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Biomedical subjects

S C Kalhan

Publications and source records attributed to S C Kalhan.

At least 109 records · Page 6Linked to original sources
PubMed1983

Glucose metabolism in chronic renal failure: adaptive responses to continuous glucose infusion.

The systemic response to a glucose infusion at 2.7 mg/kg X min was evaluated in 10 undialyzed chronically uremic patients and in 5 controls after they were fasted overnight. Systemic glucose production (Ra) was measured during the steady state using [6,6-2H2]-glucose tracer. In chronic uremic subjects, basal Ra was 1.99 +/- 0.35 ml/kg X min (mean +/- SD) and was not different from that observed in the control subjects (1.86 +/- 0.23). Basal plasma insulin and betahydroxybutyrate concentrations were significantly increased (P less than 0.01) in the uremic group. Glucose infusion resulted in complete suppression of Ra (97%) in the normal subjects. Suppression of Ra in the uremic subjects was virtually complete with the exception of 3 patients who suppressed systemic glucose production by 70%, 79%, and 87%. Glucose utilization (Ru) during glucose infusion rose from the basal state to a plateau level within the 2 hours following the start of infusion and was of the same magnitude in the uremic group as it was in the control group. During the 3rd and the 4th hour of glucose infusion, there was further increase in Ru in the normal subjects, resulting in a decrease in plasma glucose concentration. Only 4 out of 10 uremic subjects showed a similar response. There was no correlation between the metabolic changes noted and the serum creatinine concentration. These data indicate that in chronic uremia, resistance to insulin action in the peripheral tissues is present but is variable, suggesting a spectrum of metabolic disturbances unrelated to the degree of chronic renal failure.

Adolescent↗
PubMed1982

Identifying the pregnancy at risk for intrauterine growth retardation: possible usefulness of the intravenous glucose tolerance test.

Antenatal detection of intrauterine growth retardation (IUGR) remains problematic. Previous animal and human studies have documented a relationship between increased substrate delivery to the fetus, e.g., in diabetes mellitus, and the birth of large-for-gestational age infants. The purpose of the study of 55 pregnancies, in which intravenous glucose tolerance tests (IVGTTs) were performed during the third trimester, was to examine the hypothesis that evidence of decreased availability of substrates for fetal growth precedes the birth of small-for-gestational age (SGA) infants; hence, the IVGTT might be useful for the detection of pregnancies complicated by IUGR. Increased glucose utilization rates (kt) and 10-minute plasma glucose concentrations and decreased plasma glucose concentrations at fasting and 60 minutes were found to be significantly associated with decreased infant birth weight, adjusted for gestational age. The Kt and 10- and 60-minute glucose values together could account for 40% of the variance in age-adjusted birth weight (r = 0.63, p less than 0.01). The IVGTTs in the pregnancies resulting in the birth of SGA infants were characterized by kt greater than 2 and plasma glucose levels at fasting of less than 64 mg/dl, at 10 minutes of greater than 193 mg/dl, and at 60 minutes of less than 82 mg/dl. When the kt was greater than 2, six (30%) of 20 infants were SGA; when the kt was less than or equal to 2, none (0%) of the 35 infants was SGA. These results suggest that, regardless of the underlying reason for the association, parameters of maternal glucose metabolism may be useful in detecting the pregnancy at risk for IUGR.

Evaluation Studies as Topic↗
PubMed1982

Regulation of glucose production in newborn infants of diabetic mothers.

