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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regulation of zinc metabolism by dibutyryl cAMP, glucagon, and epinephrine was examined in rats fed adequate amounts of zinc. Dibutyryl cAMP, epinephrine, and glucagon each produced an increase in liver metallothionein levels by 10 h after they were first administered. The increase in liver metallothionein was inversely related to the serum zinc concentration. Treatment with dexamethasone, a glucocorticoid, accentuated these effects to some extent. Both metallothionein I and II were induced by dibutyryl cAMP and glucagon. Levels of metallothionein mRNA in total liver RNA extracts were measured by dot blot hybridization using a synthetic 21-base oligonucleotide complimentary to the 5' region of both the metallothionein I and II genes. Individual administration of dibutyryl cAMP, glucagon, and epinephrine increased the number of metallothionein mRNA molecules per cell by up to fourfold. The data suggest that glucagon and epinephrine are primary regulators of metallothionein gene expression acting at least in part via cAMP. In adrenalectomized rats, glucagon, dibutyryl cAMP, and epinephrine had a less potent effect in terms of metallothionein induction and depression of serum zinc concentrations. These effects were largely restored when dexamethasone was also given. Collectively these data suggest that changes in zinc metabolism associated with acute stress involve coordinate regulation mediated by many factors, including glucocorticoids and cAMP.
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PMID:Coordinate regulation of zinc metabolism and metallothionein gene expression in rats. 302 99

1. The present paper reports the effects of dietary modifications on the diurnal pattern of concentrations of certain metabolites and hormones in the peripheral blood of lactating dairy cows. The cows were given fixed rations of hay and high-cereal concentrates in the proportions of 30:70 or 10:90 (w/w). The concentrates were given in either two or six equal meals daily; the hay was given twice daily. 2. Previous reports of the same experiment had shown that milk-fat yield and concentration were reduced by increasing the proportion of concentrates in the diet and increased by more frequent feeding of the concentrates. These changes could be explained in part by changes in rumen volatile fatty acid (VFA) proportions and mean daily concentrations of VFA, particularly propionic acid, and insulin in the peripheral blood, but these factors failed to explain all the increase in milk-fat concentration caused by more frequent feeding. 3. Analysis of blood samples taken at hourly intervals for 24 h at two stages of lactation showed that, in the cows fed six times daily, the concentrations of metabolites and hormones remained relatively constant over the day. In the cows fed twice daily, the concentrations of VFA, 3-hydroxybutyric acid and insulin all increased after both meals whereas the concentrations of glucose and growth hormone tended to fall. The concentration of non-esterified fatty acids tended to increase overnight and fall rapidly after the morning feed. The concentrations of glucagon, thyroxine and prolactin showed no clear pattern in relation to meals. The postprandial responses of propionate, insulin and growth hormone were greater with the higher concentrate diet. 4. The maximum concentration and the diurnal range of concentrations were reduced by more frequent feeding of both diets in the case of propionic acid and of the higher concentrate diet in the case of insulin, but the effects on insulin concentrations of more frequent feeding of the lower concentrate diet were smaller and not significant. The maximum concentration and the diurnal range of concentrations of growth hormone were unaffected by meal frequency. 5. It is concluded that the severity of milk-fat depression in cows fed twice daily is increased by the rapid rise in propionic acid concentration in the peripheral blood after a meal, which in turn increases insulin secretion and may be accompanied by a suppression of growth hormone release. This causes lipogenesis to be diverted towards adipose tissue at the expense of the mammary gland.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Feeding frequency for lactating cows: diurnal patterns of hormones and metabolites in peripheral blood in relation to milk-fat concentration. 305 1

