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Biomedical subjects

K McCormick

Publications and source records attributed to K McCormick.

At least 91 records · Page 5Linked to original sources
PubMed1987

The metabolic response to prolonged walking in fed and fasted men.

Six healthy men walked 37 km (23 miles) per day over a 3-lap course for each of 4 consecutive days. Subjects were allowed breakfast and an unrestricted diet was consumed after completion of the walk, but no food was consumed during or between laps. At a later date the same subjects walked over the same course after an overnight fast and without breakfast. Completion time for each lap was 139 +/- 1 min (mean +/- SE) and exercise intensity was equivalent to 17 +/- 1% VO2max. Mean 24h energy intake was 14.5 +/- 0.8 MJ during the fed walk. Estimated daily energy expenditure was 12.0 MJ. Blood glucose concentration fell significantly on the first, third and fourth days of the fed walk, but no subject became hypoglycaemic. Glucose concentration did not fall during the fasted walk and was significantly higher pre-exercise and at the end of laps one and three when compared to the first day of the fed walk. Blood alanine concentration fell significantly after the end of the first lap of each day of the fed walk but not during the fasted walk. Blood lactate levels did not change during the course of either walk. Plasma free fatty acid, glycerol and blood 3-hydroxybutyrate concentrations were unchanged during the passage of the first lap on each day of the fed walk, but all three had increased significantly by the end of the first lap of the fasted walk.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Pancreatic exocrine aplasia, clinical features of leprechaunism, and abnormal gonadotropin regulation.

A female infant displaying morphological and clinical abnormalities is described. She had severe developmental delay, intrauterine growth retardation, and failure to thrive. Her features included an elfin facies, body and facial hirsutism, buttonlike nipples and prominent clitoris and labia. Endocrinological evaluation revealed markedly elevated serum gonadotropin levels. An LHRH stimulation test showed no LH response to LHRH but a rapid and pronounced FSH response. The patient died at 13 months following a respiratory infection. Postmortem examination revealed normal pituitary histology but an unusual pancreatic histology characterized by total absence of acinar cells. This patient had features suggestive of several clinical syndromes including leprechaunism, Shwachman syndrome, and Johanson-Blizzard syndrome, none of which, was completely satisfied. It is concluded that the infant may represent an atypical case of leprechaunism or a previously undescribed syndrome.

Facial Expression↗
PubMed1986

Effect of tolazamide on basal ketogenesis, glycogenesis, and gluconeogenesis in liver obtained from normal and diabetic rats.

The effect of tolazamide on in vitro rates of gluconeogenesis, ketogenesis, and glycogenesis was determined in liver tissue from fasted normal and diabetic rats. Hormones were not added to the incubation mixture. Two concentrations of the drug were tested, one of which was therapeutic (40 micrograms/ml) and other immoderately elevated (400 micrograms/ml). Neither drug concentration affected hepatic glycogen synthesis. However, the low dose of tolazamide inhibited ketogenesis in the diabetic liver by 39% and in the control liver by 32%; oxidative CO2 production from palmitate was reduced in parallel with ketogenesis. The drug did not alter ketogenesis in isolated intact mitochondria. Similarly, this same therapeutic dose curtailed hepatic gluconeogenesis only in control liver (74% inhibition); this reaction was unaltered by this drug concentration in the explants derived from the diabetic rats. The logarithmically higher dose inhibited hepatic gluconeogenesis in both control and diabetic liver tissue by 56% and 51%, respectively. Hence, possibly acting at a postreceptor site, therapeutic concentrations of tolazamide can decrease rat hepatic in vitro gluconeogenesis and ketogenesis.

Animals↗
PubMed1985

Partial pyruvate decarboxylase deficiency with profound lactic acidosis and hyperammonemia: responses to dichloroacetate and benzoate.

We describe the successful use of sodium benzoate in a neonate with hyperammonemia associated with congenital lactic acidosis caused by a partial deficiency of the E1 component of pyruvate dehydrogenase (PDH); of note, this biochemical disturbance has not been previously described in PDH deficiency. The pyruvate dehydrogenase complex in skin fibroblasts had 48% of normal activity with a deficiency of the E1 component. The infant presented with rapid onset of a severe metabolic lactic acidosis, hyperventilation, hyperammonemia, and coma. At 30 hours of age continuous peritoneal dialysis was started; however, plasma NH3 concentrations remained in the 300-400 micrograms/dl range over the next 12 hours. Sodium benzoate, 250 mg/kg, was infused intravenously with a decrease in plasma ammonia of 25 micrograms/dl/hr. Hippurate was documented in the urine and peritoneal fluid after benzoate therapy. At 10.5 months of age, 50 mg/kg dichloroacetate was administered orally under fasting conditions, which resulted in a 56 and 62% reduction in the serum lactate and pyruvate levels, respectively; after 2 weeks on dichloroacetate his fasting levels were significantly decreased. Fibroblast PDH activity responded similarly to this drug. In our patient sodium benzoate was rapidly effective in producing a decline in plasma ammonia that was associated with clinical improvement. We feel that its use in organic acidemias deserves further evaluation and, furthermore, that any child with suspected PDH deficiency requires a clinical trial of dichloroacetate.

Acidosis↗
PubMed1985

Fetal rat hyperinsulinism and hyperglucagonism: effects on hepatic ketogenesis, lipogenesis, and gluconeogenesis.

