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)

Studies were carried out in conscious dogs in which the effect of intravenous somatostatin on immunoreactive gastric inhibitory polypeptide (IR-GIP) release was investigated. In addition, the inhibitory action of somatostatin on the insulin response to pure porcine GIP was assessed. Intravenous administration of somatostatin resulted in a delayed IR-GIP and immunoreactive insulin (IRI) response to oral glucose. Somatostatin also delayed the IR-GIP response to the ingestion of fat. In both types of experiments, initial depression of IRI levels was followed by a sharp rise in IRI release. Intravenous infusion of somatostatin produced 80% inhibition of the IRI response to pure porcine GIP. It was concluded that somatostatin inhibits the physiological release of IR-GIP and the insulinotropic action of exogenous porcine GIP.
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PMID:The effect of somatostatin on release and insulinotropic action of gastric inhibitory polypeptide. 122 89

Concentrations of immunoreactive insulin activity (IRI) and proinsulin activity (IRP), blood glucose, free fatty acids (FFA), glycerol, cholesterol, triglycerides were analyzed in 140 subjects suspect of protodiabetes and 50 healthy persons before, during and after a glucose infusion test (GIT). The protodiabetic subjects were classified into normweight, overweight, obese, hyperlipemic groups with diet or with Regadrin therapy and each of them subdivided into such with normal and such with pathological carbohydrate tolerance. Norm- and overweight subjects with asymptomatic diabetes were characterized by a significant reduction of insulin secretion during both phases. Obese patients with or without hyperlipoproteinemia demonstrated an increased IRI reaction during the late phase of secretion. Carbohydrate intolerance was associated with an enhancement of basal triglyceride levels and a reduced depression of glycerol and FFA during the GIT. There were no differences in fasting or reactive IRP concentrations between healthy and protodiabetic subjects with normal carbohydrate tolerance. In asymptomatic diabetes the IRP levels were increased during the late secretion phase, but the percentage of IRP in total IRI was normal or--in existing high response--significantly reduced in comparison to norm response. The results do not support an enhanced IRP secretion as the cause of carbohydrate intolerance.
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PMID:Effect of glucose infusion on venous blood levels of immunoreactive proinsulin activity, insulin activity and fat parameters in healthy and protodiabetic subjects. 122 47

Since glycogen overloading is one of the outstanding features of the diabetic liver, a series of investigations were undertaken to find an enzymatic explanation of this feature. Three groups of patients were studied: non diabetics submitted to liver biopsy during surgery (group A); non diabetics submitted to percutaneous liver biopsy (group B). In both these groups G-6-PDH, PK and MDH were assayed, all these being adaptive enzymes of intermediate metabolism. Results were expressed as muU/100 mg proteins. The significant finding of the comparison of these two groups was the low concentration of these enzymes in surgical biopsies. The depression was such that for G-6-PDH the concentration was more than 10 times less in surgical specimens as compared to percutaneous ones, whereas for PK it was almost 10 times less. In view of these findings no further surgically obtained biopsy material was used in this study. The third group (C) included insulin-dependent diabetics in good metabolic control from whom percutaneous liver biopsies were obtained for the assay of the same enzymes as above and in order to compare the results with those of group B. All three enzymes were diminished in diabetics, the difference being statistically significant for G-6-PDH and PK, not for MDH in view of the wide dispersion of the values found. Comparison and analysis of these results lead to the conclusion that in view of the low concentration of these enzymes in diabetics, glucose utilization in the liver cell must be presumed to be increased via other metabolic pathways.
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PMID:The liver in human diabetes. Concentration of some induced enzymes. 123 63

Non-ketonic hyperosmolar hyperglycaemic coma (N.K.H.H.C.) is by no means uncommon in diabetes. Its picture includes sensorial depression, hyperglycaemia, hyperazotemia, marked dehydration and plasma hyperosmolarity. It is mostly found in elderly subjects with non-serious diabetes. Reference is made to 6 personal cases observed during a period of 14 months. The incidence of N.K.H.H.C. noted during this period was 2.2%; this was higher than that of ketoacidotic coma. Two patients died from hypovolaemic shock and one from septic complications. Three survived the episode. Treatment was based on three main points: high doses of insulin, though less than those employed for equal blood sugar levels in cases of ketoacidotic coma, hypotonic saline solutions, and correction of electrolyte imbalance. It is hoped that improved knowledge of the syndrome and, more particularly, earlier diagnosis and treatment, with lead to a reduction in the ta 50% mortality present associated with the disease.
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PMID:[Non-ketosic hyperosmolar hyperglycemic coma. Case reports and therapeutic consideration]. 125

