Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were conducted to determine the influence of the pancreatic hormones insulin, glucagon, and somatostatin on reticuloendothelial system (RES) phagocytosis both in vivo and in the isolated perfused livers of rats. Chronic pancreatic hormonal treatment consisted of twice daily injections SC of NPH insulin with doses ranging from 0.75 U on day 1 to 9.0 U on day 13 and unchanged doses of glucagon (200 micrograms) and somatostatin (50 micrograms). Chronic treatment with insulin significantly depressed by 48% intravascular phagocytosis of colloidal carbon administered IV at a dose of 8 mg/100 g, while glucagon and somatostatin stimulated macrophage endocytic function by 32% and 26%, respectively, compared to the control value. Acute treatment with the three pancreatic hormones at 30 min prior to carbon administration similarly produced insulin depression as well as glucagon and somatostatin stimulation of RES phagocytosis. Addition of the three hormones at near physiologic concentrations (20 ng/ml for insulin, 10 ng/ml for glucagon, and 5 ng/ml for somatostatin) to the recirculating perfusate of isolated perfused rat livers simultaneous with 24 mg of colloidal carbon likewise resulted in phagocytic reduction after insulin and enhancement after glucagon and somatostatin. Experiments involving insulin in vitro with isolated perfused livers as well as glucose replacement therapy concomitant with insulin in vivo demonstrated that hypoglycemia is not necessary for phagocytic depression by insulin while severe hypoglycemia in the perfusion medium is sufficient to depress carbon uptake by isolated perfused livers independent of insulin. Both pancreatic hormones and the level of glycemia seem to be important in modulating hepatic reticuloendothelial system phagocytosis.
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PMID:Modulation of hepatic reticuloendothelial system phagocytosis by pancreatic hormones. 676 38

Infectious or inflammatory stress in the rat causes very typical functional and metabolic alterations. Among the most typical are elevation in body temperature, insulin, and glucagon and depression in the concentrations of plasma ketones and free fatty acids. These changes occur only with infectious or inflammatory stress and not with noninflammatory stresses such as femoral fracture, screen restraint, or exercise. It appears that the depression in plasma ketone bodies during infection or inflammation is closely related to the rise in plasma insulin. During infection imposed on experimentally induced diabetes, inhibition of plasma ketones is not apparent. In a similar fashion, infection in hypophysectomized rats causes no elevation in plasma insulin and no depression in plasma ketones. Discussion concerning the implications of these observations in the rat and primate is included.
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PMID:Unique effects of infectious or inflammatory stress on fat metabolism in rats. 676 45

Liver glycogen levels of broilers with Eimeria acervulina, E. Brunetti, or E. tenella fell during the acute phase of the infection with the maximum effect at 5-6 days post-inoculation (DPI). During the early recovery phase (6-8 DPI), liver glycogen levels in the E. acervulina-infected birds increased to levels up to 3 times greater than those found in uninoculated control birds. A lesser increase was occasionally seen in E. tenella-infected birds. Pair feeding studies showed that the decrease in liver glycogen was not related to the amount of feed consumed. The magnitude of the glycogen overshoot at 7 DPI was not related to the depression of weight gain at 5 and 6 DPI. When feed was withheld from birds, liver glycogen levels of uninoculated control birds fell rapidly within 1 h after feed withdrawal. In birds infected with E. acervulina, liver glycogen levels remained high even after 3 h starvation. Injection of glucagon indicated that glycogen could be mobilized in both infected and uninfected birds.
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PMID:Changes in liver glycogen of broilers during coccidiosis. 689 Feb 69

Although it is known that caerulein exerts an action on the secretory activity of the islets of Langerhans in the pancreas, the mechanism of this hormone has not yet been ascertained. The present investigation was undertaken to observe the ultramicroscopic changes of the pancreatic islets and the peripheral blood levels of insulin, glucagon, glucose and electrolites after caerulein administration. The animals were divided into four groups, and three were injected intraperitoneally with caerulein at 25 micrograms/kg, 2 micrograms/kg and 0.2 microgram/kg body weight, respectively. The fourth group served as the control. In the first group (25 micrograms caerulein), the endocrine cells of the pancreatic islets showed accelerated functioning immediately and up to about 2 hours after injection. Then these cells degenerated due to cytoplasmic edema and evidenced decreased secretory activity. In the second group (2 micrograms) depression in the secretory activity occurred for about 2 hours immediately after the injection, but there was no destruction of cells and they gradually recovered their functioning. The third group (0.2 microgram) displayed an acceleration of secretory activity immediately after the injection and then recovered to the normal state. There were some changes of electrolites in the peripheral blood in each of the three groups, suggesting that caerulein causes acceleration and depression of the secretory activities in the islets of Langerhans in the pancreas depending on the dosage. Moreover, the cell alterations may well depend on the changes of electrolites in the inner and outer atmospheres of the cells.
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PMID:[A study of caerulein action on secretory cells, especially in the islets of Langerhans in the rat pancreas (author's transl)]. 700 39

