Biomedical subjects

S Hulman

Publications and source records attributed to S Hulman.

At least 19 recordsLinked to original sources

PubMed1998

Can cardiovascular risk be predicted by newborn, childhood, and adolescent body size? An examination of longitudinal data in urban African Americans.

OBJECTIVE: Recent retrospective studies of older adults have demonstrated a correlation between lower birth weight and hypertension and insulin resistance. We tested this finding in our sample of urban African Americans with prospective data on growth and blood pressure and also tested other variables (in addition to birth weight) for their relationship to adult cardiovascular risk. STUDY DESIGN: A prospective study of birth weight, growth, and blood pressure (Philadelphia Perinatal Collaborative Project) followed a sample of 137 African Americans, with nine examinations from birth through 28.0 +/- 2.7 years. Metabolic measurements (oral glucose tolerance testing, euglycemic hyperinsulinemic clamp, and plasma lipid concentration) were performed on the subjects as adults. Bivariate correlations among parameters were computed using the Pearson r. The chi-squared statistic was used to determine associations of outcomes with birth weight. Stepwise multiple linear regressions were computed using newborn, early childhood, adolescent, and young adult parameters to predict adult outcomes. RESULTS: Birth weight and blood pressure at age 28 years are not correlated (Pearson r = 0.06). Birth weight is also unrelated to adult obesity. However, weight at 0.3 years and after and body mass index at 7 years and after are correlated with adult weight. Furthermore, weight at age 14 years is significantly negatively correlated with measures of insulin-stimulated glucose use, indicating that obese adolescents may be at greater risk than nonobese adolescents for development of non-insulin dependent diabetes in adulthood. CONCLUSIONS: We found no relationship between birth weight and adult outcomes pertaining to cardiovascular risk in this sample of adult African Americans. However, we did find evidence that somatic growth (body weight and body mass index) is significantly related to obesity and attenuated insulin-stimulated glucose utilization in adulthood. These findings indicate that the origins of adult cardiovascular disease are related to somatic growth, but not intrauterine growth, and are evident during childhood.

Adolescent↗

PubMed1998

Birth weight versus childhood growth as determinants of adult blood pressure.

In older white American adults, recent retrospective studies have demonstrated a relationship between lower birth weight and hypertension. Black Americans have a higher occurrence of both lower birth weight and hypertension than do white Americans. To test the low birth weight-high blood pressure hypothesis, data from a prospective study (Perinatal Collaborative Project) were examined. The study followed a sample of 137 black Americans, with nine examinations. Data on birth weight, growth, and blood pressure from birth through 28.0+/-2.7 years were obtained longitudinally. Bivariate correlations among parameters were computed with the Pearson r. Birth weight and blood pressure at age 28 years are not correlated (Pearson r=.06). However, systolic blood pressures measured at 0.3 years and thereafter are correlated with adult systolic blood pressure. Also, weight at 0.3 years and body mass index at 7 years and thereafter are correlated with adult weight. Our data did not confirm the birth weight-blood pressure hypothesis. Rather, we detected significant correlations between preadult measurements of blood pressure and weight with adult measurements. These results indicate that in black Americans, childhood growth is a stronger determinant than intrauterine growth of adult blood pressure.

Adult↗

PubMed1996

Effect of estrogen withdrawal on blood pressure and insulin resistance in sucrose-fed juvenile rats.

We have previously shown that juvenile Sprague-Dawley rats, fed a diet in which complex carbohydrates are replaced by sucrose, develop insulin resistance and hypertension. These conditions develop despite the absence of genetic predisposition to either. When studied with the euglycemic hyperinsulinemic clamp technique, these rats have reduced insulin-stimulated glucose utilization, but normal suppression of hepatic glucose output. In the young sucrose-fed rats, it was noted that the degree of blood pressure elevation was greater in males than in females. The purpose of this study was to test the hypothesis that estrogen withdrawal increases insulin resistance and hypertension. Female rats were randomized at weaning (3 weeks of life) to receive control diet or sucrose diet. Animals were assessed with weekly weight and indirect tail-cuff blood pressure. At 8 weeks of life, the sucrose-fed rats were randomized to receive bilateral oophorectomy or sham surgery (anesthesia and uterine horn exposure without removal of the ovaries). At 13 to 14 weeks of life, all animals were fasted overnight, and had an oral glucose tolerance test while conscious. Weight and weight gain were not different among the groups over the 11 week study period. Animals fed the sucrose diet developed significantly higher blood pressure than animals fed the control diet; oophorectomized animals had higher blood pressure than sham-operated animals (P <.0001). Sucrose-fed oophorectomized animals developed fasting and glucose-stimulated hyperinsulinemia. Estrogen withdrawal augments blood pressure in juvenile rats made insulin resistant and hypertensive with a sucrose diet. Estrogen withdrawal in these animals also induces fasting and glucose-stimulated hyperinsulinemia, which are signs of worsening insulin resistance. Androgen:estrogen imbalance increases metabolic dysfunction and worsens hypertension in this animal model.

