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

The intravenous infusion of glucose was found to alter profoundly the response of insulin and glucagon to an intraduodenally administered fat meal in conscious dogs from that of dogs given only intravenous saline as a control. In the latter, insulin rose only 4 muu/ml and glucagon rose from 142 SEM plus or minus 8 to a peak of 221 pg/ml SEM plus or minus 50. When glucose was infused, raising plasma glucose above 173 mg/100 ml, the administration of fat was associated with a rise in mean insulin to 344 muu/ml, and glucagon remained suppressed by hyperglycemia to below baseline level, despite the fat meal. The peak insulin response to a fat meal plus glucose infusion was more than three times the peak level observed when glucose was infused alone without a meal or with a nonabsorbable intraduodenal volume load in the form of mineral oil. This suggests that the absorption of fat elicits an entero-insular signal that is greatly potentiated by exogenous glucose. These glucose-induced changes in the hormonal response to a fat meal may mediate certain of the metabolic effects of carbohydrates.
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PMID:Effect of intravenously administered glucose on glucagon and insulin secretion during fat absorption. 111 Jun 26

The isolated brains of 12 previable human fetuses obtained at 12 to 21 weeks' gestation, were perfused through the interval carotid artery with glucose (3 mM) and/or DL-B-OH-butyrate (DL-BOHB), 4.5 MM, plus tracer quantities of either glucose-6-14C (G6-14C) or beta-OH-butyrate-3-14C (BOHB3-14C). Oxidative metabolism was demonstrated by serial collection of gaseous 14CO2 from the closed perfusion system, and from the recirculating medium. Glucose and BOHB were utilized at physiological rates as indicated (mean plus or minus SEM): G6-14C at 0.10 plus or minus 0.01 mumoles/min g brain (n equal 7) or 17.5 plus or minus 1.9 mumoles/min kg fetus; and BOHB3-14C at 0.16 plus or minus 0.05 mumoles/min g (n equal to 5) or 27.3 plus or minus 7.4 mumoles/min kg. Based on fetal weight, glucose metabolism by brain apparently accounted for about 1/3 of basal glucose utilization in the fetus. On a molar basis BOHB3-14C was taken up at 1.47 times the rate of G6-14C. Both BOHB3-14C and G6 14C were converted to 14CO2. The rate of BOHB3-14C conversion to 14CO2 was equal to its rate of consumption, and exceeded the conversion of glucose to CO2 because 45% of the G6-14C was incorporated into lactate-14C. Accordingly, both substrates support oxidative metabolism by brain; and BOHB is a major potential alternate fuel which can replace glucose early in human development.
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PMID:Oxidation of glucose and D-B-OH-butyrate by the early human fetal brain. 111 94

Whole blood was stored at 4 degrees C for 42 days. At 7-day intervals, starting with day 21, aliquots were rejuvenated with a phosphate, inosine, glucose pyruvate, and adenine solution. Samples were taken for ATP assays and red cell morphology (by SEM) both before and after rejuvenation. Rejuvenation elevated all ATP levels in excess of 100% of the starting values and significantly increased the percent of cells in the discoid shape as measured by their morphological index, showing that rejuvenation not only raises the cell's metabolic level but causes partial reversion to fresh cell morphology.
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PMID:Morphology of stored, rejuvenated human erythrocytes. 111 31

