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)

Twenty to twenty-two days postcoitum mouse fetal pancreas organ bits were cultured on the dermal surface of irradiated pigskin as a substrate. The medium used for long term culture consisted of Eagle's Minimum Essential Medium with the addition of 10% bovine serum, 0.02 U/ml insulin, 0.025 microgram/ml glucagon, 3.63 microgram/ml hydrocortisone, 100 microgram/ml soybean trypsin inhibitor or 10(-8) M atropine. When the medium lacked trypsin inhibitor or atropine but contained the three hormones, the pigskin support began to be destroyed after 2 to 4 wk in culture. Thereafter, the cultured cells could not grow and survive on the digested pigskin. When 10(-6) M atropine was added to the medium, amylase secretion from cultured cells and destruction of pigskin were inhibited completely but pancreas cells could not grow or survive. In contrast, 100 microgram/ml soybean trypsin inhibitor or 10(-8) M atropine permitted cell growth, permitted amylase secretion from the cultured acinar cells, and prevented the destruction of pigskin. Under these conditions pancreas cells migrated or grew or both from the organ bits onto the surface of the pigskin dermis and organoid aggregations formed. Hydrocortisone was needed to permit growth for more than 2 wk. Glucagon and insulin had additive effects. Light and electron microscopic observations indicated the culture of at least five kinds of cells, i.e., duct, acinar, centroacinar, endocrine, and mesenchymal. The majority of cultured cells were duct cells and acinar cells. There were few mesenchymal cells. Mouse pancreas cells were cultured for at least 12 wk by this method.
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PMID:Duct, exocrine, and endocrine components of cultured fetal mouse pancreas. 618 9

Teleost fish osmoregulation is largely the result of integrated transport activities of the gill, gut and renal system. The basic 'epithelial fabric' in each of these tissues is adapted to provide the appropriate transport mechanisms depending upon whether the fish is in fresh water or sea water. Net NaCl transport by the branchial epithelium reverses direction when euryhaline species migrate between the two media, providing a useful focus in experiments designed to elucidate mechanisms of differentiation and integration of transport function. Isolated opercular membranes and skins from certain seawater-adapted species are good models to study branchial salt extrusion mechanisms. These heterogeneous tissues generate short-circuit currents equal to net chloride secretion. The vibrating probe technique has allowed localization of all current and almost all conductance to the apical crypt of chloride cells. Area-specific surface current and conductance of chloride cells are 18 mA cm-2 and 580 mS cm-2 (1.7 omega cm2), ranking them as one of the most actively transporting and conductive cells known. There is no net sodium transport under short-circuit conditions but the chloride secretion process is sodium-dependent and ouabain and 'loop'-diuretic sensitive. Sodium fluxes through chloride cells are large (PNa = 5.2 X 10(-4) cms-1) nd appear passive and rate-limited by a single barrier. A link may exist between the active transport and leak pathways since sodium fluxes always account for 50% of chloride cell conductance. The sodium pathway is probably the chloride cell-accessory cell tight junction, although this is still unresolved. Chloride secretion can be rapidly modulated by several hormones, including catecholamines, somatostatin, glucagon, vasoactive intestinal polypeptide and urotensins I and II. Regulation by these hormones may be by rapid alterations of cellular cAMP levels. Differentiation of chloride cells and chloride secretion may be controlled by cortisol and prolactin. Cortisol stimulates chloride cell proliferation and differentiation and appears to interact with NaCl to initiate salt secretion. Prolactin appears to cause chloride cell dedifferentiation by reducing both the active-transport and leak pathways proportionately.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chloride cells and the hormonal control of teleost fish osmoregulation. 636 Dec 7

To assess the role of hormonal factors in the pathogenesis of the dawn phenomenon, nocturnal (9:00 PM to 9 AM) concentrations of blood glucose, free insulin, and counterregulatory hormones were determined in eight insulin-dependent diabetic patients under feedback-controlled and continuous insulin infusions after previous blood glucose normalization. Under feedback control, mean insulin requirements, necessary for maintenance of euglycemia rose significantly in the early morning (11:00 PM to 3 AM: 8.4 +/- 1.4; 5 AM to 9 AM: 12.6 +/- 1.5 mU/kg/h; P less than 0.01). Mean free-insulin concentrations did not increase simultaneously. Correspondingly, mean insulin-clearance rates under continuous insulin infusion were higher in the morning (11:00 AM to 3 AM: 359 +/- 58; 5 AM to 9 AM: 459 +/- 72 mL/min/m2; P less than 0.05). Increases of insulin clearance rates were most marked (greater than 15%) in patients whose blood glucose rose during continuous insulin administration. Glucagon and norepinephrine concentrations were stable throughout both parts of the study. Cortisol and growth hormone exhibited the known nocturnal rhythms. Epinephrine levels were at the lower limit of detection at night and rose to normal basal concentrations at 9:00 AM. We conclude that increases of insulin clearance rates may be an important factor for the development of the dawn phenomenon while the role of most counter-regulatory hormones is still uncertain.
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PMID:Studies on the pathogenesis of the dawn phenomenon in insulin-dependent diabetic patients. 637 44

