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Biomedical subjects

T T Aoki

Publications and source records attributed to T T Aoki.

At least 19 recordsLinked to original sources
PubMed1992

Measurement of health status in diabetic patients. Diabetes impact measurement scales.

OBJECTIVE: To develop an instrument to measure health status in adult insulin-dependent (type I) and non-insulin-dependent (type II) diabetic patients. RESEARCH DESIGN AND METHODS: Correlative study to examine psychometric properties of the questionnaire. Test-retest reliability, item-scale correlations, principal-components analysis, correlations with global clinical ratings, and correlations with clinical data extracted from medical records were examined at the diabetes clinics at the University of California, Davis, Medical Center. Patients were volunteer clinic patients able to complete the questionnaire. One hundred thirty patients completed a first administration of the questionnaire, and 52 completed a second administration. RESULTS: Test-retest reliability was satisfactory. Item-scale correlations showed that 40 of 44 questionnaire items were highly correlated with subscale and total scale scores. Principal-components analysis identified one major factor measured by the questionnaire. Cronbach's alpha, a measure of the scales' internal consistency, was of satisfactory magnitude. Global ratings of clinical status by patients and clinicians were highly correlated with scale scores. Correlations of scale scores with clinical data were generally of low magnitude but, where significant, were consistently in the direction hypothesized if the scale truly measures health status or disease impact. CONCLUSIONS: The Diabetes Impact Management Scales (DIMS) is an easily administered questionnaire with internal consistency and test-retest reliability. Preliminary correlative analyses support the validity of the instrument as a measure of health status in adult type I and type II diabetic patients. Further work will be necessary to firmly establish the validity of the DIMS and its usefulness in clinical outcomes research.

Adult↗
PubMed1992

Fuel oxidation by insulin-dependent diabetics during late pregnancy in response to an oral glucose load.

1. To determine the oxidative response to a 50-g oral glucose challenge by diabetic women during late pregnancy under a more intensive therapeutic regimen than is conventionally employed, six normal pregnant women and ten insulin-dependent pregnant diabetic women were studied during the third trimester. Fuel (carbohydrate and lipid) oxidation rates were determined by indirect calorimetry, blood levels of substrates and C-peptide were measured directly, and glucose metabolism data (oxidation and nonoxidative metabolism) were estimated for both groups at the postabsorptive state and for the 2-h period following glucose ingestion. 2. The increases in the non-protein respiratory quotient (npRQ) and carbohydrate oxidation rates in response to glucose ingestion in the diabetic pregnant group were significantly smaller than in the normal pregnant individuals. The total amount of glucose oxidized by the diabetic pregnant group during the 2-h tests (6.1 +/- 0.6 g/m2) was significantly smaller than the oxidized by the normal pregnant group (8.3 +/- 0.4 g/m2), whereas there was more but not statistically significant lipid oxidation in the diabetic group (3.0 +/- 0.3 vs 2.6 +/- 0.1 g/m2). 3. The diabetic pregnant group not only oxidized less glucose (10.9 +/- 1.1 vs 14.1 +/- 0.8 g, P < 0.05) but more of this hexose remained in their glucose space (9.1 +/- 1.6 vs 3.2 +/- 1.1, P < 0.05) and they excreted 2.8 +/- 1.0 g into the urine. 4. The diabetic pregnant subjects had significantly lower blood levels of lactate, pyruvate and C-peptide than the normal pregnant subjects, but significantly higher blood levels of glucose, beta-hydroxybutyrate and acetoacetate. 5. The present data show that an intensive conventional therapeutic regimen during late pregnancy was not sufficient to completely normalize the glucose-processing capability of insulin-dependent diabetic patients.

Administration, Oral↗
PubMed1991

Responses of growth hormone and cortisol to intravenous glucose loading test in patients with anorexia nervosa.

