 1507 Sep 36

Recent data suggest that anterior pituitary dysfunction after traumatic brain injury (TBI) is common. We sought to confirm the results of earlier studies in a larger cohort of patients with dynamic testing of pituitary function. We studied 102 consecutive TBI survivors (85 males; median age 28, range 15-65 yr) who had survived severe or moderate TBI (initial Glasgow Coma Scale score 3-13) at a median of 17 months (range 6-36) post event. GH and ACTH reserves were initially assessed using the glucagon stimulation test (GST). Normative data on GH and cortisol responses to the GST were obtained from 31 matched healthy controls. Patients with subnormal GH or cortisol responses were further evaluated, using the insulin tolerance test (ITT) or arginine + GHRH test for GH assessment and the ITT or 250-microg short synacthen test for the assessment of ACTH reserve. Patients were considered to be GH or ACTH deficient if they failed both the GST and the second provocative test. Baseline thyroid function, prolactin, IGF-I, gonadotropins, testosterone, or estradiol was performed in all patients and compared with local reference ranges.In controls, normal response to the GST was a stimulated GH peak of greater than 5 microg/liter and cortisol peak greater than 450 nmol/liter (16 microg/dl). Eighteen TBI patients (17.6%) had GH response to the GST less than 5 microg/liter, 11 of whom also failed the ITT or the arginine + GHRH tests. GH-deficient patients had significantly higher body mass index (P = 0.003), and lower IGF-I concentrations (P < 0.001), than GH-sufficient patients. Twenty-three patients (22.5%) had cortisol responses to GST less than 450 nmol/liter, 13 of whom also failed the ITT or short synacthen test. GH or ACTH deficiencies were not related to age, Glasgow Coma Scale score, or the presence of other pituitary hormone abnormalities (P > 0.05). Twelve patients (11.8%) had gonadotropin and one (1%) had thyrotrophin deficiencies. Twelve patients (11.8%) had hyperprolactinemia. Twenty-nine patients (28.4%) had at least one anterior pituitary hormone deficiency. This is the largest study, to date, of hypopituitarism after TBI and confirms a high prevalence of undiagnosed anterior pituitary hormone abnormalities in survivors of TBI. Hypopituitarism is a treatable cause of morbidity after TBI. In addition to conventional pituitary hormone replacement, the potential of GH treatment to enhance recovery needs to be examined in a prospective study.
 ...
PMID:Anterior pituitary dysfunction in survivors of traumatic brain injury. 1547 87


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>