At 10 d of age miniature pigs were randomized to receive either of two total parenteral nutrition fuel mixes; oral feedings were discontinued. Both groups received 170 kcal X kg-1 X d-1 and 11 g X kg-1 X d-1 of synthetic amino acids. Nonprotein energy was supplied as glucose in group A, whereas in group B, it was divided equally between glucose and fat. Blood samples were drawn on the second and eighth postoperative days for hematologic, biochemical, and hormonal measurements. On the ninth postoperative day, total body water was determined and the animals were killed for carcass analysis. The animals tolerated the intravenous nutrition without ill effects as indicated by both clinical and biochemical parameters. Group A had significantly elevated levels of insulin and a higher insulin/glucagon ratio than group B. Cortisol levels did not differ significantly between groups. Total body fat, nitrogen, ash, K, Na, Cl, Ca, and P were similar between groups. TBW was significantly greater in group A compared with group B. Extracellular space calculated from body Cl and plasma Cl was similar between groups.
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PMID:Effect of different total parenteral nutrition fuel mixes on the body composition of infant miniature pigs. 642 45

Patients with major injury or illness develop protein wasting, hypermetabolism, and hyperglycemia with increased glucose flux. To assess the role of elevated counterregulatory hormones in this response, we simultaneously infused cortisol (6 mg/m2 per h), glucagon (4 ng/kg per min), epinephrine (0.6 microgram/m2 per min), and norepinephrine (0.8 micrograms/m2 per min) for 72 h into five obese subjects receiving only intravenous glucose (150 g/d). Four obese subjects received cortisol alone under identical conditions. Combined infusion maintained plasma hormone elevations typical of severe stress for 3 d. This caused a sustained increase in plasma glucose (60-80%), glucose production (100%), and total glucose flux (40%), despite persistent hyperinsulinemia. In contrast, resting metabolic rate changed little (9% rise, P = NS). Urinary nitrogen excretion promptly doubled and remained increased by approximately 4 g/d, reflecting increased excretion of urea and ammonia. Virtually all plasma amino acids declined. The increment in nitrogen excretion was similar in three additional combined infusion studies performed in 3-d fasted subjects not receiving glucose. Cortisol alone produced a smaller glycemic response (20-25%), an initially smaller insulin response, and a delayed rise in nitrogen excretion. By day 3, however, daily nitrogen excretion was equal to the combined group as was the elevation in plasma insulin. Most plasma amino acids rose rather than fell. In both infusion protocols nitrogen wasting was accompanied by only modest increments in 3-methylhistidine excretion (approximately 20-30%) and no significant change in leucine flux. We conclude: (a) Prolonged elevations of multiple stress hormones cause persistent hyperglycemia, increased glucose turnover, and increased nitrogen loss; (b) The sustained nitrogen loss is no greater than that produced by cortisol alone; (c) Glucagon, epinephrine, and norepinephrine transiently augment cortisol-induced nitrogen loss and persistently accentuate hyperglycemia; (d) Counterregulatory hormones contribute to, but are probably not the sole mediators of the massive nitrogen loss, muscle proteolysis, and hypermetabolism seen in some clinical settings of severe stress.
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PMID:Role of counterregulatory hormones in the catabolic response to stress. 651 25