Several lines of evidence support the hypothesis that derangements in the function of the autonomic nervous system play an important role in the development of hypothalamic obesity. Vagotomy below the diaphragm, reverses the syndrome. In diabetic rats cured of their diabetes with transplants of fetal pancreatic tissue beneath the renal capsule, ventromedial hypothalamic (VMH) lesions do not produce the characteristic rise in food intake nor do they significantly increase serum insulin. These observations indicate that the hyperinsulinaemia following VMH lesions is the result of neural connections rather than from a circulating humoral factor released following VMH injury. The smaller salivary glands, reduced level of glucagon and impaired mobilization of fatty acids during stress in VMH lesioned rats point to reduced activity of the sympathetic nervous system. The impaired mobilization of fat from retroperitoneal depots in VMH lesioned rats during fasting is similar to the effect of sympathetic denervation of the retroperitoneal fat pad. Similarly, unilateral sympathectomy caused an increased weight gain in rats almost as much as unilateral VMH lesions but significantly less than in bilaterally lesioned rats. These studies with fasting and feeding implicate the VMH in the control of the sympathetic nervous system. When atropine and epinephrine were given to VMH lesioned rats, there was a significant depression in basal and glucose-stimulated levels of insulin. Finally when VMH lesions were placed after lateral hypothalamic lesions, the effect of the VMH lesions did not seem to be reduced, suggesting that the two effects are independent. A model dealing with the effects of VMH lesions is presented in an attempt to integrate these findings.
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PMID:Hypothalamic obesity. The autonomic hypothesis and the lateral hypothalamus. 701 33

The glucagon-stimulated (coupled) activity of rat liver plasma-membrane adenylate cyclase could be selectively modulated by the anionic drug phenobarbital, whereas the fluoride-stimulated (uncoupled) activity remained unaffected. It is suggested that the cationic drug phenobarbital preferentially interacts with the external half of the bilayer, as the negatively charged phospholipids are found at the cytosol-facing side. This results in a selective fluidization of the external half of the bilayer, leading to a depression in the high-temperature onset of the lipid phase transition (from 28 degree to 16 degree C) occurring there. This was detected both by e.s.r. analysis, using a fatty acid spin probe, and also by Arrhenius plots of glucagon-stimulated activity, where the enzyme forms a transmembrane complex with the receptor and is sensitive to the lipid environment of both halves of the bilayer. However, in the absence of hormone, adenylate cyclase only senses the lipid environment of the inner (cytosol) half of the bilayer. Thus its fluoride stimulated activity and Arrhenius plots of this activity remained unaffected by the presence of phenobarbital (less than 12 mM) in the assay. These results support the view that independent modulation of the fluidity or chemical constituents of each half of the bilayer can selectively affect the receptor-coupled and uncoupled activities of adenylate cyclase.
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PMID:Phenobarbital selectively modulates the glucagon-stimulated activity of adenylate cyclase by depressing the lipid phase separation occurring in the outer half of the bilayer of liver plasma membranes. 732 77

