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Biomedical subjects

J Calles-Escandon

Publications and source records attributed to J Calles-Escandon.

32 records · Page 2Linked to original sources
PubMed1994

Effects of increased energy intake and/or physical activity on energy expenditure in young healthy men.

This study was designed to examine effects of alterations in energy balance on adaptive changes in components of total energy expenditure (TEE). Nineteen young healthy males were studied during a 10-day sedentary energy balance baseline period and then randomly assigned to one of four 10-day treatment groups: 1) no change in energy intake (EI) or physical activity (PA; energy balance at low energy flux), 2) EI increased by 50% with no change in PA (positive energy balance), 3) TEE increased by 50% by increasing PA, matched by a 50% increase in EI (energy balance at high energy flux), and 4) TEE increased by 50% by increasing PA with no change in EI (negative energy balance). TEE was measured with doubly labeled water, resting metabolic rate (RMR) by indirect calorimetry, and thermic response to feeding (TEF) by indirect calorimetry; energy expenditure of physical activity (EEPA) was estimated by subtracting RMR, TEF, and prescribed PA from TEE. TEE was significantly increased by PA (by design) but not EI. There was a significant main effect of intake and a significant intake-by-activity interaction for changes in RMR. In post hoc analysis, RMR was significantly increased during positive energy balance and energy balance at high energy flux relative to change in RMR when energy balance was maintained at low energy flux. A significant increase in RMR was also noted during negative energy balance after adjustment for change in fat-free mass. There was no significant difference in change in RMR among the three treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Discordant metabolic actions of insulin in extreme lipodystrophy of childhood.

Congenital lipodystrophy includes a group of disorders characterized by total or partial absence of adipose tissue and insulin resistance. In this study we investigated the nature of insulin resistance in an 11-yr-old girl with one form of congenital lipodystrophy. We examined in vivo insulin and glycemic responses to feeding and iv glucose and in vitro amino acid and thymidine incorporation responses of skin fibroblasts to insulin exposure. In addition, we used stable isotope infusions of glucose, glycerol, and amino acids to investigate the in vivo metabolic actions of insulin on carbohydrate, fat, and protein. At 5 yr of age, she first demonstrated clinical glucose intolerance. Her basal insulin levels were normal (129 and 114 pmol/L), but increased markedly (peak values, 1304 and 5045 pmol/L) after iv glucose and a mixed meal. Insulin antibodies were undetectable, and specific [125I]insulin binding to her skin fibroblasts was normal. Both [3H]aminoisobutyric acid transport and [3H]thymidine incorporation by her fibroblasts were similar to responses obtained using control cells. At 11 5/12 yr of age, while receiving an infusion of stable isotopes, infusions of insulin at doses of 0.1 and 0.3 U/kg BW.h were ineffective in reducing her blood glucose despite elevating her serum insulin level to approximately 2500 pmol/L. Resting metabolic rate, respiratory quotient, VCO2, carbohydrate and lipid oxidation rates, glucose production rate, glycerol appearance rate, and plasma glycerol concentrations were unperturbed by the insulin infusions. By contrast, the insulin infusions reduced plasma leucine concentrations (124.2 to 86.1 to 66.7 mumol/L) and 13CO2 production rates (0.034 to 0.017 to 0.011 mumol/kg/min; baseline, 0.1, and 0.3 U insulin/kg.h, respectively). The leucine appearance rate declined (1.96 to 1.72 mumol/kg.min) in response to the 0.1 U/kg.h dose, but did not decline further in response to the 0.3 U/kg.h dose. The leucine oxidation rate also declined (0.87 to 0.39 to 0.25 mumol/kg.min), and there was a dose-related reduction in most plasma amino acid concentrations. Finally, nonoxidative leucine disposal increased progressively (1.09, 1.34, and 1.48 mumol/kg.min), suggestive of an insulin-induced increase in protein synthesis. These data indicate profound metabolic resistance to the carbohydrate and lipid actions of insulin, with preservation of protein anabolism. These observations suggest that in this patient, the biological effects of insulin on carbohydrate, lipid, and protein are distinct metabolic actions, regulated independently.