In previous investigations, we found high rates of cholesterol synthesis in human fetal liver tissue, second only to rates in fetal adrenal tissue. Previous estimates of the amount of cholesterol in the fetus derived from the maternal compartment are in the range of 20%. Thus, the liver may be the principal source of circulating lipoproteins in the human fetus, as is true in the human adult. Low density lipoprotein is the major source of cholesterol used for fetal adrenal steroidogenesis; therefore, it follows that factors regulating cholesterol synthesis in the human fetal liver may indirectly control the rate of steroid secretion by the adrenal cortex. The purpose of the present investigation was to determine if hormones, particularly those produced by the fetal-placental unit, might serve to stimulate cholesterol synthesis in the human fetal liver. The rate of cholesterol biosynthesis was determined by measuring the rate of incorporation of [3H]water into [3H]cholesterol in hepatocytes maintained in culture or by determination of the specific activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase in microsomal preparations from human fetal liver. The addition of dexamethasone (10(-10) - 10(-6)M) stimulated cholesterol synthesis up to 2- to 4-fold between days 2 and 6 of exposure. When human fetal liver cells were maintained in the presence of dexamethasone (10(-7)M), the activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase in microsomal fractions was stimulated 4-fold compared to that in control cells. Cortisol also stimulated cholesterol biosynthesis in a concentration-dependent manner. The addition of 17 beta-estradiol (E2) to the culture medium resulted in stimulation of cholesterol biosynthesis in a concentration-dependent manner from 10(-10) - 10(-7)M. The rate of cholesterol synthesis when E2 was present (10(-7)M) was 4-fold greater than that in untreated cells. Stimulation of cholesterol synthesis by E2 was maintained between 2-7 days of incubation with E2. Estrone, estriol, and E2 (10(-6)M) caused similar increases (3- to 4-fold) in the rates of cholesterol synthesis in human fetal hepatocytes. Finally, progesterone in concentrations greater than 10(-6) M significantly stimulated cholesterol synthesis in human fetal liver cells. In contrast, other hormones and factors, including insulin, glucagon, PRL, GH, dehydroepiandrosterone and its sulfate, epidermal growth factor, fibroblast growth factor, T3, (Bu)2cAMP, and cholera toxin, had no effect on the rate of cholesterol synthesis in human fetal liver cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cholesterol synthesis by human fetal hepatocytes: effects of hormones. 672 9

Cortisol and growth hormone (GH) responses to a 100 g oral glucose load were measured in 85 Indian patients with non-insulin-dependent diabetes in the young (NIDDY) and 50 reference subjects; in 16 patients and 12 reference subjects the glucagon responses were also assessed. Fasting serum cortisol and plasma glucagon levels were significantly higher in the NIDDY group (P less than 0.001); in contrast, GH levels in the NIDDY patients were significantly lower (P less than 0.01). Plasma glucagon was only significantly suppressed 150 minutes after oral glucose loading in the NIDDY group, in contrast to the reference group, which showed maximum suppression at 90 minutes; at all time intervals plasma glucagon levels were significantly higher in the NIDDY patients. Obesity did not affect fasting plasma glucagon levels. In response to the oral glucose load serum cortisol levels in the NIDDY patients were suppressed in parallel with those in the reference group but remained significantly higher throughout the period of observation at all time intervals. Obese NIDDY patients had higher fasting cortisol levels, but their response to orally administered glucose was no different from that of the NIDDY group as a whole. GH suppression by oral glucose in NIDDY patients was less than that in the reference group, and the rebound rise occurred earlier. Obese NIDDY patients had higher fasting GH levels than their non-obese counterparts, but responses to the glucose load were not different.
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PMID:Cortisol, glucagon and growth hormone responses to oral glucose in non-insulin-dependent diabetes in the young. 675 Aug 13

Experiments were designed to estimate the effect of in vivo hormonal treatment of rats on serine metabolism in isolated hepatocytes by incubating hepatocytes in the presence or absence of 3-mercaptopicolinic acid (a potent inhibitor of phosphoenolpyruvate carboxykinase), the relative flow of [14C]serine carbon to [14C]glucose via the serine dehydratase (SDH)-initiated vs. serine amino-transferase (SAT-initiated pathways could be estimated. Streptozotocin-induced diabetes caused a tripling of the absolute rate of [14C]serine conversion to [14C]glucose, along with a shift in the relative importance of the SAT-mediated pathway. Hydrocortisone treatment had no significant effect on either the rate or route of serine metabolism. The SAT-mediated pathway was the major route of serine conversion to glucose after 4 days of chronic glucagon injections, although the absolute rate of conversion was enhanced by only 50%. This was the only treatment examined in which SDH was not the major route for serine gluconeogenesis. The enzyme activity responses of SDH and SAT to hormonal manipulation previously reported do not necessarily reflect the observed changes in pathway flux reported in the present study.
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PMID:Effects of in vivo hormonal treatment on serine metabolism in isolated rat hepatocytes. 680 68

