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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic effects of a new ketogenic regimen in which ketonemia is induced by feeding of medium chain triglycerides (MCT) are described, and comparisons are made with effects of the standard high fat ketogenic diet. Eighteen children maintained on the MCT diet for 3 months to 4 years failed to show elevations of serum cholesterol and had only a slight rise in serum total fatty acids, in contrast to the marked hyperlipidemia observed in children on the standard high fat diet. Long term use of the MCT diet did not affect pH of venous blood. Blood glucose fell below 50 mg/100 ml in one-third of the children, the lowest levels being reached 2--3 weeks after the start of the diet. Plasma D(--)-beta-hydroxybutyrate (BHB) and acetoacetate rose gradually after institution of diet therapy, maximum levels being reached after about 1 month. Higher levels of BHB and acetoacetate were achieved in children under the age of 10 years (BHB = 4.3 mM +/- 0.6 SEM, acetoacetate = 1.8 mM +/- 0.3 SEM) than in 10--18 year olds (BHB = 1.6 mM +/- 0.2 SEM, acetoacetate = 0.57 mM +/- 0.08 SEM). Plasma BHB and acetoacetate levels in children maintained on a 3:1 high fat diet were similar to those in children on a 60% MCT diet. Plasma levels of BHB showed a significant correlation with anticonvulsant effect (P less than 0.02). Both the ketonemia and the anticonvulsant action were reversed rapidly by intravenous infusion of glucose.
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PMID:Ketonemia and seizures: metabolic and anticonvulsant effects of two ketogenic diets in childhood epilepsy. 93 25

To determine whether abnormalities in glucagon secretion might precede the onset of hyperglycemia in diabetes mellitus, 32 prediabetic Pima (American) Indians, 27 normal Pima Indians and 34 normal Caucasians received an infusion of arginine monochloride (5 mg/kg/min for 40 minutes) with measurement of glucose, insulin, and glucagon. [Prediabetes is the period between conception and the development of diabetes. In most studies the term is used to characterize patients who on genetic grounds are believed to be at high risk of developing the disease, including the normoglycemic monozygotic co-twin of a diabetic or the normoglycemic offspring of two diabetic parents. The latter definition is used in the present study recognizing that in the final analysis the true prediabetic can be identified only in retrospect after the development of diabetes.] The three groups had similar mean fasting glucagon levels. During arginine infusion, the prediabetic Indians reached a mean maximum glucagon level of 315 +/- 14 pg/ml (mean +/- 1 SEM) compared with 294 +/- 20 pg/ml in the normal Indians and 292 +/- 25 pg/ml in the normal Caucasians. The calculated mean areas above baseline under the glucagon curves were 5704 +/- 324 pg-min/ml in the prediabetics, 5189 +/- 446 pg-min/ml in the normal Indians, and 4239 +/- 613 pg/min/ml in the normal Caucasians. The differences among the groups in these variables were not statistically significant. Thus, arginine induced hyperglucagonemia could not be identified as a characteristic of the prediabetic state in Pima Indians.
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PMID:Normal glucagon response to arginine infusion in "prediabetic" Pima Indians. 95 Mar 63

Using a method for measuring changes in transmural potential difference across the human jejunum in vivo, the operational kinetic parameters of 'Apparent Km' and PD max for the active electrogenic component of glucose absorption were estimated in a group of healthy volunteers and in patients with coeliac disease. Both the 'Apparent Km' (17+/2mM; mean +/SEM) and the PD max (8.6+/0.7 mV) in nine patients with untreated coeliac disease were significantly lower (p less than 0.005) than in the control group ('Apparent Km' = 74+/5mM; PD max 12.8+/0.9mV, n=20). Treatment of five coeliac patients by gluten withdrawal for less than three months increased significantly the values of both the "Apparent Km (35+/6mM) and the TPD max (11.4+/1.2mV). Treatment of five patients for more than six months caused a further increase in the values of both kinetic parameters ('Apparent Km' = 108+/13mM; PD max =15.6+/2.7mV) to levels which exceeded those in healthy subjects. The possible interpretations of the differences in the kinetic characteristics of electrogenic glucose transport between coeliac patients and healthy subjects are discussed.
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PMID:Electrogenic glucose absorption in untreated and treated coeliac disease. 95 1