A previous study demonstrated that administration of phenobarbitone to male AP Wistar rats for up to 7 days caused alterations in labelling indices (LIs) in several different tissues (including a reduction of the endocrine pancreas population LI) as determined by immunohistochemical visualisation of 5-bromo-2'-deoxyuridine (BrdU) incorporation into S-phase nuclei. The primary objective of this study was to determine whether treatment with phenorbarbitone influenced the replicative states of specific cohorts of the islet (of Langerhans) cell population or generated a uniform depression of LI. Quantitation of the LIs of individual islet cell cohorts was achieved by utilisation of a dual immunohistochemical staining method for BrdU and islet hormones (insulin, glucagon and somatostatin) using a sequential peroxidase anti-peroxidase (PAP)/alkaline phosphatase anti-alkaline phosphatase (APAAP) method employing diaminobenzidine and New Fuchsin chromogens, respectively. We observed reductions, increases and no change in LIs of insulin-, glucagon- and somatostatin-positive cells, respectively. We conclude that the decreased LI of the insulin-positive cohort was not countered entirely by the LI increase in the glucagon-positive cohort due to the larger size of the former. Furthermore, the effects of phenobarbitone treatment are not manifested generally in the islet cell population but in the insulin- and glucagon-positive cohorts only. The causation of these effects is unknown but is likely to be due to enhanced carbohydrate and hormone metabolism. We believe that the visualisation and quantitation of replicating cells in specific hormone-positive cohorts of the islet cell population provide opportunities for understanding the influence of xenobiotics and disease processes on pancreatic function.
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PMID:Assessment of the labelling index of cohorts of the pancreatic islet cell population in phenobarbitone-treated male rats using a double immunohistochemical technique for 5-bromo-2'-deoxyuridine and pancreatic hormones. 771 55

Fifty-five patients aged 15-35 years with insulin-dependent diabetes mellitus lasting 3.8 +/- 1.2 years underwent carbohydrate food loading. Within 2 hours after the meal, at 15-min intervals measurements were made of glycemia, C-peptide, insulin, glucagon, hydrocortisone, blood STH levels. Contrary to foodstuffs with low glycemia indices (GI), i.e. vermicelli, buckwheat, the intake of fast absorbed products with high GI (potatoes, hardtack, bread) stimulates glycemia and residual secretion of the islet cells. Enhanced entrance of gastrointestinal glucose into the systemic blood flow and growing insulinemia aroused glucagon secretion depression. The body responses to the above processes, assessed as metabolic stress, with increasing blood hydrocortisone and STH concentrations.
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PMID:[Products with high glycemic indices as factors in the metabolic stress of patients with insulin-dependent diabetes mellitus]. 790 57

A single-stage total-hepatectomy model in the rat is described. This model was successful in simulating the anhepatic phase for at least 4 h, with continuous intravenous glucose infusion. Advantages of the technique used for total hepatectomy in this study include ease of production, and resolution of problems encountered in previous models such as embolism and high postoperative mortality. This model was employed to observe fluctuation of pancreatic peptide hormones and glucose clearance during the anhepatic phase. Plasma insulin levels in portal blood did not vary for 120 min after removal of the liver. However, transient glucagon hypersecretion and depression in reactive secretion of somatostatin were observed during the anhepatic phase. These observations led to the following conclusions: (1) the liver seems to play an important role in regulating correlations between pancreatic peptide hormones by being part of a feedback system, and (2) hypersecretion of glucagon in the early anhepatic phase may be the initial signal for liver regeneration in the totally hepatectomized rat.
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PMID:Fluctuation of pancreatic peptide hormones in total-hepatectomy model in the rat. 790 88

The effects of the fentanyl fluanisone combination (Hypnorm) and pentobarbitone sodium (Pentobarbital) anaesthesia on blood glucose, insulin and glucagon were tested in rats in the fed and fasted state. Blood glucose was measured before and at 10, 20 and 30 min after injection of the anaesthetic agents. At 30 min the rats were sacrificed, and blood was drawn for measurement of glucagon and insulin. Pre-anaesthetic values for insulin and glucagon were established in separate groups of fasted and fed rats. In fasting rats given Hypnorm, blood glucose and plasma insulin were unchanged while there was a non-significant increase in plasma glucagon. The fasted rats given Pentobarbital had unchanged blood glucose and plasma insulin and a non-significant depression of glucagon. The fed rats given Hypnorm had a significant increase in blood glucose at 10 min and nearly a doubling of glucose values at 20 and 30 min (P < 0.001). Glucagon increased far less than in the fasted group, whereas insulin was doubled from preanaesthetic values (P < 0.05). The fed rats given Pentobarbital, had unchanged blood glucose, a slight non-significant depression of glucagon and a significant increase in insulin (P < 0.01). Thus Hypnorm induced hyperglycaemia in fed but not in fasted rats, probably because more glucose was available in the fed state. Fed animals are a modification of the standard fasted animal model, and may be preferable when exploring hyperglycaemic or other reactions to anaesthetic agents.
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PMID:Increased plasma glucose levels after Hypnorm anaesthesia, but not after Pentobarbital anaesthesia in rats. 796 63


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