The hypothalamic satiety and hunger centers appear to be affected by changes in circulating blood glucose concentrations. The response of the centers, in turn, is reflected by alterations in growth hormone (GH) and cortisol levels. There are no studies attempting to relate blood glucose and GH and cortisol changes in patients with anorexia nervosa (AN) during an intravenous glucose tolerance test (IVGTT). In the present inquiry, IVGTT (10 g) were performed on AN patients to characterize the satiety and hunger centers' responses to changes in glucose and insulin levels as reflected by GH and cortisol levels. Study participants were 15 female AN patients and eight healthy female volunteers. No significant differences in blood glucose levels were observed between the two groups. However, immunoreactive insulin (IRI) levels in AN patients were significantly lower than those in the control group. Although GH and cortisol concentrations were significantly suppressed after the infusion in the control group, the AN patients' GH levels paradoxically increased, and cortisol levels did not change. Moreover, a negative correlation was observed between delta GH and delta IRI in all individuals in this study (r = -.61, P less than .01). In conclusion, abnormal GH and cortisol responses to a 10-g IVGTT were found in patients with AN. delta GH levels correlated negatively with delta IRI levels. These data suggest that hypothalamic satiety and hunger centers in AN respond abnormally to change in blood glucose levels.

Adolescent↗
PubMed1989

Impaired glucagon secretion to insulin-induced hypoglycemia in anorexia nervosa.

In order to clarify the role played by pancreatic alpha-cell dysfunction in the impaired glucose recovery from hypoglycemia in patients with anorexia nervosa, the response of pancreatic alpha-cells to insulin-induced hypoglycemia was investigated in 16 patients with anorexia nervosa before and after treatment. The results were compared with those obtained after loading with arginine. Before treatment, despite comparable falls in plasma glucose levels, glucagon secretion was significantly reduced in the anorectic patients compared with control subjects. In addition, glucose recovery from hypoglycemia in the patients was attenuated. However, after treatment, both glucagon secretory activity and plasma glucose recovery following insulin-induced hypoglycemia were restored to normal. Plasma glucagon responses to arginine infusion were not significantly different in the untreated anorectic patients and control subjects. However, the plasma insulin response in the patients was significantly lower than in the control group. These results suggest that the impaired recovery of plasma glucose levels from insulin-induced hypoglycemia in patients with anorexia nervosa is primarily attributable to impaired pancreatic alpha-secretory capability. In addition, this abnormality in pancreatic alpha-cell function is reversible with treatment leading to improved nutrition and weight gain.

Adolescent↗
PubMed1989

Carbohydrate, lipid and amino acid metabolism of insulin-dependent diabetic patients regulated by an artificial beta-cell unit.

To characterize the effects of artificial beta-cell directed insulin therapy on carbohydrate, lipid and amino acid metabolism, five insulin-dependent diabetic patients were challenged with a 100-g glucose meal while on conventional (single or split mixed insulin injections) therapy and again after 72 hr on an artificial beta-cell unit. It was verified that the high levels of blood glucose of the conventionally treated diabetics were marked reduced toward normal by the artificial beta-cell therapy, while the blood lactate and pyruvate concentrations increased significantly to levels higher than in normal controls. The elevated levels of FFA, glycerol, and ketones in the diabetics under conventional therapy were entirely normalized during the artificial beta-cell regulation. Furthermore, the artificial beta-cell insulin therapy showed capable to restore the abnormalities in the blood profiles of alanine, glutamine and branched-chain amino acids, exceeding in some points the normal response. It was also detected hyperinsulinemia in the diabetics treated with the artificial beta-cell unit and no change in the pancreatic beta-cell function during this period of regulation, evidenced by low and unchanged blood levels of C-peptide. Marked suppression of pancreatic alpha-cell secretion was detected by the significant decrease of the hyperglucagonemia in the conventionally treated diabetics by the artificial beta-cell therapy. These studies reveal that the artificial beta-cell insulin therapy is capable of restoring to normal not only the abnormal glucose metabolism of conventionally treated diabetics, but also other substrate metabolism related to the lipid and protein homeostasis of the organism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Glucagon secretion in anorexia nervosa.