Amino Acids↗
PubMed1991

Reduced mononuclear leukocyte ascorbic acid content in adults with insulin-dependent diabetes mellitus consuming adequate dietary vitamin C.

Several recent studies suggest that vitamin C (ascorbic acid [AA]) status may be altered in insulin-dependent diabetes mellitus (IDDM). We measured the AA content of mononuclear leukocytes (MN-AA) as an indicator of tissue vitamin C status in adults with IDDM and nondiabetic adults matched for age and sex. Dietary vitamin C intake and plasma AA were analyzed to ensure that vitamin C availability was adequate. Dietary vitamin C intakes were above recommendations and were not different between the groups. MN-AA was reduced by 33% on average (P less than .05) in adults with IDDM (1.75 microgram/mg total protein [TP]) when compared with nondiabetics (2.60 micrograms/mg TP). When MN-AA is indexed to the dietary vitamin C intake (MN-AA/100 mg diet C), the storage deficit in adults with IDDM averages 50% (P less than .05). This observation suggests an impaired tissue AA storage in adults with IDDM and supports the theory that intracellular scurvy contributes to the chronic degenerative complications of the disease.

Adult↗
PubMed1987

Loss of early phase of insulin release in humans impairs glucose tolerance and blunts thermic effect of glucose.

Loss of the early phase of insulin release has been documented in both type I (insulin-dependent) and type II (non-insulin-dependent) diabetes; however, the physiological importance of this loss is unsettled. We created a model of loss of the early phase of insulin release in normal volunteers. Somatostatin (SRIF) was briefly infused (from -5 to 15 min) during intravenous (IVGTT) and oral (OGTT) glucose tolerance tests. The thermic response to oral glucose was determined under these conditions by indirect calorimetry. Early insulin release was totally blocked during IVGTT and OGTT by SRIF infusion. During the IVGTT, glucose tolerance was deteriorated in association with loss of the early phase of insulin release as indicated by a decrease in the K value (control 1.9 +/- 0.36 vs. SRIF 1.1 +/- 0.27, P less than .001). Higher plasma glucose concentrations were observed during SRIF tests in the OGTT at 60, 90, 120, 150, and 180 min; total glycemic excursion was larger during the SRIF test (9473 +/- 3089 mg X dl-1 X 5 h-1) when compared with the control condition (6583 +/- 2329 mg X dl-1 X 5 h-1). During the OGTT the total amount of glucose oxidized (control 56 +/- 4.2 vs. SRIF 55 +/- 3.4 g/5 h) was similar in both conditions, suggesting that nonoxidative pathways of glucose disposal were responsible for the deterioration in glucose tolerance. Surprisingly, we found that glucose-induced thermogenesis was reduced in association with loss of the early phase of insulin release (control 102 +/- 21.3 vs. SRIF 72 +/- 27.8 J/5 h, P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1986

Effects of preexercise snack feeding on endurance cycle exercise.

We studied the effects of ingesting either a snack food (S) (260 kcal) or placebo (P) 30 min before intermittent cycle exercise at 70% maximal O2 consumption on endurance performance and muscle glycogen depletion in eight healthy human males. Immediately before exercise there were significantly greater increases in plasma glucose (PG) (S +28 +/- 9.7; P +0.1 +/- 0.8 mg/dl) and insulin (S +219 +/- 61.5; P -7 +/- 5.5 pmol/l) (P less than 0.05) following S feeding compared with P. These differences were no longer present by the end of the first exercise period. There were no differences in endurance times (S 52 +/- 6.4; P 48 +/- 5.6 min) or in the extent of muscle glycogen depletion following exercise (S 56 +/- 14.7; P 50 +/- 15.5 micrograms/mg protein) between the two groups. PG was maintained at base-line (prefeeding) concentrations following S, whereas there was a tendency for PG to steadily decrease after P. Total grams of carbohydrate oxidized during exercise did not differ between the two groups (S 120; P 118 g). These results demonstrate that the ingestion of a mixed-macronutrient snack 30 min before exercise does not impair endurance performance nor increase the extent of muscle glycogen depletion during high-intensity cycle exercise in untrained adult male subjects.