The effects of insulin (In) on contractile activity of isolated cardiac muscle were studied in right ventricular moderator band (MB) of piglets and papillary muscle (PM) of cats and kittens. The muscles were bathed in modified Krebs solution containing 5.6 mM glucose at 30 degrees C and gassed with 95% O2 and 5% CO2. They were paced at 24 contractions per minute isometrically at Lmax. Addition of In (1 U/ml) to the bath induced a biphasic inotropic response to piglet MB. The initial negative effect was due to the preservative (0.2% phenol) in the regular commercial In solution. Following the transitory depression, both active isometric tension (AT) and maximal rate of tension development increased to a maximum (about 120% of control) within 15 min and then declined slightly toward control. Similar positive responses were observed in both cat and kitten PM, but without the initial negative effect. Maximal responses were not diminished by the absence of glucose in the bath. Increases in AT and dT/dt of both MB and PM in response to NE were significantly attenuated in the presence of In compared with untreated muscle. These findings demonstrate that In elicits a positive inotropic effect on mammalian cardiac muscle and that it impairs the inotropic action of NE.
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PMID:Effects of insulin on cardiac muscle contraction and responsiveness to norepinephrine. 127 78

The effects of glucose-insulin-potassium infusion (GIK) on atrial pacing-induced angina, ST depression, abnormal left ventricular end-diastolic pressure during pacing interruption (LVEDPi) and lactate metabolism (L), were studied in 18 patients: ten had angina during pacing = Ischemic group, and eight (5 normals and 3 with coronary artery disease) remained asymptomatic = Nonischemic group. The study consisted of 8-10 minute periods of control, pacing and recovery, before and after GIK. No untoward effects were observed. Comparison of the pacing responses (GIK vs pre-GIK states) showed that during GIK, angina occurred in only 4 patients, while significantly less severe changes were observed in ST depression (1.4 +/-0.5 vs 2.4 +/- 0.4 mm) and LVEDPi (16 +/- 3 vs 23 +/- 3 mm Hg). Lactate extraction was also higher (8.1 +/- 10.9 vs -5.2 +/- 11.1%), but not significantly so, although L became normal in 4 subjects and improved in another. These results indicate that GIK infusion was well tolerated and had a beneficial effect on pacing-induced myocardial ischemia.
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PMID:The protective effect of glucose-insulin-potassium on the response to atrial pacing. 127 28

Flow cytometry with monoclonal antibody Leu-7 (CD57), Leu-11 (CD56) and Leu-19 (CD56) were used to study the content of different subpopulations of natural killer cells (NK-cells) in the blood of type I diabetes mellitus patients before and after insulin treatment and in healthy people. After a course of insulin therapy most patients showed restoration of the total cell number with antigens on their surface characteristic of NK-cells, especially CD56, that indicates the essential role of hypoinsulin in the depression of the NK-system. At the same time a small group of patients was distinguished who did not show such normalization. This may indicate participation of other mechanisms in the formation of natural immunity failure, in particular, the genetic.
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PMID:[The effect of insulin therapy on the level of natural killer cells of different immunological phenotypes (CD16+, CD56+ and CD57+) in the blood of patients with diabetes mellitus type I]. 128 83