Patients with anorexia nervosa frequently manifest impaired glucose tolerance. However, alterations in pancreatic glucagon secretion have also been associated with alterations in diabetes mellitus. For this reason, pancreatic alpha- and beta-cell responses to glucose load were measured in 25 anorexic patients both before and after treatment. The baseline glucose challenge failed to suppress plasma glucagon levels in the patients. However, in the control subjects and patients after treatment, glucagon levels were suppressed after glucose ingestion. Plasma glucose levels during the baseline challenge were significantly higher than those of the control subjects; however, after treatment glucose responses were nearly normal. Finally, insulin responses at baseline and after treatment were lower in the patients than in control subjects. These results suggest that the impaired glucose tolerance manifested by anorexic patients may be attributable to significant alterations in both pancreatic alpha- and beta-cell secretions and in pancreatic alpha-cell and glucose interrelationships.

Analysis of Variance↗
PubMed1988

Effects of glucose loads of 50 and 100 g on carbohydrate and lipid oxidation in normal human subjects.

1. The effects of 50- and 100-g glucose loads on carbohydrate and lipid oxidation and substrate metabolism of seven normal subjects were studied in the postabsorptive state and for 3 h following glucose ingestion. 2. The increases in the non-protein respiratory quotient (npRQ) and carbohydrate oxidation rate were larger after the ingestion of 100 g glucose than after the 50-g glucose load. The total amount of glucose oxidized during the test with 100 g of glucose ingested orally (100-g OGT) (13.4 +/- 0.8 g/m2) was significantly greater than that oxidized during the 50-g OGT (9.5 +/- 0.6 g/m2), whereas lipid oxidation predominated in the tests with the smaller dose of glucose. The difference between the amounts of glucose oxidized during the two tests was greater when the increments above the basal values of glucose oxidation were compared (100-g OGT = 8.0 +/- 0.5 g/m2 vs 50-g OGT = 3.8 +/- 0.5 g/m2; P less than 0.001). 3. The glucose disposal data revealed that the subjects not only oxidized more of the hexose after the ingestion of 100 g of glucose but they also stored more than after the 50-g glucose meal. 4. The changes in the concentrations of glucose, lactate, pyruvate, alanine and insulin in the blood were also related to the amount of the glucose load. 5. It is suggested that the modulation of this oxidative response to glucose ingestion occurs in the insulin-dependent tissues.

Adult↗
PubMed1987

A computer-assisted image-analysis system for analyzing polymorphonuclear leukocyte chemotaxis in patients with diabetes mellitus.

A computer-assisted image-analysis system that precisely tracks the cell movements of up to 50 polymorphonuclear leukocytes (PMNLs) was developed and used to quantitatively measure cellular chemokinesis and chemotaxis in normal individuals and in diabetic patients with hyperglycemia. The PMNLs were tested in Zigmond chambers with or without a gradient of 10(-7) M n-formylmethionylleucylphenylalanine (f-Met-Leu-Phe). Cellular movement was recorded on videotape by using a videocamera mounted on the microscope. The videotapes were analyzed by computer programs to calculate the speed and direction of each PMNL at 10-sec intervals. Average rates of chemokinesis were 19.6 microns/min without and 25.3 microns/min with f-Met-Leu-Phe. McCutcheon indices, which measure chemotaxis, were 0.01 without and 0.48 with f-Met-Leu-Phe. Similar values were observed in diabetic patients after fasting (average glucose, 217 mg/100 ml) and 2 hr after glucose challenge (average glucose, 309 mg/100 ml). These values demonstrate that PMNLs from diabetic patients with hyperglycemia move at normal rates and respond appropriately to f-Met-Leu-Phe.

Adolescent↗
PubMed1986

Insulin stimulates branched chain amino acid uptake and diminishes nitrogen flux from skeletal muscle of injured patients.