To study the direct effects of hyperglucagonism and hyperinsulinism (both with glucose excess) on fetal intermediary metabolism, rat liver explants from 19-day-gestated fetuses were maintained in culture for 48 h. The liver cubes were exposed to 0, 250, or 500 mU/ml porcine insulin or 5 micrograms/ml glucagon. In addition, lipogenesis from 3H2O was cumulated throughout the 48 h. Chronic hyperinsulinism in the fetal rat doubled hepatic lipogenesis and curtailed hepatic gluconeogenesis and ketogenesis by 80% and 50%, respectively. Chronic hyperglucagonism was without effect; however, the fetal liver did yet respond to 1 mM (Bu)2cAMP.

Animals↗
PubMed1984

Thyrotropin (TSH)-induced hyperthyroidism: response of TSH to dopamine and its agonists.

A 12-yr-old girl with the syndrome of hyperthyroidism due to inappropriate TSH secretion, who had no evidence of pituitary tumor, was studied in detail. She had undergone two thyroidectomies for recurrent goiter and hyperthyroidism before referral. Basal serum TSH levels were extremely high (maximum 173 microU/ml), and the TSH response to TRH was exaggerated (peak, 675 microU/ml). The serum alpha-subunit of TSH was normal. PRL and other anterior pituitary hormone studies were normal. Dopamine infusion at 2 and 4 micrograms/kg X min partially suppressed TSH and PRL secretion and their responses to TRH. Bromocriptine had a paradoxical effect, resulting in an increase in TRH-stimulated TSH levels. Pergolide, a newer dopamine agonist, significantly decreased per basal serum TSH and blunted the TSH response to TRH; however, despite progressive dose increases, her TSH level was not reduced to normal.

Child↗
PubMed1984

Equation error.

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Aminophylline↗
PubMed1983

Importance of albumin binding in the assay for carnitine palmitoyltransferase.

Alterations in the long-chain acyl-CoA binding to albumin in the carnitine palmitoyltransferase (CPT) assay appreciably affect the reaction at commonly used substrate concentrations. Since in the CPT assay the latter are typically well below saturation or Vmax. values, the measured enzyme activity depends on both the absolute quantity of albumin in the CPT assay and any biochemical modification of its binding. The present study verifies the striking dependence of the K0.5 for palmitoyl-CoA on albumin and the misleading 'activation' of the enzyme by compounds that also avidly bind to albumin. In assessing the intracellular physiological relevance of any modifier of CPT, the effects of protein binding in the assay assume particular importance. Indeed, any compound that alters CPT activity may do so, not directly, but as an assay artifact changing the free or unbound substrate concentrations.

Acyltransferases↗
PubMed1983

Inhibition by acetyl-CoA of hepatic carnitine acyltransferase and fatty acid oxidation.

At micromolar concentrations, acetyl-CoA inhibited hepatic carnitine acyltransferase activity and mitochondrial fatty acid oxidation. The inhibitory effects were not nearly as potent on a molar basis as those of malonyl-CoA; nevertheless, the cytosolic concentrations of acetyl-CoA, as yet unknown, may be sufficient (greater than 30 microM) to curtail appreciably the mitochondrial transfer of long-chain acyl-CoA units and fatty acid oxidation. Hence acetyl-CoA may also partially regulate hepatic ketogenesis.

Acetyl Coenzyme A↗
PubMed1983

Autoradiographic demonstration of high affinity nuclear binding and finite binding capacity of [3H]estradiol in mouse vaginal cells.

Vaginae from adult C57Bl/6J mice were analyzed for nuclear estrogen-binding sites by biochemical as well as in vitro steroid autoradiographic methods. Finite binding capacity (saturability) and high affinity binding were demonstrated in stromal cell nuclei (Kd = 1.0 nM) by autoradiographic methods and in nuclear extracts of vaginal homogenates (Kd = 1.9 nM) by biochemical techniques. The results of this study demonstrate that all criteria considered definitive for estrogen receptors can be met by autoradiographic analysis, which makes feasible the assessment of estrogen receptor activity in the individual cell types that comprise fetal and neonatal estrogen target organs.

Animals↗
PubMed1980

Growth factor- and cyclic nucleotide-induced proliferation of normal and malignant mammary epithelial cells in primary culture.

Sustained growth of normal mouse mammary epithelial cells in primary culture, leading to an increase in cell number, in response to growth factors [epidermal growth factor (EGF) and fibroblast growth factor (FGF)] or cholera toxin has been achieved by embedding the cells inside collagen cells. Inclusion of agents known to increase the level of cellular cAMP have been found to be favorable for mammary epithelial cell proliferation. Cholera toxin is by far the best of all of the agents tested (prostaglandins E1 and E2, isoproterenol, theophylline, and dibutyryl cAMP). When growth factors (EGF or FGF) are added with cholera toxin, a synergistic effect resulting in a response much greater than with either of them alone is seen. This synergism was best seen in normal mammary epithelial cells from nonpregnant mice. The extent of this synergistic effect was found to be less in normal cells from pregnant mice, suggesting that these cells may be less responsive to EGF during pregnancy. Tumor cells were found to be rather inconsistent in their responses to EGF and cholera toxin, ranging from a minimal response, similar to that of normal cells from pregnant animals, to a maximal response, similar to that of normal cells from nonpregnant animals.

Animals↗