Animals↗

PubMed1994

Gender differences in insulin-stimulated glucose utilization among African-Americans.

The purpose of this study was to determine whether there are gender differences in plasma insulin levels or insulin resistance in young adult African-Americans. Male (n = 53) and female (n = 45) subjects (age 23 to 28 years) included normotensives (N, blood pressure [BP] < 135/85 mm Hg) and borderline hypertensives (BH, BP > 135/85 mm Hg). Plasma insulin concentration was measured during an oral glucose tolerance test (OGTT) in all subjects. In 50 cases, insulin clamps were performed. Plasma estradiol and free testosterone were analyzed in a subsample (n = 15) of women. Data were analyzed for BP and gender groups by two-way ANOVA. Compared to men, women in each BP group had higher plasma insulin: glucose ratios (P < .01) and sums of insulin on OGTT (P < .02). The insulin clamp data also demonstrated significantly lower insulin-stimulated glucose utilization (M) in women compared to men in each BP group (N males 7.28 +/- 0.72 v N females 4.94 +/- 1.2 mg/kg-min; BH males 5.28 +/- .56 v BH females 2.59 +/- 0.50 mg/kg-min; P < .004 for gender differences). Analysis of the sex hormone data found a significant correlation in the ratio of free testosterone/estradiol (T/E) with plasma glucose, insulin, insulin/glucose, and systolic BP (P < .05), and no correlation of T/E with body mass index or triceps skinfold thickness. These data indicate that there are significant gender differences in plasma insulin levels and in insulin sensitivity in African-Americans. The relationship of plasma insulin to sex hormones suggests that in females, hyperinsulinemia cosegregates with increased androgenicity.

Adult↗

PubMed1994

The effect of excess dietary sucrose on growth, blood pressure, and metabolism in developing Sprague-Dawley rats.

To determine the effects of sucrose-enriched feeds on somatic growth, blood pressure development, and insulin-stimulated glucose metabolism, Sprague-Dawley rat pups (n = 94) were randomly assigned at weaning (3 wk) to a control diet (15% sucrose, by calories, n = 48) or an isocaloric diet in which starch is replaced by sucrose (66% sucrose, by calories, n = 46). Weight and blood pressure were followed until 13 wk. Chronic catheters were placed in a subset of male animals (n = 13), fasting glucose production was measured, and euglycemic hyperinsulinemic clamps were performed while the rats were in the conscious, nonstressed state. There was no difference in weight gain between control and sucrose rats in each sex group. Blood pressure in sucrose rats was significantly higher than in control rats after 4 wk of diet (7 wk of age, p < 0.001) in both sex groups and persisted for the duration of sucrose-enriched feeds. Insulin resistance was confirmed in sucrose rats with the euglycemic hyperinsulinemic clamp technique. In juvenile rats that have no genetic predisposition to hypertension, excess dietary sucrose induced high blood pressure without obesity. Sucrose feeding also induced insulin resistance. The sucrose-fed Sprague-Dawley weanling rat provides a model

Aging↗

PubMed1993

Insulin resistance in the conscious spontaneously hypertensive rat: euglycemic hyperinsulinemic clamp study.