Resistance to insulin-mediated glucose disposal occurs in uninjured skeletal muscle of trauma patients but the effect of insulin on the accelerated proteolysis of trauma is unknown. We examined the influence of insulin on forearm amino acid and substrate exchange in five normals and four trauma patients using the hyperinsulinemic glucose clamp technique. Forearm substrate and amino acid flux (Q, nM/100 ml tissue/min), the product of blood flow and arterial deep venous concentration difference, was calculated before and during insulin infusion. Total nitrogen release (NQ, nM/100 ml tissue/min) was calculated as the algebraic sum of all nitrogen groups contained in the amino acids released. Among normal subjects, total nitrogen release from the forearm did not change (581 +/- 197 nM/100 ml tissue/min to 1167 +/- 455) during insulin infusion nor did total branched chain amino acid flux (0 +/- 30 nM/100 ml/min to 106 +/- 36). Under conditions of hyperinsulinemia, neither glutamine nor alanine changed in control subjects. In trauma patients, total nitrogen release (3843 +/- 1383 nM/100 ml/min) was inhibited during insulin administration (819 +/- 314, P less than 0.05). Total branched chain amino acid flux went from a net release of 460 +/- 134 nM/100 ml/min to a net uptake of 10 +/- 82 (P less than 0.05). In patients, statistically significant (P less than 0.05) differences were seen in individual amino acids as well. Forearm nitrogen flux was directly related to total branched chain amino acid flux in patients (r2 = 0.89). Additional studies in normals (n = 4) at higher insulin infusion rates confirmed that these effects were unique to injured subjects and not an effect of the insulin dose. Insulin attenuates the accelerated release of skeletal muscle amino acid in trauma patients. This effect may be mediated in part by facilitated branched chain amino acid uptake. The manipulation of both insulin and branched chain amino acid concentrations may provide a method to reduce post-traumatic protein catabolism.

Adult↗
PubMed1986

Plasma level of 13,14-dihydro-15-keto-PGE2 in patients with diabetic ketoacidosis and in normal fasting subjects.

Plasma levels of 13,14-dihydro-15-keto-PGE2, a stable derivative of PGE2, are elevated in rats with diabetic ketoacidosis (DKA) and decrease in response to insulin therapy. In patients with insulin-dependent diabetes mellitus type I (IDDM) the plasma levels of this derivative also rise in response to insulin withdrawal and then fall in response to insulin replacement. We wished to determine whether the level of this substance is elevated acutely when patients present with DKA and to determine whether the levels fall during treatment. We also wished to identify the origin of the circulating 13,14-dihydro-15-keto-PGE2 in patients with DKA and in normal fasting subjects. We measured the plasma level of 13,14-dihydro-15-keto-PGE2 in five patients with DKA and in six normal subjects during a 24-h fast. In the patients with DKA before treatment, the plasma 13,14-dihydro-15-keto-PGE2 level was threefold above normal. During therapy, the 13,14-dihydro-15-keto-PGE2 level fell toward normal. There was a significant direct correlation between the plasma free fatty acid (FFA) level and the plasma 13,14-dihydro-15-keto-PGE2 level before and during treatment. In addition, the inverse correlation between the plasma free-insulin level and the plasma 13,14-dihydro-15-keto-PGE2 level approached significance (P = .06). In contrast, in the normal fasting subjects the plasma FFA level rose to values comparable to those observed in the patients with DKA, but there was no significant increase in the plasma 13,14-dihydro-15-keto-PGE2 level.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1985

Fuel utilization following injury: relationship to hormonal environment.

To investigate the relationship between fuel metabolism, insulin resistance, and hormonal environment, insulin clamp studies and indirect calorimetry were performed in nine normal volunteers after they had received a continuous infusion of the three "stress" hormones, cortisol, glucagon, and epinephrine, for 3 days. Studies after a 3-day infusion of saline served as control. Diets were constant and matched on both occasions. Hormonal infusion achieved hormone concentrations similar to those seen following mild to moderate injury. In this altered environment, insulin failed to suppress endogenous glucose production and resulted in reduced glucose disposal. The glucose that was taken up was oxidized, not stored. Furthermore, insulin failed to suppress fat oxidation. The altered hormonal environment achieved by triple hormonal infusion, simulated many of the features of post-traumatic fuel metabolism.