The glucose homeostasis in the infants of normal and diabetic mothers was elevated by examining the effects of exogenous glucose infusion at 4 mg/kg . min and quantifying the rats of glucose production and utilization. Five infants of insulin-dependent diabetic mothers (IDM), one infant of a gestationally diabetic mother and five infants of normal mothers were studied between 2-4 h of age. The rates of glucose production and utilization before and during glucose infusion were quantified by tracer dilution technique using [6,62H2] glucose tracer and gas chromatography-mass spectrometry. Fractional glucose uptake (Kt) was measured at the end of infusion by administering 0.5 g/kg glucose pulse. All diabetic women were under rigid metabolic control during pregnancy. Although basal plasma glucose levels at e 2-4 h were lower in the IDMs as compared with normal newborns (43.4 +/- 3.7 and 65.2 +/- 3.6 mg/dl, mean +/- S.E., respectively), the glucose production and utilization rates were not significantly different (3.35 +/- 0.26 and 3.39 +/- 0.08 mg/kg . min); therefore, the metabolic clearance rates were higher inthe IDMs (7.69 +/- 0.41 ml/kg . min) as compared with the normal newborn infant (5.20 +/- 0.20 ml/kg . min). Glucose infusion resulted in a greater suppression of endogenous glucose production rate in the normal newborn infants than in the IDMs. Glucose infusion resulted in an acceleration of Kt in the normals (2.38 +/- 0.25%/min). We conclude that rigid regulation of maternal diabetes normalizes glucose production rate in IDM; however, intermittent maternal hyperglycemia may result in altered regulation of hepatic glucose production.

Blood Glucose↗
PubMed1981

The effect of enteric galactose on neonatal canine carbohydrate metabolism.

Newborn pups were assigned to a fasting group or to a group receiving intravenous glucose alimentation. Glucose turnover was determined during steady state equilibration of simultaneously infused [6-3H] glucose. Thereafter, pups from each group received 0.625 g/Kg of either oral [U-14C] galactose or [U-14C] glucose. In fasted or intravenously alimented pups enteric glucose resulted in a rapid and sustained elevation of blood glucose concentrations. Systemic appearance of carbon-14 label from enteric glucose increased rapidly as did the enrichment of blood [14C] glucose specific activity. In those pups given enteric galactose, blood glucose values were equivalent to that in the glucose fed groups, however carbon-14 appearing in blood glucose and blood glucose specific activity was significantly lower. The peak values for rates of appearance and disappearance of systemic glucose were significantly lower in pups fed galactose than among pups fed glucose. Glucose clearance was also significantly lower in these pups despite equivalent plasma insulin responses. Among fasting pups hepatic glycogen content was significantly higher in those given either oral glucose or galactose when compared to a completely starved control group. In contrast, among alimented pups galactose administration significantly enhanced hepatic glycogen content compared to those fed glucose. Similarly, enteric substrate label incorporation into hepatic glycogen was enhanced in both groups given oral labeled galactose. In addition, hepatic glycogen synthase (glucose-6-phosphate independent) activity was increased only among alimented pups fed galactose when compared to completely fasted pups. In conclusion these data suggest that following gastrointestinal galactose administration, hepatic carbohydrate uptake is augmented while glycogen synthesis may be enhanced. Augmented glycogen synthesis following galactose administration may reflect alterations in hepatic glycogen synthase activity or enhanced hepatic carbohydrate uptake.

Animals↗
PubMed1981

A rapid, simple, and sensitive procedure for the determination of free fatty acids in plasma using glass capillary column gas-liquid chromatography.

A rapid and sensitive method for the analysis of plasma free fatty acids with glass capillary column gas-liquid chromatography and flame ionization detection is described. The plasma sample, together with n-pentadecanoic acid as an internal standard, was treated with 2,2-dimethoxypropane and hydrochloric acid. 2,2-Dimethoxypropane serves as water scavenger, deproteinizing agent, and as a methylating agent. Under the assay conditions, only free fatty acids were converted to their methyl esters; esterified fatty acids, such as those in triglycerides and phospholipids, were not significantly transmethylated. This advantage eliminated the need for thin-layer chromatography for the separation of free and esterified fatty acids. The methyl esters of fatty acids were then extracted into isooctane and analyzed with a 10-meter glass capillary column coated with SP-2100. Splitless mode of injection was used to increase the sensitivity. Only 20 microliter or less of plasma was required for analysis. The coefficient of variation was 4.6%, which was better than the conventional gas-liquid chromatographic methods. These latter methods require 20 to 50 times larger samples, as compared with the present assay. This method is suitable for the measurement of both total free fatty acids and individual fatty acid patterns in small plasma samples.

Adult↗
PubMed1980

Estimation of glucose turnover and 13C recycling in the human newborn by simultaneous [1-13C]glucose and [6,6-1H2]glucose tracers.