The effects of acute doses of soman (40, 60, or 80 micrograms/kg sc) in rats were evaluated for toxic symptoms as well as for changes in plasma levels of glucose, insulin, glucagon, corticosterone, norepinephrine, and epinephrine. The relationship between changes in these levels and depressed acetylcholinesterase activity in the hypothalamus was determined. Soman 40 micrograms/kg did not manifest significant changes in any of the parameters evaluated. However, both the 60 and 80 micrograms/kg doses of soman caused dose- and time-related increases in plasma levels of glucose, corticosterone, norepinephrine, epinephrine, and a depression of insulin. Many of these increases, as well as the severity of toxicity, appear to be inversely related to the hypothalamic acetylcholinesterase levels. The hyperglycemia following the higher doses of soman is likely due to the combined effects of elevated levels of corticosterone, catecholamines, possibly glucagon, and depressed insulin levels. Stress from the toxic effects of soman is likely partially responsible for the endocrine effects since most of the changes observed are consistent with changes in these levels that would be manifested in an animal stress model.
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PMID:Effect of acute soman on selected endocrine parameters and blood glucose in rats. 306 86

Calcium channel blockers (CCBs) may produce profound myocardial depression. Glucagon antagonized verapamil-induced hypotension and bradycardia in rats; however, glucagon's ability to antagonize other CCBs is unexplored. This study determined: a) if glucagon reverses verapamil-induced depression by a direct cardiac effect, b) if myocardial depression induced by diltiazem and nifedipine (representing different classes of CCBs) is also reversed by glucagon, and c) the glucagon concentration needed to reverse myocardial depression. Isolated rat hearts were perfused at a constant flow rate in a Langendorff preparation. Developed pressure (dP), contractility (+dP/dtmax), relaxation (-dP/dtmax), heart rate, and coronary vascular resistance were recorded. A CCB (n = 6, each blocker) was infused until greater than 50% depression of contractility was achieved. Glucagon was then simultaneously infused (perfusion concentration of 0.6-1.1 x 10(-7) M), and repeat cardiac variables were recorded. In a separate group of 36 hearts, glucagon dose response was determined. After producing a greater than 50% depression in dP/dtmax with 3 mumol of diltiazem, a single concentration of glucagon was infused simultaneously into each heart (perfusion concentrations between 10(-6) and 10(-9) M) and percent recovery of baseline function was determined. Glucagon restored baseline contractility and dP with all three CCBs. Complete reversal of diltiazem-induced myocardial depression occurs at glucagon concentrations greater than or equal to 5 x 10(-7) M. We conclude that a) glucagon directly reverses myocardial depression from three classes of CCBs at concentrations achieved in vivo, and b) glucagon may be useful in the treatment of CCB-induced myocardial toxicity.
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PMID:Glucagon antagonism of calcium channel blocker-induced myocardial dysfunction. 327 81

The multisystem involvement in acute pancreatitis (AP) is a reflection of the pancreatic gland's capacity to produce a number of potent vasoactive peptides, hormones, and enzymes. The various prognostic criteria are early evaluations of these metabolic derangements. The pathogenesis of hypocalcemia, long recognized as an indicator of severity of AP, is multifactorial. Imbalances of parathyroid hormone (PTH)-calcitonin, the interactions of glucagon, gastrin and other pancreatic hormones with PTH-calcitonin, the role of free fatty acids in binding serum calcium with albumin, and the translocation of calcium ion in muscles and liver, have been recently described but remain conflicting theories. Yet, the time-honored theory of calcium-soap formation enjoys wide acceptance. Hyperglycemia, hypoglycemia, and occasional ketoacidosis in acute pancreatitis have been studied thoroughly. The complex cause-and-effect relationship between hyperlipidemia with acute pancreatitis needs further study. The coagulation abnormalities seem to be initiated by activated trypsin, and their role in microvascular coagulation appears to form a unifying hypothesis for major organ dysfunction, but this requires further investigation. Adult respiratory distress syndrome may be the result of active enzymes that digest pulmonary surfactant and/or microvascular thrombosis. The depression of cardiac function and shock are suspected to be secondary to vasoactive peptides such as bradykinin, or myocardial depressant factor, whose structure has yet to be elucidated. The renin-angiotensin alterations and renal complications in acute pancreatitis have received scant attention in the literature. The onset of moderate visual disturbances, or even blindness, in a patient with acute pancreatitis as a result of retinal vessel thrombosis is fortunately uncommon. Rare but interesting are the manifestations such as subcutaneous fat necrosis, arthralgia, and pancreatic encephalopathy. Despite the extensive literature on the complexities of the pathogenesis of complications of acute pancreatitis, there have been very few advances in the prevention and management of specific complications. It is hoped that further work on modification of enzymatic disturbances induced in acute pancreatitis will result in its effective treatment and prevention of serious complications.
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PMID:Systemic complications of acute pancreatitis. 328