Basal Metabolism↗
PubMed1985

Role of muscle in CO2 production after oral glucose administration in man.

A significant increase in CO2 production, reflecting carbohydrate oxidation and/or fat synthesis, is observed in normal subjects after the ingestion of glucose. The anatomic site(s) of this CO2 production has not yet been localized, although liver and muscle are logical considerations. To assess the contribution of skeletal muscle to this process, we measured whole-body and forearm CO2 flux in normal, postabsorptive subjects after the ingestion of 100 g of glucose and calculated their total muscle CO2 production. In the basal state, muscle accounted for 19% of total CO2 production, and, after glucose administration, muscle CO2 production did not change significantly. Thus, muscle is not the principal site of the observed increase in CO2 production.

Adult↗
PubMed1984

Post-traumatic insulin resistance in uninjured forearm tissue.

Insulin resistance is a hallmark of post-traumatic metabolism. The mechanism and site of this resistance, however, have not been elucidated. To further define the site of this abnormality, glucose uptake across the uninjured forearm was measured in conjunction with hyperinsulinemic glucose clamp studies in 21 normals and 5 patients with multiple trauma. Under these conditions, glucose infused approximates whole body glucose disposal (M, milligrams/kilogram/min). Forearm glucose flux (Q, milligrams/100 ml tissue/min) is the product of blood flow and arterial-deep venous glucose difference (A-DV). In the basal, unperturbed state forearm glucose uptake (Q) was significantly lower in the patients (0.01 +/- 0.04 mg/100 ml/min) than in the normals (0.06 +/- 0.02) and not significantly different from zero. Basal serum insulin in patients (17 +/- 3 microU/ml) was significantly greater than controls (11 +/- 1). During steady-state conditions of euglycemia and hyperinsulinemia, forearm glucose uptake in the patients (0.36 +/- 0.18 mg/100 ml/min was not significantly different from the basal value. At comparable serum insulin levels in controls, forearm glucose uptake was approximately three times that of the injured patients. This is the first in vivo confirmation of the hypothesis that post-traumatic insulin resistance occurs in uninjured forearm tissue, primarily skeletal muscle. Diminished forearm glucose uptake is present in the resting basal state and cannot be overcome by increasing insulin concentrations.

Adult↗
PubMed1984

Metabolic, endocrine, and reproductive changes of a woman channel swimmer.

We report the coordinated metabolic, hormonal, and reproductive data of a female channel swimmer during the pre-swim training period, immediately post-swim, and in the post-swim untrained state. Urine and blood samples collected at these times were assayed for diurnal urinary catecholamines, urinary C-peptide and 3-methylhistidine, total blood ketone bodies, glycerol, the reproductive hormones, adrenal androgens, and thyroid hormones. Subcutaneous fat was measured by ultrasonography. All of the metabolic and hormonal data post-swim except cortisol reflected the severe physiological stress. Urinary catecholamines returned to near-normal levels by 12 hours post-swim. The metabolic changes were associated with reproductive changes, including a shortened luteal phase, absence of ovulation, and increased LH secretion relative to FSH. The swimmer maintained high levels of body fat; she did not become amenorrheic. Metabolic and reproductive hormone levels returned to normal by 2 months post-swim.

Adipose Tissue↗
PubMed1984

Combined hormonal infusion simulates the metabolic response to injury.