To determine whether spontaneously hypertensive rats (SHR) are insulin resistant when compared with their genetic control, Wistar-Kyoto rats (WKY), insulin-stimulated glucose utilization was studied in both strains with the euglycemic hyperinsulinemic clamp technique. This methodology can determine if insulin resistance is present and whether it is due to ineffective stimulation of peripheral glucose utilization, or to incomplete suppression of (hepatic) endogenous glucose production (EGP) by insulin, or both. Twelve WKY and 15 SHR (all male) had long-term catheters surgically placed. After surgical recovery, fasting metabolic parameters were measured in the conscious, unstressed state. Clamp studies were then performed on nine WKY and eight SHR. EGP was measured before and during euglycemic hyperinsulinemia with the tracer-dilution technique (6-3H-glucose). Indices of fasting metabolism (plasma glucose, insulin, and hepatic EGP) were not different between WKY and SHR. During the clamp studies, the glucose infusion rate (GIR) required to maintain euglycemia was significantly lower in SHR (SHR, 0.055 +/- 0.003 v WKY, 0.106 +/- 0.001 mmol/kg.min-1; P < .001). EGP was completely suppressed during euglycemic hyperinsulinemia in all WKY and in six of eight SHR. We conclude that conscious, nonstressed SHR are insulin resistant when compared with WKY. Attenuated insulin-stimulated peripheral glucose utilization implicates skeletal muscle, and not liver, as the primary site of insulin resistance in SHR.

Animals↗

PubMed1993

Insulin-stimulated glucose utilization and borderline hypertension in young adult blacks.

The purpose of this investigation was to determine whether there is a relation between impaired insulin-stimulated glucose utilization, or insulin resistance, and blood pressure (BP) in a young adult black population. Clinically well, young black men and women, including normotensive (BP < 135/85 mm Hg, n = 23) and borderline hypertensive (BP > or = 135/85 mm Hg, n = 27) individuals, were studied. Each subject had an oral glucose tolerance test (OGTT) and underwent a euglycemic hyperinsulinemic clamp procedure. A two-way analysis of variance demonstrated a significantly greater fasting insulin plasma concentration (P < .02) and sum of insulin levels during the OGTT (P = .04) in the borderline hypertensive compared with normotensive subjects. In both BP groups, women had significantly higher fasting plasma insulin levels than men (P < .02 and P = .009). Body mass index was a significantly covariate of the plasma insulin concentration. Data obtained from the clamp demonstrated significant insulin resistance in borderline hypertensive compared with normotensive subjects (4.69 +/- 0.50 versus 6.57 +/- 0.63 mg/kg per minute, P = .002). A stepwise multiple linear regression analysis demonstrated that there are significant multiple correlations of insulin resistance with body mass index, clamped insulin level, BP group, and systolic BP (multiple R = .7862, P < .001). Application of this analysis to the nonobese sample (n = 33) found significant correlations of insulin resistance with sex, BP group, and systolic BP (multiple R = .6817, P < .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Red blood cell sodium-proton exchange in hypertensive blacks with insulin-resistant glucose disposal.

To define the potential pathogenic role of hyperinsulinemia as a mediator of alterations in sodium transport, we have examined red blood cell Na(+)-H+ and Na(+)-Li+ exchanges in a young adult black population characterized for blood pressure and insulin-mediated glucose disposal. Normotensive and mildly hypertensive blacks (blood pressure, 120 +/- 2/76 +/- 2 and 139 +/- 3/94 +/- 2 mm Hg, respectively) with a mean age of 26.1 years were studied for insulin sensitivity with the euglycemic hyperinsulinemic clamp (molar index of insulin sensitivity, M/I = moles glucose metabolized/insulin in milliliters of plasma). Na(+)-H+ exchange (U = mmol/L cell.h) was measured before and after the insulin clamp as a function of cell pH to determine the maximum transport rate. In the normotensive subjects, 18 were insulin sensitive (M/I = 9.37 +/- 0.6 x 10(4)) and 4 were insulin resistant (M/I = 3.64 +/- 0.6 x 10(4)). In the hypertensive subjects, 4 were insulin sensitive (M/I = 9.15 +/- 1.1 x 10(4)) and 16 were insulin resistant (M/I = 3.02 +/- 0.3 x 10(4)). The maximum rate of Na(+)-H+ exchange was significantly higher in all hypertensive vs normotensive individuals (35 +/- 3 vs 23 +/- 3 U, P < .005). Na(+)-H+ exchange activity was higher in insulin-resistant vs insulin-sensitive hypertensive subjects (40 +/- 3 vs 20 +/- 2 U, P < .001) but not in insulin-resistant normotensive subjects. Na(+)-Li+ exchange was not different in hypertensive and normotensive individuals but was higher in all insulin-resistant compared with all insulin-sensitive subjects (0.26 +/- 0.03 vs 0.16 +/- 0.02 U, P < .01). Na(+)-Li+ exchange also was higher in insulin-resistant vs insulin-sensitive normotensive subjects (0.35 +/- 0.03 vs 0.15 +/- 0.02 U, P < .001) and in insulin-resistant hypertensive subjects vs insulin-sensitive normotensive subjects (0.24 +/- 0.03 vs 0.15 +/- 0.02 U, P < .001). A stepwise multiple regression analysis for all variables revealed that with Na(+)-H+ exchange as a dependent variable the main determinant was blood pressure, which in turn had insulin sensitivity as the main determinant. In conclusion, these results indicate that in hypertensive blacks, insulin-resistant glucose disposal is strongly associated with elevated red blood cell Na(+)-H+ exchange activity. Thus, despite impaired insulin-mediated glucose disposal, cellular Na+ gain via enhanced activity of Na(+)-H+ exchange is not blunted in hypertensive blacks.

