Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:034761 (insulin)
 211,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in the concentration of blood glucose, fructose and galactose and their disappearance rate, concentration of plasma insulin, free fatty acids, blood lactate and pyruvate after intravenous glucose, fructose and galactose loads (1 g/kg) were studied in 23 infants of insulin treated diabetic mothers (IDM). The control group consisted of 42 infants of healthy mothers (IHM). The disappearance rate of these monosaccharides was higher in IDM that in IHM (P less than 0.01). All monosaccharides enhanced plasma insulin levels, but the plasma insulin concentration varied considerably. The highest insulin response with difference between IDM and IHM occurred after loading with glucose. Fructose was the least effective insulin stimulator which did not increase glucose levels. All monosaccharides decreased free fatty acid levels. Lactate levels and lactate:pyruvate ratio in IHM were increased after fructose loading. The results of this study suggest that galactose is of some physiological importance for maintaining glucose levels and that the islet apparatus of newborns of diabetic mothers is less loaded with galactose than with glucose.
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PMID:Plasma insulin, carbohydrate, and free fatty acid changes in newly born infants of diabetic and non-diabetic mothers after loading with glucose, fructose, and galactose. 15 32

Rates of incorporation of [4,5-(3)H]leucine into insulin plus proinsulin, designated ;(pro)insulin', and total protein in rat pancreatic islets were measured. Glucose stimulates rates of total protein and (pro)insulin biosynthesis, but (pro)insulin biosynthesis is stimulated preferentially. Mannose and N-acetylglucosamine also stimulate (pro)insulin and total protein biosynthesis; inosine and dihydroxyacetone stimulate (pro)insulin biosynthesis specifically. Fructose does not stimulate (pro)insulin biosynthesis when tested alone, but does so in the presence of low concentrations of glucose, mannose or N-acetylglucosamine. Many glucose analogues do not stimulate (pro)insulin biosynthesis. Mannoheptulose inhibits synthesis of (pro)insulin and total protein stimulated by glucose or mannose but not by dihydroxyacetone, inosine or N-acetylglucosamine; phloretin (9mum) inhibits N-acetylglucosamine-stimulated (pro)insulin biosynthesis preferentially. The data are in agreement with the view that the same glucose-sensor mechanism may control both insulin release and biosynthesis, and ;substrate-site' model is suggested. The threshold for stimulation of biosynthesis of (pro)insulin and total protein is lower than that found for glucose-stimulated insulin release; moreover the biosynthetic response to an elevation of glucose concentration is slower than that found for insulin release. The physiological implication of these findings is discussed. Caffeine and isobutylmethylxanthine, at concentrations known to increase islet 3':5'-cyclic AMP and potentiate glucose-induced insulin release, were without effect on rates of glucose-stimulated (pro)insulin biosynthesis.
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PMID:The effect of sugars on (pro)insulin biosynthesis. 36 Oct 36

Two regimens (A and B) for TPN were designed to meet the requirements of newborn infants for calories, amino acids, fatty acids, electrolytes, trace elements and vitamins. Both "A" and "B" included fat emulsion (Intralipid). "A" contained fructose and glucose, "B" glucose only. "A" provided amino acids (Vamin) in proportions similar to those of whole egg, "B" similar to those of human milk. All nutrients were given simultaneously into peripheral veins by constant infusion. Nineteen patients (11 newborns, 8 infants) were studied for 1-28 days. Twelve infants recovered, 7 died. In none could TPN be regarded as the cause of death. Treatment was complicated by sepsis in 5 infants. During the course of treatment, blood levels of substrates and insulin were measured before, during and 30 min after discontinuation of TPN. Highly raised concentrations of circulating substrates seen in 3 infants seemed to be related to a poor clinical condition rather than to the regimen used. Infants in good condition tolerated TPN well. Low levels of branch-chained amino acids and tendency to ketonemia, when infusion was stopped, suggested that minimal rather than optimal supply of energy and of amino acids in relation to energy was provided with both regimens. Low insulin levels associated with elevated blood levels of substrates suggested that insulin administration to selected cases might be indicated. Fructose (0.30 g/kg X hour-1) given with regimen A increased blood lactate concentrations. Homocystinaemia appeared in 2 cases; disappearance after excess vitamin B6 administration indicated increased B6 requirement.
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PMID:Total parenteral nutrition in infants. Blood levels of glucose, lactate, pyruvate, free fatty acids, glycerol, d-beta-hydroxybutyrate, triglycerides, free amino acids and insulin. 40 94

