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

The mechanisms controlling secretion of glucagon and other pancreatic hormones were studied in a patient affected with multihormone-secreting islet-cell tumor. Fasting glucagon levels (3,000 pg./ml.) rose to 10 ng./ml. following arginine stimulation. While oral glucose load and intravenous glucose infusion did not suppress glucagon secretion, insulin administration induced a prompt depression in glucagon levels. Glucagon, insulin, and gastrin levels were suppressed by somatostatin while calcium infusion caused a paradoxical increase. It is suggested that only some of the stimulation-inhibition mechanisms were conserved in this case of glucagon-secreting pancreatic tumor.
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PMID:Suppression and stimulation mechanisms controlling glucagon secretion in a case of islet-cell tumor producing glucagon, insulin, and gastrin. 0 26

This article discusses the results of recent neuroendocrinological research in depressions. The abnormalities found in a given category of vital depressive patients--cortisol hypersecretion, decreased growth hormone response to insulin hypoglycaemia and decreased luteinizing hormone secretion in menopause--are believed to be due to deficient noradrenalin-(NA)-ergic activity in the hypothalmus. Thus explained, they support the so-called MA (monoamine) hypothesis, which postulates that a functional NA deficiency in the brain plays a role in the pathogenesis of certain types of vital depression. Disorders in certain central MA-ergic systems are predictive of disorders in the hormone secretion of the anterior pituitary. Inversely, disorders in the hormone secretion of the anterior pituitary can be indicative of disorders in the MA-ergic transmission in the hypothalamus. Consequently we can expect a convergence of transmitter research and neuroendocrinological research--two lines of research which have so far been largely separated in studies of human individuals.
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PMID:Neuroendocrine disorders in depressions and their significance for the monoamine hypothesis of depression. 2 49

The effects of a 0.5 g/kg body weight arginine infusion on plasma inorganic phosphates and potassium were examined in nineteen normal subjects. Plasma phosphorus displayed a highly significant (p less than 0.001) fall with a maximum depression below baseline of 1.11 +/- 0.15 mg/100 ml or 33 +/- 3% (mean +/- SEM); there was a significant correlation (p less than 0.01) between this fall and the insulin peaks induced by arginine. Plasma potassium levels displayed a distinct and significant increase in eleven of the twelve subjects studied; the maximum increase above baseline was 1.02 +/- 0.14 mEq/1 or 27 +/- 4.5% (p less than 0.001). No change occurred in blood pH values determined in four subjects. In six normal subjects, the test was repeated with the addition of somatostatin (250 micrograms bolus, followed by 500 micrograms/hr), which abolished the insulin and growth hormone response to arginine. It also abolished the fall in plasma phosphorus but appeared (if anything) to augment the increase in potassium. These findings show that arginine is responsible for a fall in plasma phosphorus related to the insulin response, and for an increase in plasma potassium of clinical significance, the mechanism(s) of which, however, are still obscure.
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PMID:Arginine-induced hypophosphatemia and hyperkaliemia in man. 4 74

1. Cultured rat hepatoma cells accumulate 2-aminoisobutyrate to high concentrations by a transport mechanism probably of the A type mediation. 2. Transport is enhanced by the presence of serum. When cells are deprived of serum the rate of transport declines over a period of hours; conversely addition of serum leads over a period of hours to increase in transport activity. In the presence of serum the apparent Km for aminoisobutyrate uptake is about 8 mM. In cells deprived of serum the Km is much higher. 3. Addition of insulin produces both an immediate increase in the rate of aminoisobutyrate uptake and a time-dependent rise. 4. The presence of alanine diminished aminoisobutyrate uptake in a concentration-dependent fashion. Competition is seen both in the presence and absence of serum but not when cells are incubated at 4 degrees C. 5. Preincubation with alanine for 1 h also diminishes aminoisobutyrate uptake when the alanine is removed. Cells take a period of several hours to recover from the depression of transport induced by alanine. 6. Transport of aminoisobutyrate rapidly declines in the presence of cycloheximide. Actinomycin had no effect for at least 8 h.
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PMID:Influence of serum and insulin on the accumulation of aminoisobutyrate by rat hepatoma cells. 6 Jan 38