The past decade has seen a shift in the strategy for hypertension treatment from stepped therapy--a highly structured monolithic series of steps--to recommendations for a more individualized selection of treatment. Severe hypertension is a clear indicator to bypass traditional steps. Demographic factors, such as age, gender, and race, are often cited, but have proved to be less helpful. Concomitant medical conditions and problems are very common and are more often the crucial determinants in the selection of antihypertensive therapy. Coronary artery disease, diabetes mellitus, heart failure, azotemia, asthma, and chronic obstructive pulmonary artery disease, anxiety, and depression are all common, and each has implications for the selection of antihypertensive therapy. Blood pressure reduction is a surrogate for reduction of cardiovascular risk, and therefore, consideration of concomitant medical problems has extended to left ventricular hypertrophy, obesity, mild hyperlipidemia, and insulin resistance, as additional risk factors in hypertension. Consideration of all these factors makes it possible to individualize antihypertensive therapy in most patients today.
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PMID:Treatment of hypertension: the place of angiotensin-converting enzyme inhibitors in the nineties. 128 28

Addition of 10 mM citrate at constant free extracellular Ca concentration [( Ca]o; 2 mM) reduced contraction in rabbit ventricular muscle and isolated myocytes. We have recently shown that extracellular citrate decreases contraction and Ca current (ICa) in cardiac muscle by a direct effect on Ca channels rather than by Ca buffering per se [D. M. Bers, L. V. Hryshko, S. M. Harrison, and D. Dawson. Am. J. Physiol. 260 (Cell Physiol. 29): C900-C909, 1991]. Citrate rapidly depressed peak ICa and shifted both the peak ICa and the apparent reversal potential (Erev) to more negative potentials. When the impermeant cations, tetraethylammonium or N-methylglucamine were used instead of intracellular Cs, the citrate-induced shift in Erev was reduced or eliminated but depression of ICa was still observed. Thus citrate appears to alter the selectivity (PCa/PCs) of the Ca channel and reduce ICa. We also studied the effects of citrate on Na current through the Ca channel, observed when the divalent cation concentration is submicromolar. This current, termed INS for nonspecific, also exhibited leftward shifts in peak INS and smaller changes in Erev in the presence of citrate. However, neither peak INS nor single-channel conductance were affected by citrate. Thus the reduced PCa/PCs is due primarily to alteration of Ca permeation rather than monovalent cation permeation. Activation and inactivation curves for both ICa and INS were shifted toward more negative potentials by citrate. The shifts in gating and peak current to more negative membrane potentials would be consistent with a surface charge effect. The much larger shift in Erev for ICa (than for INS) is consistent with a reduction in Ca selectivity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Citrate alters Ca channel gating and selectivity in rabbit ventricular myocytes. 131 Feb 10

We electromagnetically measured blood flow to one cerebral hemisphere and determined cerebrovascular reactivity to vasoconstrictor and vasodilator stimuli during normoglycemia and insulin-induced hypoglycemia in unanesthetized goats. Control blood glucose concentration was 84 +/- 4 mg, and insulin, injected intravenously, decreased glycemia with a concomitant increment in cerebral blood flow and reduction in cerebrovascular resistance in all the animals. When glycemia decreased to 60 to 65 mg/dl, the animals began to show signs of increased adrenergic activity, and when it decreased to less than 30 mg/dl, they showed signs of CNS depression. Cerebral blood flow began to rise significantly at a glycemia of 50 to 55 mg/dl, and progressively increased to reach an increment of 36% +/- 4% when glycemia was less than 30 mg/dl. Norepinephrine (0.3 to 9 micrograms), tyramine (50 to 500 micrograms), and 5-hydroxytryptamine (0.1 to 9 micrograms) reduced cerebral blood flow, and this effect was lower during severe hypoglycemia. Acetylcholine (0.01 to 1 microgram), isoproterenol (0.03 to 3 micrograms), diazoxide (0.3 to 9 mg), and inhalation of 10% CO2 in air increased cerebral blood flow, and this effect was also lower during severe hypoglycemia. The results show that insulin-induced hypoglycemia causes cerebral vasodilation and reduction of the capacity of cerebral blood vessels to constrict and dilate. They also show that the glycemic thresholds for increasing cerebral blood flow are near to, or slightly lower than, the thresholds for hypoglycemic symptoms. This experimental model of hypoglycemia closely resembles the conditions in hypoglycemic patients and permits serial evaluation of the cerebrovascular effects of hypoglycemia without using anesthesia.
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PMID:Effects of hypoglycemia on the cerebral circulation in awake goats. 131 45


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