1. The present paper reports the effects on rumen fermentation and plasma metabolites and hormones of giving fixed rations of hay and high-cereal concentrates at different meal frequencies to lactating cows. In Expt 1 the total ration was given in two and twenty-four meals daily and in Expts 2-4 the concentrates were given in two and five or six meals and the hay in two meals daily. The diets contained 600-920 g concentrates/kg. 2. In Expt 1, minimum rumen pH was higher but mean pH was lower when cows were given their ration in twenty-four meals/d rather than two meals/d. 3. In all the experiments, the effects of increased meal frequency on the molar proportions of rumen volatile fatty acids (VFA) were small and not significant, although there was a general tendency for the proportion of acetic acid to increase and that of propionic acid to fall. Increasing the proportion of concentrates in the diet reduced the proportion of acetic acid and increased the proportions of propionic and n-valeric acids. 4. In Expt 3, more frequent feeding was found to reduce the concentration of non-esterified fatty acids in the blood, but changes in other metabolites were small and not significant. Increasing the proportion of concentrates in the diet reduced the concentrations of acetic acid and 3-hydroxybutyric acid and increased the concentrations of propionic acid and glucose. 5. The mean daily concentration of insulin in the blood was reduced by more frequent feeding of the higher-concentrate diet but not of the lower-concentrate diet. The concentration of glucagon also tended to fall with more frequent feeding. Increasing the proportion of concentrates in the diet increased the concentration of insulin. 6. More frequent feeding reduced the depression in milk-fat concentration caused by feeding the low-roughage diets. About three-quarters of the variation in milk-fat concentration could be related to changes in rumen VFA proportions, but the relations for the two meal frequencies had different intercepts although similar curves. The results suggest that milk-fat depression on low-roughage diets with twice-daily feeding was due to a change in rumen VFA proportions accompanied by elevated plasma insulin concentrations. The improvement in milk-fat concentration due to more frequent feeding could be explained partly by the small change in rumen VFA proportions and partly by a reduction in mean plasma insulin concentrations, but these mechanisms did not fully account for the milk-fat responses observed.
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PMID:Feeding frequency for lactating cows: effects on rumen fermentation and blood metabolites and hormones. 331 80

Verapamil-induced cardiovascular depression has been examined in dial-urethane-anesthetized open chest dogs. Verapamil was administered slowly intravenously until the mean arterial pressure was decreased by approximately 45 mm Hg. The dose of verapamil required to reach the hemodynamic endpoint was 1,495 +/- (SE) 165 micrograms/kg. In a second group, interactions between beta-adrenergic blockade, propranolol 1 mg/kg (i.v.), and verapamil were examined. Although propranolol alone had only minor hemodynamic effects, the cardiac depressant dose of verapamil was reduced significantly to 450 +/- 105 micrograms/kg. After cardiovascular depression with verapamil or verapamil plus propranolol, glucagon was administered to assess its inotropic activity using cumulative doses of 5, 15, and 45 micrograms/kg over 20 min. Glucagon produced a dose-dependent recovery of heart rate, mean arterial pressure, and PR interval. Depressed contractility assessed by peak positive dP/dt and right ventricular isometric contractile force also recovered after glucagon. These results suggest a significant interaction between the potency of verapamil as a myocardial depressant and the state of the myocardium as affected by beta-blockade. Cardiac depression by verapamil or verapamil in combination with propranolol was reversible by glucagon.
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PMID:Cardiovascular depression by verapamil: reversal by glucagon and interactions with propranolol. 342