Depression of lymphocyte transformation and an increase in insulin resistance are common to pregnancy, oral contraceptive use, widespread malignancy, infection, and tissue destruction. We suggest that these abnormalities are caused by a rise in the plasma-glycoprotein level which is also common to these clinical states. There is evidence that glycoproteins can inhibit cell division, lymphocyte transformation, and the action of hormones on target cells. Because of the increase in plasma glycoprotein the cells in many organs and their hormone receptors may have a thicker coating of glycoproteins which blunts their response to variuos stimuli.
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PMID:Do plasma glycoproteins induce lymphocyte hyporesponsiveness and insulin resistance? 8 44

Overnight metabolic studies in 39 poorly controlled insulin-treated diabetic patients aged 9 to 66 years showed hypoglycaemia (blood-glucose less than 2 mmol/1) in 22 patients; it lasted 3 h or more in 17. Hypoglycaemic symptoms were very mild or absent, but 19 patients had other features of overtreatment with insulin. These included lethargy, depression, night sweats, morning headaches, fits (3 patients), glycogen-laden hepatomegaly (3), and acquired tolerance to high doses of insulin (mean 1 u/kg/24 h). The best clinical clue to recurrent nocturnal hypoglycaemia was the intermittent occurrence of symptoms, however "mild" and infrequent these appeared to be. Reduction of insulin by a mean of 25% in these patients (without change of species) did not result in loss of overall control; 1 patient with recurrent ketoacidosis was stablished on 40% of his initial dose. It is difficult, sometimes impossible, to achieve good overnight control with conventional once or twice daily insulin therapy. Since patients readily become tolerant of low blood-glucose levels, reliance on urine tests and symptoms of hypoglycaemia as a guide to dosage easily produces a spiral of overtreatment.
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PMID:Unrecognised nocturnal hypoglycaemia in insulin-treated diabetics. 8 75

15 patients with formerly endogenous recurrent depression or manic-depressive illness free of psychotic symptoms, who are under lithium prophylaxis about 3,9 years, and 16 healthy controls with approximately the same age and sex were tested with 0,1 U Insulin/kg, 200 micrograms TRH and 50 micrograms LHRH for their hGH-, TSH-, hPRL-, FSH-, LH-and Cortisol levels about 2 hours. hPRL, FSH and LH did not show any change under lithium salts. All patients under lithium showed elevated TSH-levels under basal conditions and after stimulation compared with the control groups. For the young women before menopause the difference was highly significant. Men and praemenopausal women had significantly higher hGH-levels after stimulation under lithium than the normal controls. However postmenopausal women did not show this lithium effect on their hGH levels.
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PMID:[Neuroendocrinological changes under longterm therapy with lithium salts (author's transl)]. 11 22

Previous in vitro studies of the metabolism of the peripheral nerve have been based on incorporation of radioactive precursor into components isolated from whole nerve. In this study we have determined incorporation secifically into myelin components of peripheral nerve by isolating myelin after incubating whole nerves with lipid or protein precursors and by determining the specific activity of the components of that membrane. The effect of diabetes on such incorporation was also studied. In the rat, in vitro incorporation of DL-[1-14C]leucine into protein components of myelin was decreased by 30-88% in diabetic animals as compared to controls. The major polypeptide constituent of rat sciatic nerve myelin (mol st 28,000; 58.5% of total mass of proteins) was not labeled in either the diabetic or the control group. In diabetes incorporation rate into a polypeptide of mol wt 23,000, which constitutes 21% of total mass, was approximately one half that of controls. In polypeptides of mol wt 38,000-49,000, which are heavily labeled in normal animals, but constitute only about 5% of total mass of proteins, depression of incorporation was e-en more marked in the diabetics. While these marked differences in incorporation between diabetic and control animals were observed, the amount of protein and its distribution among the constituent polypeptides was the same in both groups. In young rats made diabetic with streptozotocin and young rabbits made diabetic with alloxan, there was a lower rate of incorporation of the lipid precursors, [1-14C]sodium acetate or [3H]water, into myelin components. In older animals of both species incorporation in the controls was considerably lower than in the yount animals, and the effect of diabetes was no longer apparent. In nondiabetic animals, the in vitro addition of insulin (10-7 M) stimulated incorporation of DL-[1-14C]leucine into myelin proteins 1.6-3.1 times that of controls. This stimulation by insulin in vitro was not seen in diabetic animals. In animals in which diabetes had spontaneously recovered, however, incorporation rate in the in vitro experiments approached that of controls and were significantly above that in animals whose diabetes persisted. Since myelin is the palsma membrane of the Schwann cell, these studies provide evidence that the Schwann cell is affected by insulin and that some aspects of the metabolism of myelin are altered in insulin-deficient states.
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PMID:Metabolism of peripheral nerve myelin in experimental diabetes. 12 35