The effects of insulin on the renal handling of sodium, potassium, calcium, and phosphate were studied in man while maintaining the blood glucose concentration at the fasting level by negative feedback servocontrol of a variable glucose infusion. In studies on six water-loaded normal subjects in a steady state of water diuresis, insulin was administered i.v. to raise the plasma insulin concentration to between 98 and 193 muU/ml and infused at a constant rate of 2 mU/kg body weight per min over a total period of 120 min. The blood glucose concentration was not significantly altered, and there was no change in the filtered load of glucose; glomerular filtration rate (CIN) and renal plasma flow (CPAH) were unchanged. Urinary sodium excretion (UNaV) decreased from 401 plus or minus 46 (SEM) to 213 plus or minus 18 mueq/min during insulin administration, the change becoming significant (P smaller than 0.02) within the 30-60 min collection period. Free water clearance (CH2O) increased from 10.6 plus or minus 0.6 to 13 plus or minus 0.5 ml/min (P smaller than 0.025); osmolar clearance decreased and urine flow was unchanged. There was no change in plasma aldosterone concentration, which was low throughout the studies, and a slight reduction was observed in plasma glucagon concentration. Urinary potassium (UKV) and phosphate (UPV) excretion were also both decreased during insulin administration; UKV decreased from 66 plus or minus 9 to 21 plus or minus 1 mueq/min (P smaller than 0.005), and tupv decreased from 504 plus or minus 93 to 230 plus or minus 43 mug/min (P smaller than 0.01). The change in UKV was associated with a significant reduction in plasma potassium concentration. There was also a statistically significant but small reduction in plasma phosphate concentration which was not considered sufficient alone to account for the large reduction in UPV. Urinary calcium excretion (UCaV) increased from 126 plus or minus 24 to 200 plus or minus 17 mug/min (P smaller than 0.01). These studies demonstrate a reduction in UNaV associated with insulin administration that occurs in the absence of changes in the filtered load of glucose, glomerular filtration rate, renal blood flow, and plasma aldosterone concentration. The effect of insulin on CH2O suggests that insulin's effect on sodium excretion is due to enhancement of sodium reabsorption in the diluting segment of the distal nephron.
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PMID:The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man. 112 Jul 86

Four healthy adult subjects received intravenous tolbutamide (TOL) at six different doses (twenty-four tests): 0.0625 gm., 0.125 gm., 0.25 gm., 0.5 gm., 1.0 gm. and 1.5 gm. Blood glucose (BG), serum immunoreacctive insulin (IRI) and serum TOL levels were determined before and for 180 minutes after TOL. There was a highly significant correlation of the dose of TOL with the peak IRI (p less than .01), zero to ten minute IRI area (p less than .001), and zero to sixty minute IRI area (p less than .001) and with the decline in BG expressed as zero to sixty minute BG area (p less than .001). Similar significant correlations were observed between levels of TOL and both IRI and BG. At each dose level the IRI response correlated significantly with the BG fall. An additional eighteen subjects received the 1.0 gm. dose. In these, serum TOL levels did not correlate with either BG or IRI. These subjects also received intravenous glucose (0.5 gm. per kilogram body weight). BG levels did not correlate with IRI. However, there were striking correlations between TOL and glucose-stimulated peak IRI (p less than .001), zero to ten minute IRI area (p less than .05). The mean (plus or minus SEM) space of distribution for glucose (G.S.) and tolbutamide (TLS.) was found to be 13.45 plus or minus 0.71 and 6.34 plus or minus 0.31 L., respectively. There was a significant dose-response relationship exists between TOL and IRI. TOL- and glucose-induced IRI secretion dynamics suggest strong similarities between mechanisms of rapid IRI release and/or size of available IRI storage pools.
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PMID:Dynamics of tolbutamide, glucose, and insulin interrelationships following varying doses of intravenous tolbutamide in normal subjects. 113 1

Since chronic pentagastrin stimulates pancreatic and proximal duodenal growth (15), we studied jejunal structure and function following subcutaneous pentagastrin (2 mg-100 g-1 day-1). After 15 days, macroscopic enlargement was confined to the proximal duodenum with a significant increase in wet weight (from 231 +/- SEM 6 to 308 +/- 13 mg) but there was no significant difference in wet and defatted dry intestinal weights, histological measurements of villous height and mucosal thickness or in glucose absorption per unit length of distal duodenum and proximal jejunum. Since chronic pentagastrin causes parietal cell hyperplasia and hypersecretion of gastric acid, the results suggest that the adaptive changes seen in the jejunum after ileectomy are neither mediated by gastrin nor by factors present in gastric secretions.
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PMID:Effect of pentagastrin on small bowel structure and function in the rat. 115 69