The inhibitory effect of glucagon on exocrine pancreas has been the subject of controversial reports. On the other hand, oxyntomodulin (bioactive enteroglucagon or glucagon-37), a 37 amino acid peptide isolated from porcine lower intestine, has been shown to be 10-20 times more potent than glucagon in inhibiting gastric acid secretion in the rat. In view of this, the effect of glucagon and oxyntomodulin on basal and caerulein-stimulated pancreatic secretion has been studied, during re-introduction of pancreatic juice into duodenum, in the conscious rat provided with pancreatic and duodenal fistulas. A depression of pancreatic function was observed with both peptides on the three parameters studied: (volume of juice secreted, bicarbonate and protein output), either under basal conditions or during stimulation by caerulein. In all the experimental conditions used, oxyntomodulin was ca. ten times more potent than glucagon in its inhibitory effect. The fact that oxyntomodulin, as what is observed in the stomach, is one order of magnitude more potent than glucagon in inhibiting pancreatic secretion suggests that the biological mechanisms by which the peptides of the glucagon-family act on exocrine pancreas are similar, or related to that present at the gastric level.
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PMID:The effect of oxyntomodulin (glucagon-37) and glucagon on exocrine pancreatic secretion in the conscious rat. 344 47

Diabetes is known to result in depression of myocardial function, whereas hearts from insulin-treated diabetic rats exhibit functional characteristics similar to controls. In the present study, we have studied the effect of insulin perfusion on cardiac performance of 3-day and 6-week streptozotocin (STZ) diabetic rats. Three days of diabetes did not result in depressed cardiac performance when the hearts were isolated and perfused in the working heart mode. Increasing the concentration of glucose from 5 to 10 mM in the perfusion fluid did not alter the function in either control or in diabetic rat hearts. However, when regular insulin or glucagon-free insulin (Humulin) (5 mU/mL) was included in the perfusion medium, the ventricular function of hearts from control rats was significantly enhanced, while diabetic myocardial function remained unaffected. When the study was repeated on hearts from 6-week diabetic animals, cardiac function of diabetic rats was significantly depressed as compared with controls. As in the 3-day study, contractility was not affected in either group by increasing glucose concentration in the perfusion medium. Again, inclusion of insulin in the medium enhanced cardiac contractility only in control hearts. These results suggest that diabetes results in a loss of myocardial sensitivity to insulin which seems to occur as early as 3 days after induction of diabetes with STZ. The study also demonstrates that the beneficial effects of in vivo insulin treatment on myocardial alterations induced by diabetes are not due to its direct myocardial effects.
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PMID:Effects of insulin perfusion and altered glucose concentrations on heart function in 3-day and 6-week diabetic rats. 351 48

Endotoxemia is a frequent complication of many health disorders. It is characterized by systemic release of a variety of endogenous inflammatory mediators which effect cardiovascular depression, reductions in organ blood flow, tissue ischemia and derangements in cellular metabolism leading to death. During a continuous intravenous infusion of Escherichia coli lipopolysaccharide, the chronology of alterations in hepatosplanchnic blood flow, hepatic carbohydrate metabolism and pancreatic insulin secretion has been studied in awake Yucatan miniature pigs (Sus scrofa). Endotoxic shock in this model is characterized by reductions in portal venous and hepatic arterial blood flow, early transient increases in pancreatic insulin secretion, increases in the 3H-glucose-derived rates of glucose appearance and disappearance, profound hypoglycemia, hyperlactatemia and metabolic acidosis. Reductions in hepatic oxygen delivery are compensated for by enhanced oxygen extraction efficiency, but hepatic gluconeogenesis continues at an inadequate rate to compensate for increased glucose utilization. Experimental therapies including lidocaine, naloxone, captopril, dichloroacetate and glucagon each effect specific improvements in cardiovascular or metabolic function, but none significantly alter the composite derangements responsible for lethality in this model.
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PMID:Endotoxemia in Yucatan miniature pigs: metabolic derangements and experimental therapies. 353 41


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