Blood Glucose↗
PubMed1986

Hypercorticosteronuria and diminished pituitary responsiveness to corticotropin-releasing factor in obese Zucker rats.

Metabolic defects in obese (fa/fa) Zucker rats have previously been shown to be reversed by adrenalectomy; however, hypercorticosteronemia has not been demonstrated. We now report that the total daily excretion of corticosterone and urea nitrogen are significantly greater (P less than 0.01) in obese Zucker rats than in age-matched lean Zucker rats. This excessive excretion of corticosterone is not of autonomous adrenal origin, since dexamethasone treatment (20 micrograms/kg X day) for 2 days induced a proportionate reduction in corticosterone excretion (approximately 50%) in both obese and lean Zucker rats. Corticosterone excretion was further suppressed to levels not different from those in lean rats after 2 days of dexamethasone (40 micrograms/kg X day). Both the peak and total pituitary beta-endorphin secretion in response to an iv bolus of corticotropin-releasing factor (CRF) were diminished in obese Zuckers. The response to CRF in obese Zucker rats was dampened and superimposable on that of dexamethasone-treated lean Zucker rats, suggesting the existence of chronic hypercorticosteronemia as a component of this genetic obesity. These observations provide evidence for a compensatory alteration of the pituitary-adrenal axis. We suggest that corticosterone turnover may be increased in obese Zucker rats.

Animals↗
PubMed1985

The analysis of glucose kinetics using a single jugular catheter in awake rats.

The rates of glucose production and utilization can be estimated by a primed-constant infusion technique using separate catheters for the infusion of radiolabelled glucose and periodic blood withdrawal. In rats, a carotid artery catheter is most often combined with a jugular or femoral venous catheter in such studies. We presently describe a method which utilizes a single jugular catheter for both infusion and sampling in the awake rat. This method is directly compared with simultaneous carotid artery sampling during both the dynamic steady state and a nonsteady state induced by a constant infusion of insulin. Our results demonstrate the validity of a single vein design for the analysis of glucose kinetics in either state. Rapid sampling and complete flushing prevent disruption of infusate equilibrium and sample contamination respectively. This single catheter method requires less technical skill for placement, reduces surgical intervention and enhances the comfort of the awake rat.

Animals↗
PubMed1984

The plasma amino acid response to cafeteria feeding in the rat: influence of hyperphagia, sucrose intake, and exercise.

The plasma amino acid response to voluntary hyperphagia was evaluated in rats fed a "cafeteria" diet for 4 to 8 weeks and compared to chow-fed controls. The influence of the sucrose content of the cafeteria diet was examined by studying rats given a low-sucrose, highly palatable, liquid diet (Magnacal). In a second series of studies the cafeteria diet was fed to rats housed in wheel cages and who ran 2.0 +/- 0.1 milles per day and compared with a sedentary cafeteria-fed group housed in standard cages. As expected, the cafeteria diet resulted in hyperphagia (45% to 55%) and in increased weight gain (35% to 50%). In response to cafeteria feeding there was an increase in plasma threonine, serine, proline, citrulline, alpha-amino butyric acid (ABA), and tyrosine. Significant decreases were observed in the branched chain amino acids (BCAA), valine and leucine. All of these changes were also observed when hyperphagia was induced with the low-sucrose diet, with the exception of the rise in ABA. In the exercised cafeteria-fed rats, excessive weight gain did not occur. Nevertheless, the amino acid response to the cafeteria diet was the same as in sedentary rats with excessive weight gain. The plasma amino acid pattern in those rats that developed glucose intolerance during cafeteria feeding and those that maintained normal glucose tolerance was similar. We conclude that hyperphagia induced by cafeteria feeding in the rat results in a specific plasma amino acid profile characterized by elevations in some amino acids (threonine, serine, proline, citrulline, ABA, and tyrosine) and reductions in the BCAA.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1984

Influence of exercise on urea, creatinine, and 3-methylhistidine excretion in normal human subjects.