To investigate the role of hormones as mediators of the metabolic response to injury, nine normal male volunteers received a continuous 74-hour infusion of the three 'stress' hormones: cortisol, glucagon, and epinephrine. As a control, each subject received a saline infusion during another 4-day period. Diets were constant and matched on both occasions. Hormonal infusion achieved hormone concentrations similar to those seen following mild-moderate injury. With this alteration in the endocrine environment significant hypermetabolism, negative nitrogen and potassium balances, glucose intolerance, hyperinsulinemia, insulin resistance, sodium retention, and peripheral leukocytosis were observed. Additional studies with single hormone infusions indicated that these responses resulted from both additive and synergistic interactions of the hormones. Triple hormone infusion simulated many of the metabolic responses observed following mild-moderate injury and other catabolic illnesses.

Blood Flow Velocity↗
PubMed1983

The relationship between glutamate deamination and gluconeogenesis in kidney.

The effect of 3-mercaptopicolinate, an inhibitor of phosphoenolpyruvate carboxykinase [GTP:oxaloacetate carboxy-lyase (transphosphorylating), EC 4.1.1.32], was tested on NH3 formation via the purine nucleotide cycle and glutamate dehydrogenase (EC 1.4.1.2). NH3 excretion in rats increased 70-fold after 48 h of NH4Cl feeding, from 12.2 +/- 4.5 to 862 +/- 190 mumol/mg of creatinine. At 4 h after a single intraperitoneal injection of 3-mercaptopicolinate into NH4Cl-fed rats, NH3 excretion was inhibited by 93%. Kidneys of NH4Cl-fed plus 3-mercaptopicolinate-treated rats, compared with those of NH4Cl-fed rats, showed a 3.5-fold increase in the content of IMP, 5-fold increase in adenylosuccinate, 4-fold increase in aspartate, and a 30% increase in AMP. 3-Mercaptopicolinate completely inhibited NH3 and glucose formation from glutamate in tubules from acidotic rats and NH3 formation from aspartate in kidney perfusion experiments. When transamination in tubules was prevented by 2-amino-4-methoxy-trans-but-3-enoic acid, formation of glucose, but not of NH3, from glutamate was inhibited. 3-Mercaptopicolinate completely inhibited NH3 formation from aspartate in the presence of the aminotransferase inhibitor in kidney tubules. The data show that NH3 can be formed via glutamate dehydrogenase and the purine nucleotide cycle at significant and approximately equal rates. 3-Mercaptopicolinate has no direct effect on NH3 formation via glutamate dehydrogenase, but inhibits that via the purine nucleotide cycle. We conclude that gluconeogenesis is not regulatory for NH3 formation in kidney.

Aminobutyrates↗
PubMed1983

Early events in the initiation of ammonia formation in kidney.

Experiments were designed to examine the early events in the initiation of glutamate deamination in kidney. Perfused kidneys from methionine sulfoximine-treated rats formed ammonia from [15N]glutamate via the purine nucleotide cycle. The turnover of the 6-amino group of adenine nucleotides to yield ammonia occurred at the rate of 0.30 mumol/g of kidney/min. This rate is 3-4 times larger than in liver and is in agreement with published rates of the purine nucleotide cycle in kidney. The addition of 0.1 mM fluorocitrate to glutamate perfusions stimulated ammonia formation 3 1/2-fold. The turnover of the 6-amino group of adenine nucleotides increased during the first 5 min after adding fluorocitrate to form ammonia predominately from tissue glutamate and aspartate. This turnover correlates with a 3 1/2-fold increase in kidney tissue IMP levels. As the ATP/ADP ratio fell the purine nucleotide cycle was inhibited and glutamate dehydrogenase was stimulated to form ammonia stoichiometric with glutamate taken up from the perfusate. Ammonia formation via glutamate dehydrogenase occurred at a rate of 1.0 mumol/g of kidney/min. Fluorocitrate completely blocked ammonia formation from aspartate in perfusions. The perfused kidney formed ammonia from aspartate via the purine nucleotide cycle at a rate of 1.0 mumol/g of kidney/min. The results indicate a discrete role for aspartate in renal metabolism. Ammonia formation via the purine nucleotide cycle can occur at significant rates and equal to the rate of ammonia formation from glutamate via glutamate dehydrogenase.

Amino Acids↗