1. Chronic ethanol administration enhances rat brain 5-hydroxytryptamine synthesis by increasing the availability of circulating tryptophan to the brain. This increased availability is not insulin-mediated or lipolysis-dependent. 2. Under these conditions, tryptophan accumulates in the liver and apo-(tryptophan pyrrolase) activity is completely abolished, but could be restored by administration of regenerators of liver NAD+ and/or NADP+. 3. All four regenerators used (fructose, Methylene Blue, phenazine methosulphate and sodium pyruvate) prevented the ethanol-induced increase in liver tryptophan concentration and the increased availability of tryptophan to the brain. 4. It is suggested that the enhancement of brain tryptophan metabolism by chronic ethanol administration is caused by the decreased hepatic tryptophan pyrrolase activity. The results are briefly discussed in relation to previous work with ethanol. 5. Fructose enhances the conversion of tryptophan into 5-hydroxyindol-3-ylacetic acid in brains of ethanol-treated rats, whereas Methylene Blue inhibits this conversion in both control and ethanol-treated animals.
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PMID:Enhancement of rat brain tryptophan metabolism by chronic ethanol administration and possible involvement of decreased liver tryptophan pyrrolase activity. 45 65

Fasting blood glucose is elevated and the rate of disappearance of a glucose load is reduced after major surgery. Resistance to insulin is considered to play a part in post-traumatic glucose intolerance. Fructose metabolism is partly independent of insulin. Glucose and fructose clearance were compared in two groups of 6 matched male patients with normal glucose tolerance who were studied before and after major vascular surgical operations of the same severity. Fructose or glucose (25 g) was given intravenously over a 2-min period before, during and at intervals for 8 days after surgery. The rate of clearance of fructose increased significantly during operation (P less than 0.01), but returned to the preoperative level by the first postoperative day. Glucose clearance, in contrast, was reduced during and throughout the 8 days of the study. The fructose load produced a brisk insulin response before operation which was diminished and delayed during surgery. These findings suggest that administered fructose may be removed more rapidly than glucose during and immediately after surgical operation.
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PMID:The plasma clearance of fructose and glucose during and after surgical operation. 69 41

Glucose, fructose, sorbitol or xylitol were infused for four hours at different dose levels to metabolically healthy volunteers. The metabolic effects of the so-called glucose substitutes were compared to that of glucose. Even at very high doses (2.0 g/kg bodyweight per hour) of infusion of glucose or fructose a steady state was attained. This, however, was not the case with xylitol or sorbitol at lower doses (i.e. 0.5 g/kg bodyweight per hour), where no steady state was reached. The blood glucose concentration is not influenced by any of the glucose substitutes. During infusion of very high doses of fructose a small increase in serum insulin level is found, however, without any alteration in blood glucose concentration. Glucose as well as glucose substitutes cause an immediate suppression of free fatty acid concentrations in serum. In case of glucose there is a manifold increase in fatty acid concentration after the infusion is terminated. On the other hand, the free fatty acid concentration remains low even several hours following termination of the high-dosed fructose infusion. Theoretically one would expect an increase in triglyceride concentration, at least at the high dosed carbohydrate infusions. In contrast to this theoretical expectation, in the case of glucose and of xylitol a significant reduction of triglyceride concentration in serum was observed. Fructose and sorbitol did not exhibit this effect. Glucose and fructose are well utilized in metabolically healthy subjects. The maximum turnover rates for both polyols are lower. Unlike glucose, the glucose substitutes obviously do not cause any serious disturbation in hormonal regulations. Only in the case of glucose, counterregulation is seen following the termination of the infusion.
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PMID:[Comparison of side effects of infusion of glucose and glucose substitutes at different doses]. 73 96