The retention of degradation of insulin by isolated perfused liver have been examined. Noncyclically perfused livers from streptozotocin-diabetic rats retained 25% and degraded 10% of 125I-insulin administered as a 1-min pulse. On gel filtration (Sephadex G50F), the degradation products released into the vascular effluent eluted in the salt peak. During the 45-min interval after the end of the 125I-insulin infusion, 0.19% of the total dose was excreted in the bile. 60-90% of this material consisted of iodinated, low-molecular-weight degradation products. Inclusion of native insulin with the 125I-insulin in the pulse depressed both the retention and degradation of iodinated material; however, this reflected increased retention and degradation of the total insulin dose (125I-insulin plus native hormone). The log of the total amounts of insulin retained and degraded were linearly related to the log of the total amount of insulin infused at concentrations between 12.7 nM and 2.84 muM. Increasing the amount of native insulin in the infused pulse also depressed the total amount of iodinated material found in the bile and led to the appearance in the bile of intermediate-sized degradation products that did not simultaneously appear in the vascular effluent. Addition of high concentrations of glucagon to the infused 125I-insulin had no effect on the retention or degradation of the labeled hormone, or on the apparent size and amount of iodinated degradation products found in the vascular effluent or in the bile. Preinfusion of concanavalin A inhibited both 125I-insulin retention and degradation. A greater depression by concanavalin A of degradation than binding was also observed with isolated hepatocytes. In contrast to 125I-insulin, the retention and degradation of two iodinated insulin analogues of relative low biological potency, proinsulin and desalanyl-desasparaginyl insulin, were small. The amount of radioactivity appearing in the bile after infusion of these analogues was almost negligible. However, degradation products of these analogues that appeared in the bile and in the vascular effluent was qualitatively similar to those found after the infusion of 125I-insulin. Our findings suggest that the rapid initial uptake of 125I-insulin after its infusion into noncyclically perfused liver, as well as its subsequent degradation, behaves in a qualitatively similar fashion to the binding of 125I-insulin and its degradation by isolated rat hepatocytes. This uptake and the subsequent phase of degradation may be attributable to binding of insulin at specific recognition sites, preliminary to its transfer to a degradative site(s) presumed to be located inside the cell.
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PMID:Retention and degradation of 125I-insulin by perfused livers from diabetic rats. 13 20

The blastogenic responses of lymphocytes from chemically-induced (streptozotocin) and genetically-diabetic C57B1/6J (ob/ob) obese mice were assessed using mixed-lymphocyte cultures (MLC) and mitogens selective for thymus-derived (T cell) and bone marrow-derived (B cell) lymphocytes. Splenic lymphocytes from obese and normal C57B1/6 mice exhibited similar responses to the nonspecific T and B cell mitogens, Concanavalin A (Con A) and E. coli lipopolysaccharide (LPS), respectively. A small (25%) depression of the blastogenic response in MLC was observed for lymphocytes from obese mice. The generation of cytotoxic T cells in vitro in response to trinitrobenzene sulphonic acid (TNP)-modified syngeneic spleen cells was the same for normal and obese mice. In contrast, splenic lymphocytes from 7-14 day streptozotocin-diabetic mice had lower (56-60%) proliferative responses in MLC. The generation of cytotoxic effector cells in vitro was lower for spleen cells for spleen cells from 22-day streptozotocin mice, although blastogenic responses in MLC were not depressed. The insulin-deficient streptozotocin mice appear to have a depression of some thymus-derived cell functions that may be associated with streptozotocin rather than the diabetic state. Direct immunosuppressive effects of streptozotocin are indicated by the marked decrease in the number of lymphocytes in the thymus, lymph nodes, and spleen.
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PMID:Immune responses of diabetic animals. Comparison of genetically obese and streptozotocin-diabetic mice. 14 82


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