Adult↗

PubMed1992

Hyperinsulinemia and blood pressure sensitivity to sodium in young blacks.

The relationship of blood pressure sensitivity to sodium with plasma insulin concentration was examined in young adult (22 to 28 yr) blacks (N = 45). The study included normotensive and borderline hypertensive subjects. Blood pressure sensitivity to sodium was determined by the change in mean blood pressure after 14 days of sodium loading (10 g of NaCl daily plus usual diet). Plasma insulin concentration was determined during an oral glucose tolerance test (OGTT). The correlation of fasting plasma insulin concentration with blood pressure or blood pressure sensitivity to sodium was not statistically significant. There was a significant correlation (after adjustment for adiposity) of blood pressure sensitivity to sodium with both the sum of insulin (r = 0.41; P < 0.01) and the 60-min plasma insulin concentration during the OGTT. The plasma insulin concentration at 60 min during the OGTT correlated significantly with the change in mean arterial pressure over a 5-yr interval (r = 0.36; P < 0.02). There was a similar significant correlation of blood pressure sensitivity to sodium with change in mean arterial pressure over 5 yr (r = 0.48; P < 0.001). These data demonstrate an association of hyperinsulinemia and blood pressure sensitivity to sodium in the young. The data also suggest that insulin may contribute to the pathogenesis of hypertension in the black population.

Adult↗

PubMed1991

Insulin resistance in the spontaneously hypertensive rat.

To determine experimentally if insulin resistance is associated with spontaneously occurring hypertension, insulin-stimulated glucose metabolism was studied in an animal model of genetic hypertension. The spontaneously hypertensive rat (SHR) and its genetic control, the Wistar-Kyoto strain (WKY) were studied with the euglycemic hyperinsulinemic clamp technique. Clamp studies demonstrated reduced insulin-stimulated glucose uptake in SHR (P less than .001). These data indicate that SHR is insulin-resistant when compared with WKY. A reduction of insulin-stimulated glucose metabolism occurred in older animals of both strains, providing evidence of an aging effect on insulin-stimulated glucose metabolism. However, the reduction of insulin-stimulated glucose metabolism was more pronounced in the hypertensive animals. This study demonstrates the presence of peripheral (skeletal muscle) insulin resistance in the SHR.

Animals↗

PubMed1991

Blood pressure patterns in the first three days of life.

Current blood pressure data for healthy newborn infants consist primarily of single measurements of systolic and diastolic pressure in the first 48 hours of life. The purpose of this study was to determine if blood pressure levels are stable or are changing during the first few days of life. To determine blood pressure level and trend, indirect blood pressure was measured on day 1 through day 3 of life in all infants admitted to the well newborn nursery at Hahnemann University Hospital in Philadelphia. Systolic pressure correlated significantly with birthweight on day 1 of life (P less than .03). Repeated measures analysis of variance demonstrated a significant increase in both systolic and diastolic pressures over the first 72 hours of life (P less than .001). There was no difference in blood pressure among racial groups (black, Hispanic, white, Asian). In healthy newborns, there was no correlation of blood pressure with maternal conditions: toxemia, diabetes, substance abuse. These data demonstrate that blood pressure correlates with birthweight in well newborns. There is, however, a significant progressive increase in both systolic and diastolic blood pressure over the first 3 days of life, regardless of birthweight or maternal conditions.

Analysis of Variance↗

PubMed1990

Relationship between plasma renin concentration and atrial natriuretic peptide in the human newborn.