Monosaccharides were intravenously injected to eight adult heads of cattle, between 380 kg and 670 kg in live weight, to study, in the context of stress endurance, the half-life values of the sugars as well as monosaccharide effects upon concentrations of various blood components. The fructose concentration in the blood plasma went up temporarily following the infusion of glucose solution. Fructose infusion usually caused only little rise of the glucose concentration in blood plasma, with hypoglycaemia occurring quite often towards the end of an experimental period. The half-life values of sugar in blood plasma were between twelve and 29 and those of fructose between ten and 17 minutes. The rate of fructose conversion was higher than that of glucose conversion, but values were identical in some cases. The pyruvate concentration in the blood and the insulin level in blood plasma went up in response to infusion of monosaccharide solutions. Urine excretion of monosaccharides following invert sugar infusion was less than half of that in response to glucose infusion.
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PMID:[Behavior of various blood constituents (glucose, fructose, insulin, lactate, pyruvate, free fatty acids, inorganic phosphate) and half-life of monosaccharides in the plasma after i.v. infusion of glucose, fructose, galactose and invert sugar solutions in ruminants. 2. Studies in cattle]. 73 16

Blood sugar, insulin, NEFA, triglycerides and cholesterol were evaluated in metabolically healthy subjects following oral glucose (100 g in 12 subjects), fructose (50 g in 9 subjects), and saccharose (100 g in 9 subjects). As shown in the literature, glucose led to a slight sugar increase at 60', a marked increase in insulin at 60', and a pronounced fall in NEFA at 120'. Fructose had no effect on sugar and NEFA, whereas there was significant and gradual rise in the insulin curve until 180' (P less than 0.01). In the case of saccharose, the changes in blood sugar, insulin and NEFA were slightly less evident than with glucose. No significant alterations in cholesterol and triglyceride levels were noted throughout the experiment.
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PMID:[Effects of oral glucose, fructose and saccharose loads on blood sugar, insulin and lipids in normal subjects]. 75 9

The effect of addition of different carbohydrates (starch, glucose, fructose) to the feed was investigated using the experimental animal. Additionally, the admixture of cholesterol and of cholesterol plus cholic acid was tested. Fructose (70% of the feed) causes a slight increase in serum triglyceride concentration and a very slight increase in triglyceride concentration in the liver. Fructose and to a lesser degree glucose cause an increase in pyruvate kinase activity in the liver. The activity of glucose-6-phosphate dehydrogenase is increased slightly following high-dosed glucose, whereas the increase is very pronounced following fuctose-rich feed. The admixture of cholesterol (with cholic acid) causes a decrease in glucose-6-phosphate dehydrogenase activity up to 70%. The activity of glutamate dehydrogenase is decreased also following cholesterol admixture. A fructose-rich diet causes a slight degree of hyperlipemia with a metabolic situation similar to a latent diabetic state. This effect is greatly intensified by the addition of cholesterol and cholic acid to the diet of the rats. Especially striking was the increase in serum-free-fatty-acid concentrations in all groups of animals. This is speculated to be a sign of insulin deficiency. The so-called "carbohydrate-induced hypertriglyceridemia" is obviously intensified within a short period by the admixture of cholesterol plus cholic acid to the experimental diet.
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PMID:[Effect of various dietary carbohydrates on supplementary cholesterol]. 89 66

Glucose and fructose were studied in eight healthy volunteers who fasted twice for 4 days. Before and after the fasts each subject received a 4-hr glucose or fructose infusion providing 0.5 g/kg/hr. Glucose infusion during starvation resulted in a mean maximal plasma glucose rise of 401 +/- 21 mg/100 ml (+/- SEM) as compared to 119 +/- 10 mg/100 ml before starvation. Insulin/glucose ratios were lower than normal in fasted subjects. Fructose infusion during fasting produced a maximal plasma glucose rise of 91 +/- 9 mg/100 ml as opposed to 5+/-1 mg/100 ml before starvation. During fructose infusion in the fasted state, plasma fructose levels were higher than control and the rise in blood lactate and pyruvate was delayed, but finally lactate concentrations were above control values. The antiketotic effects of intravenous glucose and fructose were similar during fasting but fructose was significantly less potent in reducing free fatty acid levels. After starvation, urinary carbohydrate losses during glucose infusion were 5 times higher than those observed during fructose infusion. Thus, fructose utillization was less impaired during fasting than was glucose utilization, although fasting induced abnormalities in both glucose and fructose metabolism.
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PMID:Comparison of glucose and fructose tolerance before and after starvation. 90 56


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