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Biomedical subjects

R Buckspan

Publications and source records attributed to R Buckspan.

5 recordsLinked to original sources
PubMed1992

The effects of acute elevations in plasma cortisol levels on alanine metabolism in the conscious dog.

The present study was undertaken to determine whether an acute physiological increase in plasma cortisol level had significant effects on alanine metabolism and gluconeogenesis within 3 hours in conscious, overnight-fasted dogs. Each experiment consisted of an 80-minute tracer and dye equilibration period, a 40-minute basal period, and a 3-hour experimental period. A primed, continuous infusion of [3-3H]glucose and continuous infusions of [U-14C]alanine and indocyanine green dye were initiated at the start of the equilibration period and continued throughout the experiment. Dogs were studied with (1) a hydrocortisone infusion ([CORT] 3.0 micrograms.kg-1.min-1, n = 5), (2) hydrocortisone infused as in CORT, but with pancreatic hormones clamped using somatostatin and basal intraportal replacement of insulin and glucagon (CLAMP+CORT, n = 5), or (3) saline infusion during a pancreatic clamp (CLAMP, n = 5). Glucose production and gluconeogenesis were determined using tracer and arteriovenous difference techniques. During CLAMP, all parameters were stable except for a modest 67% +/- 6% increase in gluconeogenic conversion of alanine to glucose and a 53% +/- 26% increase in gluconeogenic efficiency. When plasma cortisol levels were increased fourfold during CLAMP+CORT, there was no change in the concentration, production, or clearance of glucose. Gluconeogenic conversion of alanine to glucose increased 10% +/- 34% and gluconeogenic efficiency increased 65% +/- 43%, while net hepatic alanine uptake (NHAU) increased 60% +/- 19% and hepatic fractional extraction of alanine increased 38% +/- 12%. Cortisol did not cause an increase in the arterial glycerol level or net hepatic glycerol uptake.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗
PubMed1987

Extrapancreatic effects of L-leucine infusion in leucine-sensitive and control subjects.

We studied the extrapancreatic effects of L-leucine infusion (2.5 mumol/kg/min) in six controls (three females, three males) and three members of a family with leucine-sensitive hypoglycemia (LSH). Total glucose disposal and endogenous glucose production (EGP) rates were assessed after an overnight fast (12 to 14 hour) during somatostatin (SRIF) infusion (500 micrograms/h) with insulin replacement (0.2 mU/kg/min), combined with D-(3-3H)-glucose infusion. Additional studies of forearm arterial-venous (A-V) balances of amino acids, glucose, and other substrates, combined with L-(1-14C)-leucine kinetics, were done in these two groups. L-leucine infusion resulted in a 15% decrease in whole-body total glucose utilization in controls (P less than .05) during SRIF-insulin infusion, but did not affect glucose utilization in LSH subjects. EGP was not affected by L-leucine infusion in either group. Control subjects demonstrated a significant reduction in forearm glucose uptake and greater lactate release during L-leucine infusion, compared to the basal state. In contrast, subjects with LSH showed a slight increase in forearm glucose uptake and significantly less lactate release during L-leucine infusion. Subjects with LSH demonstrated significantly lower forearm leucine uptake, and lower rates of appearance and oxidation of L-(1-14C)-leucine during leucine infusion, compared to controls. Our data suggest that members of this LSH kindred have a defect in intracellular leucine metabolism in skeletal muscle, resulting in a lack of leucine-induced inhibition of glucose utilization. This may contribution to the development of hypoglycemia in these subjects.

Adolescent↗
PubMed1986

alpha-Ketoisocaproate is superior to leucine in sparing glucose utilization in humans.

The present study was designed to examine the glucose-sparing effect of leucine and its keto acid alpha-ketoisocaproate (KIC) in vivo. Two groups of overnight-fasted normal volunteers were studied. In the first group, eight subjects received an intravenous infusion of leucine and six subjects received KIC (2.3 mumol X kg-1 X min-1) for 3 h; on another occasion, all subjects received saline and acted as their own controls. In the second group, 11 subjects received an infusion of 1 mU X kg-1 X min-1 for 3 h with a variable glucose infusion to maintain euglycemia. On another occasion, five subjects received an additional infusion of leucine and six subjects received KIC each at 2.3 mumol X kg-1 X min-1 for 3 h. The amount of exogenous glucose required to maintain euglycemia (M, mg X kg-1 X min-1) was used as an index of total body glucose utilization. Forearm exchange of leucine, KIC, glucose, and lactate was determined in both groups. Both leucine and KIC infusions alone decreased glucose uptake (42 and 40%) and increased lactate release (37 and 116%, respectively). Hyperinsulinemia (6-fold basal) and euglycemia resulted in a fivefold increase in glucose uptake across the human forearm. The amount of exogenous glucose required to maintain euglycemia averaged 7.4 +/- 0.5 mg X kg-1 X min-1. The combination of leucine and insulin infusions did not alter the stimulated forearm glucose uptake nor did it change M (7.25 +/- 0.6 mg X kg-1 X min-1, P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Insulin's effect on Leucine turnover changes during early fasting in the conscious dog.

To study the effects of insulin on leucine turnover during fasting, acute insulin deficiency was induced by the simultaneous infusion of somatostatin and glucagon in conscious dogs fasted 18 h (N = 10) and 48 h (N = 11). Insulin levels during the basal period (before hormone perturbation) were similar in both groups of dogs (12 +/- 3 versus 10 +/- 3 microU/ml, respectively). Glucagon levels were similar in the two groups (94 +/- 9 versus 106 +/- 19 pg/ml). Leucine levels rose from 118 +/- 9 mumol/L to 155 +/- 12 mumol/L as fasting progressed (P less than 0.005). Its rate of appearance also increased by 30% (P less than 0.005) from 3.4 +/- 0.3 to 4.3 +/- 0.4 mumol/kg/min (P less than 0.005), while its clearance remained unchanged. Acute insulin deficiency caused an increase in leucine levels in both 18-h and 48-h-fasted dogs by 55% (to 181 +/- 10 mumol/L) and 45% (to 225 +/- 20 mumol/L), respectively (P less than 0.005). However, while the rate of appearance of leucine remained unchanged in dogs fasted overnight, it rose to 5.1 +/- 0.3 mumol/kg/min (P less than 0.01) in those fasted 48 h. The metabolic clearance rate fell in both groups, although this drop was twice as great in the 18-h group (from 28 +/- 3 to 17 +/- 3 ml/kg/min, P less than 0.005) as in the 48-h group (from 28 +/- 3 to 23 +/- 2 ml/kg/min, P less than 0.005). We conclude that insulin has disparate effects on protein turnover as fasting becomes more prolonged.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