In two groups of pts with diabetic derangements the effect of infusion therapy was investigated with regard to metabolic and endocrine functions. The rate of infusion was adapted to the height of the central venous pressure and the administration of electrolytes to their serum concentration. Insulin was withheld until no further decrease of blood glucose was noted. Group A consisted of 8 pts with severe diabetic ketoacidosis (blood glucose higher than 25 mmol/l, pH below 7.0 and/or bicarbonate below 10 mmol/l). The duration of insulinfree rehydration was 8.8 +/- 1.3 (x +/- SE) hrs and the fluid retention 4060 +/- 3 633 ml. The osmolality in serum decreased from 356 +/- 12 to 340 +/- 8 mosm/kg H2O and the blood glucose from 37.9 +/- 2.9 to 28.6 +/- 3.4 mmol/l. No correlation existed between the decrease of blood glucose and the expansion of the intravascular volume. Therefore, the decrease of blood glucose was not caused by a simple dilution effect. High renal glucose excreation was observed (408 +/- 83 mmol) but could not explain the decrease of blood glucose. The glucose clearance fell from 25.9 +/- 6.9 to 21.5 +/- 3.8 ml/min/1.73 m2 body surface from the first to the last 2-hr periods. It must be concluded that the initial rehydration deminished gluconeogeneses and/or increased tissue glucose utilization without exogenous insulin administration. This conclusion is supported by the decrease in the plasma concentration of the contrainsular hormons. Glucagon decreased 579 +/- 209 to 319 +/- 88 pg/ml (n.s.). Cortisol from 49.9 +/- 4.6 to 35.8 +/- 6.7 micrograms/100 ml (p < 0.05) and Adrenalin from 2.43 +/- 1.03 to 0.4 +/- 0.22 ng/ml (p < 0.05). Blood gas analysis revealed only minimal and ketobodies in serum no changes. Therefore, it can be concluded that rehydration and decrease of plasma concentration of contrainsular hormones do not influence the enhenced lipolyses in diabetic ketoacidosis. Group B consisted of 8 pts with nonacidotic diabetic derangements (blood glucose higher than 25 mmol/l, pH above 7.3 and/or bicarbonate above 18 mmol/l) and an acute weightloss of more than 3 kg. The insulinfree rehydration lasted 13 +/- 1.6 hrs and the fluid retention was 4620 +/- 380 ml. The serum osmolality decreased from 317 +/- 5.3 to 288 +/- 1.9 mmol/l. The decrease of blood glucose could not be explained by delution effect. The renal glucose excreation was 370 +/- 120 mmol/l in total and the glucose clearance decreased from 15.3 +/- 8.4 to 8.0 +/- 2.8 ml/min/1.73 m2 body surface (p < 0.01). Decrease of gluconeogenese and/or increase of glucose assimilation of the tissues can also be expected for the pts with nonacidotic diabetic derangements during plain rehydration.
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PMID:[Influence of insulinfree rehydration on diabetic derangements (author's transl)]. 700 20

1. Glucose metabolism and changes in the concentrations of several hormones in jugular plasma were measured in growing lambs fed on fresh pasture ad lib. One group of lambs acted as control while the second received a continuous abomasal infusion supplying 44 g sodium caseinate+0.5 g L-methionine/d. 2. Hormone concentrations were determined by radioimmunoassay procedures and glucose irreversible loss measured from continuous infusion of D-[U-14C]glucose. 3. Protein infusion increased plasma concentrations of insulin, glucagon and thyroxine (T4), depressed those of growth hormone, prolactin and somatostatin and had no effect on triiodothyronine (T3) concentrations. Cortisol concentrations also tended to be slightly higher in the plasma of protein-infused lambs. 4. Increases in herbage intake within the ad lib, range were associated with increases in plasma insulin and glucagon concentrations and decreases in growth hormone concentration, and it is suggested that these effects could be mediated in part by the accompanying increases in protein absorption from the intestines. The T4:T3 value also decreased with increasing herbage intake, and it is suggested this was due to conversion of T4 to T3. 5. After correction by covariance to equal herbage intake, rates of irreversible glucose loss for control and protein-infused lambs were 9.2 and 10.0 mg/min per kg body-weight 0.75. It was calculated that respectively 0.12 and 0.19 of the total glucose production in control and protein-infused lambs could be accounted for by net synthesis from protein. 6. It was concluded that changes in the circulating concentration of several hormones in protein-infused compared with control lambs were likely to have been implicated in protein deposition forming a greater proportion of energy retention in the infused lambs (0.41 v. 0.27).
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PMID:Protein metabolism in growing lambs given fresh ryegrass (Lolium perenne)--clover (Trifolium repens) pasture ad lib. 2. Endocrine changes, glucose production, and their relationship to protein deposition and the partition of absorbed nutrients. 706 91


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