To test the hypothesis that atrial natriuretic peptide (ANP) concentration in the newborn is negatively related to plasma renin concentration (PRC), as it is in the adult, we measured the concentration of both substances in the same plasma sample. We studied 24 well term newborns and 20 samples of umbilical venous blood from normal deliveries. Both ANP and PRC are elevated in newborn plasma, but not in umbilical venous plasma. ANP levels on the second day of life are greater than either day 1 or day 3. Linear regression of ANP and PRC demonstrates a highly significant negative correlation [r = -0.65, p less than 0.001], which suggests that the suppression of the renin-angiotensin system by ANP seen in the adult may be intact in the newborn. ANP may act to blunt the effects of the augmented renin-angiotensin system of the newborn and promote normal neonatal diuresis.

Atrial Natriuretic Factor↗

PubMed1990

Insulin resistance and blood pressure in young black men.

Insulin resistance, independent of obesity or non-insulin-dependent diabetes mellitus, has been demonstrated to be associated with high blood pressure. To determine if insulin resistance could be an antecedent to hypertension in a high-risk population, we studied normotensive (112 +/- 12/70 +/- 10 mm Hg) and borderline hypertensive (135 +/- 8/85 +/- 5 mm Hg) lean young black men (22-26 years old) with the euglycemic hyperinsulinemic clamp technique. All subjects had clinically normal oral glucose tolerance. Body mass index and percent adipose mass were the same in both groups. Fasting plasma insulin concentration was significantly higher in the borderline hypertensive group (p less than 0.01). Insulin-directed exogenous glucose metabolism at the same degree of steady-state hyperinsulinemia was significantly lower in the borderline hypertensive group (5.98 +/- 2.22 versus 8.22 +/- 1.96 mg/kg/min; p less than 0.01). For the total population, a significant inverse correlation existed between the glucose infusion rate and systolic blood pressure (p less than 0.01). These data indicate that there is a relation between insulin-mediated glucose uptake and blood pressure. Furthermore, in this high-risk population insulin resistance may precede the onset of established essential hypertension.

Adult↗

PubMed1990

Evaluation of active versus passive AIDS surveillance in Oregon.

We searched for unreported AIDS cases in Oregon through death certificate and medical record review, and enhanced infection control practitioner and physician surveillance. Fifty-six AIDS cases diagnosed between February 1, 1986 and January 31, 1987 were reported passively. Twenty-nine additional cases diagnosed during this time were retrospectively identified by active methods. Ninety percent of those 29 cases were diagnosed by physicians and cared for in hospitals that had previously reported cases. Completeness of reporting under the passive system was 64 percent.

Acquired Immunodeficiency Syndrome↗

PubMed1989

Effect of euglycemic hyperinsulinemia on neonatal canine hepatic and muscle metabolism.

The effects of euglycemic hyperinsulinemia on hepatic and muscle metabolism were determined in the fasted newborn dog during the first day of life. Hyperinsulinemia was sustained with a primed constant infusion of insulin whereas euglycemia was maintained with an intravenous infusion of 10% glucose using the insulin clamp technique. Euglycemic hyperinsulinemia caused an increase of glucose utilization from 43.9 +/- 3.7 to 66.5 +/- 5.4 mumol/kg/min (p less than 0.001) and reduced endogenous glucose production to 44.4 +/- 5.4% of basal values obtained before the induction of hyperinsulinemia. Hepatic tissue glycogen, triglycerides, or intermediates were not altered by hyperinsulinemia nor was the incorporation of [3H]glucose into glycogen. However, the hepatic cytoplasmic redox state was more oxidized, and the incorporation of [3H]glucose into triglycerides was higher among hyperinsulinemic pups. Pups who demonstrated incomplete suppression of endogenous glucose production had metabolite perturbation suggestive of ongoing gluconeogenesis. Despite very few changes in hepatic tissue metabolite levels, pups subjected to hyperinsulinemia demonstrated a linear uptake of 2-deoxyglucose into hepatic tissue as a function of circulating insulin levels during hyperinsulinemia. Muscle tissue demonstrated no alterations of tissue metabolites, glycogen, or triglycerides levels or precursor incorporation into these storage pools. Nonetheless, 2-deoxyglucose incorporation into neonatal muscle tissue was a significant linear function of plasma insulin concentration. Total tissue 2-deoxyglucose uptake was lower in muscle tissue than in hepatic tissue (245 +/- 19 versus 514 +/- 20 dpm/g/min) (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Beneficial effects of early hypocaloric enteral feeding on neonatal gastrointestinal function: preliminary report of a randomized trial.