Treatment with oral prednisone (15 mg every 6 h) for 1 day plus a 4-h glucose infusion at 2.8 mg/min kg body weight to 5 normal, healthy individuals raised their blood glucose to 137 +/- 4.5 mg per 100 ml (mean +/- SEM). In order to evaluate the effects of steroid-induced hyperglycemia on insulin responses, a model for the duplication of blood glucose concentration in serial studies was developed. During glucose infusion at 5.7 mg/min kg body weight, the fractional uptake of glucose at the end of infusion (KG) was 2.08 +/- 0.2%/min and the apparent volume of distribution (V) was 285 +/- 10.5 ml/kg. Further increase in the rate of glucose infusion did not affect KG and V. Based on these parameters, KG and V, the stable blood glucose achieved during the prednisone study (C) was duplicated both after short (4 h) and prolonged (28 h) glucose infusions (138 +/- 4.5 and 146 +/- 4.5 mg/100 ml, respectively) at rates calculated as the product of KG.C.V. The effects of prednisone treatment on insulin secretion were examined (1) during fasting, (2) at identical glucose concentrations during glucose infusions at constant rates, and (3) in response to glucose pulse (0.1 g/kg) during the infusions. During fasting, there was a significant elevation of mean blood glucose with prednisone (99 +/- 1.8 mg/100 ml) compared with that in the control study (88 +/- 1.7 mg/100 ml). The plasma IRI, however, remained unchanged (10 +/- 2.3 vs 10 +/- 1.6 muU/ml). During glucose infusions in the presence of similar blood glucose levels, the IRI was lower after prednisone treatment (18 +/- 1.5 muU/ml) than during the short and prolonged glucose infusions (42 +/- 5.1 and 63 +/- 7.0 muU/ml). The insulin response to the glucose pulse also was significantly lower during steroid treatment. Thus, prednisone apparently has an early inhibitory effect on the insulin response to glucose.
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PMID:Inhibitory effect of prednisone on insulin secretion in man: model for duplication of blood glucose concentration. 115 64

Plasma glucose, glucagon, and insulin responses to oral feedings of L-alanine were assessed in 44 healthy term infants during the first three days of life. Alanine administration produced significant increases in glucagon and glucose concentrations on day 1, but not on days 2 and 3. These increases occurred within 30 minutes (mean and SEM for glucagon, 127 plus or minus 7 to 219 plus or minus 16 pg/ml, P smaller than 0.001; glucose, 45 plus or minus 3 to 60 plus or minus 7 mg/100 ml, P smaller than 0.01) and persisted at the P smaller than 0.05 level at four hours. Responsiveness to alanine seemed to be related to the baseline blood glucose levels since constant infusions of glucose inhibited the response; These results indicate that the pancreatic islet alpha cell secretion mechanism(s) is functioning in the newborn.
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PMID:The effect of oral alanine on blood glucose and glucagon in the human newborn infant. 116 64

Umbilical blood flow (UBF) and fetal glucose uptake were measured in 5 lamb fetuses 4-20 days following single umbilical artery ligation (SUAL). The ligation was performed at 108-119 days gestation (sheep pregnancy = 145-150 days), and the blood flow and glucose uptake studies were performed as chronic preparation at 120-137 days of gestation. In comparison with 9 control subjects at matched gestation, the SUAL fetuses had significantly lower UBF (mean plus or minus SEM, 735 plus or minus 70 vs. 475 plus or minus 24 ml/min, p less than 0.01) and fetal glucose uptake (2190 plus or minus 1.6 vs. 14.8 plus or minus 1.9 mg/min, p less than 0.05). When the values were expressed per kilogram fetal weight, the UBF decreased with increasing gestational age in SUAL fetuses. In the control fetuses, the UBF increased with increasing gestational age. The fetal glucose uptake (FGU), when expressed per kilogram fetal weight, was essentially similar to that of the control subjects. The glucose gradients across the placenta were similar in both groups of fetuses. These data suggest that in lamb fetuses with placental vascular insufficiency induced by SUAL, the reduction of UBF and FGU may account for growth retardation in utero. It was also suggested that placental transfer of substrate other than glucose may also be impaired as a result o
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PMID:Umbilical blood flow and glucose uptake in lamb fetus following single umbilical artery ligation. 116 79

The effects of somatostatin on GLI release during the absorption of intraduodenally administered glucose, casein hydrolysate and longchain triglycerides were studied in conscious dogs. Whereas, after an intraduodenal glucose load, GLI rose promptly in saline-infused control experiments to a peak of 5 ng/ml (SEM +/- 4) in 60 minutes, significantly lower values were observed during somatostatin infusion (P less than 0.025 -- 0.05). A similar reduction in the magnitude of the GLI response to intraduodenally administered casein hydrolysate (P less than 0.05) and fat (p less than 0.05) was observed.
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PMID:The effect of somatostatin on the response of GLI to the intraduodenal administration of glucose, protein, and fat. 118 67


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