Fifteen red cell enzyme activities of growth-retarded patients with and without growth hormone (GH) deficiency were investigated before and after GH administration. The 15 enzymes were Hexokinase, phosphoglucomutase, glucose phosphate, isomerase, phosphofructokinase, fructose diphosphate aldolase, glyceraldehyde-3-phosphae dehydrogenase, triosephosphate isomerase, 2,3-diphosphoglycerate mutase, 3-phosphoglycerate kinase, 3-phosphoglycerate mutase, enolase, pyruvate kinase, glycose-6-phosphate dehydrogenase, 6-phosphogluconic dehydrogenase, glutathione reducase. Sixty-six subjects were studied: 30 normal control subjects (group N) and 36 patients (aged 5-23 years) with short stature. Complete endocrine evaluation showed 21 (group I) to have GH deficiency (10 patients with isolated GH deficiency) and 15 (group II) to have normal hypothalamic and pituitary function except for two patients with a moderate hypothyroidism. Both had been receiving thyroid hormone treatment for a long time before our studies. All 36 patients were treated with 2 mg human growth hormone intramuscularly for 7 days. Before GH treatment no significant difference was observed between hematologic data in group I (GH deficiency) and group II (no GH deficiency). After GH therapy there was a significant increase in reticulocyte count in both groups of patients with short stature. The mean pretreatment value in group I was 1.294% +/- 0.084 (SEM); the mean post-treatment value was 2.081% +/- 0.287 (SEM)< P less than 0.005. The mean pretreatment value in group II was 1.0% 0.184 (SEM); the mean post-treatment value was 1.407% +/- 0.193 (SEM), P less than 0.01. In group II (no GH deficiency) mean pretreatment erythrocyte enzyme activities were not significantly different from those activities observed in normal control subjects (group N). However, in patients who lacked GH, the pretreatment activities of five red cell enzymes (glucose phosphate isomerase, triosephosphate isomerase, glyceraldehyde-3-phosphate dehydrogenase, 2,3-diphosphoglycerate mutase, 3-phosphoglycerate kinase) were significantly decreased before GH administration compared with the values in normal control subjects...
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PMID:Action of growth hormone on erythropoiesis: changes in red blood cell enzyme activities in growth-retarded patients with and without growth hormone deficiency. 95 53

Cerebral blood flow (CBF) was measured by means of Celabeled microspheres in infant (20-day-old) and adult (3-month-old) rats, anesthetised with Na-5-ethyl-5-(1-methylpropyl)2-thiobarbituric acid. Cerebral arteriovenous differences of acetoacetate, D-beta-hydroxybutyrate, glucose, lactate, and oxygen and brain DNA content were determined in other groups of similarly treated infant and adult animals fed or starved for 48 or 72 hr. The mean CBF values of 0.48+/-0.04 and 0.62+/-0.07 ml/(g X min), +/- SEM, in infant and adult animals, respectively, were not significantly different. CBF was unaffected by starvation. At any given arterial concentration the cerebral arteriovenous difference of acetoacetate was significantly higher in infant than adult rats. The same was true for D-beta-hydroxybutyrate at arterial concentrations above 1 mmol/liter. There was an approximately linear relationship between arterial concentration of acetoacetate and its cerebral arteriovenous difference in both infant and adult rats. A similar relationship was found for D-beta-hydroxybutyrate only in infant animals. In the fed state, the cerebral uptake of glucose and ketone bodies (micromoles per (mg DNA X min)) was not different in infant and adult rats. During starvation, cerebral uptake of ketone bodies expressed as micromoles per (mg DNA X min) was higher in infant than adult rats, indicating a higher rate of utilization of ketone bodies per cell in these animals. For glucose, no such difference was found in either fed or starved groups (Table 3). The average percentage of the total cerebral uptake of substrates (micromoles per min) accounted for by ketone bodies increased in both infant and adult rats during starvation. This percentage value was clearly higher in infant than adult rats during starvation. After 72 hr of starvation the values were 38.8% and 15.2% in infant and adult rats, respectively (Fig. 3). Calculated cerebral metabolic rate for oxygen (CMRO2), assuming complete oxidation of glucose and ketone bodies and expressed as micromoles per (mg DNA X min), was similar in fed and starved rats of both age groups (Table 3), indicating that ketone bodies serve as an alternative substrate for glucose during starvation. Calculated CMRO2 for glucose plus ketone bodies was similar to the measured CMRO2 in adult rats both in the fed and the starved groups. For infant rats, calculated CMRO2 for glucose plus ketone bodies was higher than measured CMRO2, indicating that in this age group a portion of substrate was used for synthesis or storage rather than for complete oxidation.
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PMID:The rate of cerebral utilization of glucose, ketone bodies, and oxygen: a comparative in vivo study of infant and adult rats. 98 May 50

The effects of carbohydrate (CHO) restriction on the hypoglycemic phase of the glucose tolerance test were studied in ten normal subjects. The mean nadir plasma glucose was 64 +/- 4 mg/dl (x +/- SEM) for the control test, and 48 +/- 4 mg/dl (P less than 0.01) after 3 days of an isocaloric low CHO diet. Following the low CHO diet, six of ten subjects had a nadir plasma glucose less than 50 mg/dl, and five of these six had mild symptoms of hypoglycemia compared to no biochemical or symptomatic hypoglycemia during the control test. Hormone secretory patterns under the two experimental conditions were measured. CHO restriction produced a significant decrease in early insulin release followed by excessive insulin relative to the control test at 3-4 h of the test. Glucose ingestion produced a depression of plasma, glucagon from fasting levels during the control test, which was impaired following CHO restriction. Plasma growth hormone and cortisol responses were not different under the two experimental conditions. These studies demonstrate that CHO restriction followed by concentrated CHO ingestion produces hypoglycemia in normals. They emphasize the need to consider dietary history in evaluation of hypoglycemia. CHO restriction may provide a useful model for further study of the mechanisms of hypoglycemia.
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PMID:Effects of carbohydrate restriction on the hypoglycemic phase of the glucose tolerance test. 99 13