In a prospective randomized trial, we studied the effects of early hypocaloric enteral feedings (PO) begun at 48 hours of age in 19 infants compared with 20 infants who received no enteral feedings (NPO) for at least the first 9 days of life. Both groups initially received the majority of their calories by parenteral alimentation. The groups were similar with respect to birth weight, gestational age, sex, Apgar score, and major neonatal diagnoses. The early enteral feeds proved to be significantly beneficial without an increased incidence of complications. The PO group reached full enteral feedings faster than the NPO group (31.2 vs 47.3 days). The PO group had a greater decline in serum bilirubin concentration over the first 2 weeks of life and spent less time under phototherapy (6.8 vs 9.5 days). Less cholestasis was observed among the PO infants (6.7% vs 33%), and peak direct bilirubin levels were also lower (0.7 vs 2.5 mg/dL). Osteopenia of prematurity, manifested by significantly lower alkaline phosphatase activity, was also decreased in the PO group, perhaps because of greater calcium intake during the first month among PO infants (1.3 vs 0.8 g). Compared with complete bowel rest, early onset of hypocaloric enteral feedings has beneficial effects on indirect hyperbilirubinemia, cholestatic jaundice, and metabolic bone disease of very low birth weight infants.

Alkaline Phosphatase↗

PubMed1988

Relationship of substrate level to turnover rate in fasted adult and newborn dogs.

Glucose turnover, clearance and response to insulin were determined in fasted newborn and adult dogs. Fasting levels of glucose and insulin and rates of glucose turnover and clearance were not different between the two groups. Blood glucose correlated with basal glucose turnover in newborn pups but not in adult dogs. Glucose turnover was not related to fasting plasma insulin levels. Glucose clearance was an inverse function of blood glucose levels among newborn but not adult dogs. Glucose clearance and blood glucose levels were not related to insulin concentrations. In response to euglycemic hyperinsulinemia, glucose metabolism increased 4-fold among adults but only 1.7-fold in pups. Hyperglycemic hyperinsulinemia increased glucose metabolism in both groups but to a much greater extent in the pups. Euglycemic hyperinsulinemia increased the metabolic clearance rate of glucose 4.2-fold among adults but only 1.8-fold in newborn dogs. In response to hyperglycemic hyperinsulinemia glucose clearance rates were now similar. Despite euglycemic hyperinsulinemia, the newborn dog had an attenuated response to insulin, demonstrating lower rates of glucose metabolism and glucose clearance. The response to the hyperglycemic stimuli suggests that maximal glucose uptake was not achieved during hyperinsulinemia alone. This response supports the concept of glucose-mediated regulation of glucose disposal in newborn animals.

Animals↗

PubMed1988

The effect of euglycemic hyperinsulinemia on cerebral cortical glucose metabolism in newborn beagles.

There is a paucity of information on the significance of insulin on neonatal cerebral glucose metabolism. The effect of insulin on neonatal cerebral glucose uptake and cerebral cortical metabolic intermediates was investigated with the euglycemic hyperinsulinemic clamp in unanesthetized beagles during the first day of life. Insulin was infused at various rates to sustain an elevated steady state plasma insulin concentration in individual pups. Furthermore, blood glucose and 2-deoxyglucose levels were also maintained ("clamped") in a steady state by infusion of glucose and 2-deoxy-[14C]-glucose. Mean (+/- SD) plasma insulin levels were 20 +/- 12 and 2971 +/- 3386 (33-14330) microU/ml in control and hyperinsulinemic pups. Blood glucose concentration was 4.43 +/- 2.64 mM during basal periods and 4.54 +/- 2.87 mM during the clamp period in study pups. Basal fasting glucose utilization in study pups was 43.9 +/- 24 mumol/kg/min and increased to 60.9 +/- 35.2 mumol/kg/min (p less than 0.001) during hyperinsulinemia. Immediately after the euglycemic hyperinsulinemic clamp or fasting in control pups, the cerebral cortex was frozen to the temperature of liquid nitrogen. No differences were noted for any cerebral cortical intermediate between the two pup groups. In addition, there was no relationship between the cerebral intermediates concentration when analyzed as a function of plasma insulin levels. The uptake of cerebral 2-deoxyglucose was analyzed as a function of plasma insulin concentration (120-6900 microU/ml). Brain tissue demonstrated a positive linear relationship for 2-deoxyglucose uptake as a function of plasma insulin concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