To compare two methods of estimating systemic glucose production rates and to quantify carbon tracer recycling, six newborn infants, aged 2 h to 3 days, were infused simultaneously with [1-13C]glucose and [6,6-2H2]glucose tracers. The older infants were studied 6 h after a meal. [1-13C]Glucose was infused at 6 microgram/kg.min. Systemic glucose production rates were calculated from tracer dilution, assuming steady state kinetics. Although 13C was expected to randomize away from the C-1 of glucose, recycling occurred and was estimated from the difference in the rate of systemic glucose production quantified by the dilution of the two tracers. Systemic glucose production rates ranged from 4.2--5.4 mg/kg.min. Recycling on the glucose C-1 was 3--20% of the systemic glucose production rate and did not change with the age of the infant. Because recycling of glucose carbon signifies gluconeogenesis from lactate or pyruvate, it is concluded that the human newborn is able to initiate gluconeogenesis soon after birth.

Blood Glucose↗
PubMed1979

Glucose production in pregnant women at term gestation. Sources of glucose for human fetus.

The effects of pregnancy and diabetes on systemic glucose production rates and the sources of glucose for the human fetus in utero were evaluated in five normal, four gestationally diabetic, and one insulin-dependent diabetic subject undergoing elective caesarean section at term gestation. Five normal nonpregnant women were studied for comparison. Systemic glucose production rates were measured with stable tracer [1-(13)C]glucose according to the prime-constant rate infusion technique. Even though the plasma glucose concentration during normal pregnancy had declined as compared with the nonpregnant subjects (P < 0.0005), the systemic glucose production rate was 16% greater, a rate sufficient to provide the glucose requirement of the fetus at term gestation. The decline in glucose concentration could be the result of an increase in apparent volume of distribution of glucose. Systemic glucose production rates in well-controlled, gestationally diabetic subjects were similar to those in normal pregnant subjects (2.07+/-0.53 vs. 2.42+/-0.51 mg/kg.min). The sources of glucose for the human fetus at term gestation were evaluated by comparing (a) natural variation in (13)C:(12)C ratio of plasma glucose and (b) enriched (13)C:(12)C ratio of plasma glucose during [1-(13)C]glucose infusion in maternal and fetal blood at delivery in both normal and diabetic subjects. These data showed that the fetal glucose pool was in equilibrium with the maternal glucose pool in both normal and diabetic subjects, indicating that a brief maternal fast did not initiate systemic glucose production in human fetus. A materno-fetal gradient was observed for betahydroxybutyrate.

Adolescent↗
PubMed1977

Estimation of glucose turnover with stable tracer glucose-1-13C.

Glucose turnover was measured in normal and disbetic dogs by the dilution of glucose-1-13C and glucose-1-14C tracers infused simultaneously at constant rates. In order to quantify the stable isotope, an enzymatic assay for the analysis of glucose-1-13C was developed and evaluated. CO2 from C-1 glucose was evolved by coupling hexokinase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconic dehydrogenase activities. The 13C/12C ratio of the CO2 was measured with a high-precision magnetic-deflection double-collector mass spectrometer, and the radioactivity of 14CO2 was quantified by liquid scintillation. The ratio of 13C/12C was reproducible in assays of CO2 evolved from either naturally occurring or 13C-enriched glucose. Furthermore, systemic glucose production rates measured with 13C- and 14C-labeled tracers were similar over a wide range from 2 to 12 mg./kg.-min. Thus, glucose-1-13C may be employed as a tracer for glucose metabolism in human subjects without incurring the risk of radiation.

Animals↗
PubMed1976

Measurement of glucose turnover in the human newborn with glucose-1-13C.

Systemic glucose production rates were measured in 6 normal newborn infants by dilution of glucose-1-13C tracer according to the prime constant-rate infusion technique. Glucose production rates were 4.4 +/- 0.39 mg/kg. min. (Mean +/- S.D.) in 4 infants at 2 hours of age, and were 3.83 and 3.86 mg/kg. min. in 2 infants at 1 day of age. Systemic glucose production accounts for 50% of the substrate utilized for oxidative metabolism in newborn infants.

Blood Glucose↗
PubMed1975

Inhibitory effect of prednisone on insulin secretion in man: model for duplication of blood glucose concentration.

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.

Blood Glucose↗