To evaluate the effects of exercise on net protein catabolism, the losses of urea in sweat and urine and urinary creatinine and 3-methylhistidine (3MH) excretion were determined in eight healthy subjects during cycle ergometer exercise performed at approximately 45% of VO2max for 90 min. The subjects ingested a meat-free diet for 5 days starting 3 days before and continuing for 1 day after the day of exercise. During exercise, total urea excretion (urine + sweat losses) increased 100% above pre- and postexercise values. Thirty percent of the total urea excretion during exercise was in the form of sweat losses. Total protein breakdown (as reflected by urea excretion), however, could account for less than 5% (21 +/- 4 kcal) of total calorie expenditure during the exercise (567 +/- 83 kcal). Urinary creatinine excretion increased by 50% during exercise. Urinary excretion of 3MH also tended to rise, but the ratio of urinary 3MH to creatinine showed no change in response to exercise. We conclude that 1) light to moderate exercise results in an increase in net protein catabolism and an increase in creatinine excretion; 2) sweat losses are an important route for urea excretion during exercise; 3) there is no evidence of a disproportionate increase in breakdown of myofibrillar contractile proteins; and 4) in spite of the increase in the rate of protein catabolism, protein is only a minor source of energy during light to moderate exercise.

Adolescent↗
PubMed1984

Fuel-hormone metabolism during exercise and after physical training.

In this review the metabolic changes encountered in response to exercise in normal humans are considered in the context of the following categories: (1) fuel utilization and production, (2) hormone secretion, (3) the post-exercise recovery period, (4) effects of physical training on fuels and hormone secretion, and (5) effects of exercise on lipoprotein metabolism.

Carbohydrate Metabolism↗
PubMedDate not supplied

Postprandial oscillatory patterns of blood glucose and insulin in NIDDM. Abnormal diurnal insulin secretion patterns and glucose homeostasis independent of obesity.

Compared with control subjects, non-insulin-dependent diabetes mellitus (NIDDM) subjects had both quantitative and qualitative abnormalities in blood insulin and glucose concentrations. The purpose of this study was to determine whether and to what extent normally observed multiphasic patterns of insulin and glucose responses to mixed meals are deranged in NIDDM. A total of 24 volunteers were studied while eating three meals of identical composition at 0745, 1145, and 1645. Twelve had NIDDM, and the remainder were healthy nondiabetic age- and weight-matched control subjects. Blood was withdrawn every 10 min from 0630 to 1930 for measurement of C-peptide, insulin, and glucose concentrations. Peaks were analyzed by computer-based algorithms. Diabetic volunteers displayed several differences from control subjects. First, although the number of insulin peaks was similar, there was a consistent delay of 20-30 min in the appearance of the first postprandial peak. Second, insulin concentrations after lunch were higher than after breakfast, whereas the reverse pattern occurred in control subjects. Third, integrated glycemia was greater after breakfast than after lunch. Fourth, glucose concentrations decreased during the first 30 min after lunch, suggesting accelerated glucose disposal and/or enhanced suppression of endogenous glucose production at this time of day. These data demonstrate that insulin secretion and action and glucose homeostasis in NIDDM are more complex than commonly appreciated. This dynamic state is undetected unless there is frequent blood sampling for measurement of insulin and glucose. The quantitative and qualitative abnormalities that we observed in these parameters are independent of obesity and suggest the need to expand the pathophysiological definition of NIDDM.

Adult↗