Maize glucose was used as a natural tracer for studies of metabolism. It is richer in 13C than common vegetables and foods derived from these, and the C02 formed from it is consequently richer in 13C than the CO2 expired by man fed on a diet of common vegetables. The quantitative results, obtained by measurement of delta 13C of the expired CO2 and of VCO2 during the oxidation of an exogenous glucose load (about 100 g) in eight normal subjects over 7 hr, have shown a consumption of 28.64 +/- 1.44 g of glucose (mean +/- SEM), which represents about 30% of the load given. A comparison is made with the results obtained from other methods and the originality and usefulness of this new quantitative procedure is outlined.
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PMID:Quantitative evaluation of the oxidation of an exogenous glucose load using naturally labeled 13C-glucose. 99 39

An experimental model of clinical liver failure, using total devascularization of the liver is described in the pit. The survival time was 1495 +/- 75 (SEM) minutes. Clinically the pigs showed a uniform course. They became lethargic after eight to ten hours and following a period of increasing drowsiness they became comatose. The immediate cause of death was cardio-vasculary collaps. The ammonium ion concentration in the blood increased to 696 +/- 57 umol/l and in cerebrospinal fluid to 664 +/- 57 umol/l. Cerebrospinal fluid glucose concentration was significantly decreased.
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PMID:Total devascularization of the Liver: an experimental model of acute liver failure. 106 34

UO22+ 1.3 mM added as UO2(NO3)2 to the mucosal solution consistently inhibited the P.D. and ISC evoked by 11 mM glucose and 35 mM 3-O-methyl glucose across isolated strips of bullfrog small intestine bathed by symmetrical Ringer solutions in which SO42- was the major anion. The average degree of inhibition in the presence of glucose was 42 +/- 7(SEM) percent. P.D. and ISC in the absence of transported solutes were not significatnly altered by mucosal UO22+ at this concentration. Increasing the mucosal UO22+ concentration to 2.6 mM did not significantly increase its inhibitory action on glucose-evoked P.D. and ISC. Further increasing the UO22+ concentration to 13 mM completely inhibited glucose-induced P.D. and ISC but also markedly reduced these parameters in the absence of glucose. Serosal UO22+ (1.3mM) had no effect on the P.D. and ISC evoked by glucose and 3-O-methyl glucose. It is suggested that the inhibitory action of UO22+ involves binding of this ion to anionic sites located in the apical membrane of the absorptive cells. Mucosal or serosal UO22+ (1.3 mM) had no effect on the P.D. and ISC elicited by 20 mM valine, indicating that under the conditions of these experiments UO22+ selectively inhibits sugar-induced P.D. and ISC and, by implication mucosal sugar uptake.
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PMID:Sugar-induced potential difference and short circuit current in bullfrog small intestine: effect of UO22+. 108 34

Using an in vitro rabbit pancreas system, we studied the effect of monoamine oxidase (MAO) inhibitors on flucose-stimulated insulin secretion. We evaluated the effect of both brief (15 min) and prolonged (60 min) exposure of pancreas segments to non-hydrazine (harmine, alpha-methyltryptamine, tranylcypromine and pargyline) and hydrazine (phenelzine, nialamide, iproniazid) type MAO inhibitors. All of the hydrazine type MAO inhibitors potentiated glucose-stimulated insulin secretion. Of the non-hydrazine inhibitors, only harmine and alpha-methyltryptamine potentiated glucose-stimulated insulin secretion. Hydrazine, although not itself an MAO inhibitor, also potentiated insulin secretion. Sixty minutes of exposure to tranylcypromine or alpha-methyltryptamine caused a decrease in insulin secretion. These MAO inhibitors are primary amines and primary amines can inhibit insulin secretion. The dopamine (DA) or serotonin (5-HT) content of the B-cells was increased by incubating rabbit pancreas with L-3, 4-dihydroxyphenylalanine (L-Dopa) or 5-hydroxytryptophan (5-HTP) for forty-five minutes prior to stimulation with glucose. Non-hydrazine MAO inhibitors increased dopamine inhibition of insulin secretion and either did not alter, or decreased serotonin inhibition of insulin secretion. Rabbit pancreatic islets were isolated using the collagenase digestion technique. The MAO activity of islet homogenates was determined using 5-HT and DA as substrates. Rabbit islet MAO has only one-tenth the specific activity against 5-HT (35 +/- 8.7 mumumoles/mg/min, M +/- SEM) that it has against DA (357 +/- 62.3 mumumoles/mg/min). This suggests that one reason that MAT inhibitors do not increase serotonin inhibition of insulin secretion is because MAO is not the major pathway for 5-HT inactivation in rabbit pancreatic islets. These studies suggest that MAO inhibitors alter insulin secretion, by both decreasing B-cell monoamine degradation and by mechanisms that do not involve MAO inhibition.
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PMID:Monoamine oxidase inhibitors: nature of their interaction with rabbit pancreatic islets to alter insluin secretion. 110 23


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