Biomedical subjects
Publications and source records attributed to D J Cox.
By using the luciferase-luciferin ATP assay and whole cells of Leuconostoc oenos, we have demonstrated that malolactic fermentation does yield ATP. This energy-yielding mechanism did not occur in a cell extract and was inhibited in the presence of dicyclohexylcarbodiimide or an ionophore such as monensin. A lactate:proton efflux mechanism for this proposed pathway is presented.
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Whereas self-monitoring of blood glucose (SMBG) is the recommended source of information on which to make self-care decisions, patients frequently use estimates of their own blood glucose (BG). This study evaluated whether patients with insulin-dependent diabetes mellitus (IDDM) could learn to improve accuracy of BG estimations and whether this would lead to improved metabolic control. Subjects in BG awareness training improved both their BG-estimation accuracy and glycosylated hemoglobin (HbA1) compared with the control group. Initial BG-estimation accuracy was marginally associated with pretreatment HbA1 and months of previous SMBG experience. Posttreatment improvement was associated with pretreatment BG-estimation accuracy and the ability to counterregulate to insulin-induced hypoglycemia.
1. Intragastric administration of ethanol (75 mmol/kg body wt.) at 1 h before glucose refeeding of 24 h-starved rats inhibited hepatic glycogen deposition (by 69%) and synthesis (by approx. 70%), but was without significant effect on muscle glycogen deposition and synthesis. 2. Treatment of ethanol-administered rats with methylpyrazole (an inhibitor of alcohol dehydrogenase) did not significantly diminish the inhibitory effect of ethanol on hepatic glycogen deposition after glucose refeeding, suggesting that the inhibition was not dependent on ethanol metabolism. 3. Ethanol delayed and diminished intestinal glucose absorption, at least in part by delaying gastric emptying. 4. At a lower dose (10 mmol/kg body wt.), ethanol inhibited hepatic glycogen repletion and synthesis without compromising intestinal glucose absorption. Ethanol inhibited glycogen deposition (by 40%) in hepatocytes from starved rats provided with glucose + lactate + pyruvate as substrates, consistent with it having a direct effect to diminish hepatic glycogen synthesis by inhibition of gluconeogenic flux at a site(s) between phosphoenolpyruvate and triose phosphate in the pathway. 5. It is concluded that ethanol acutely impairs hepatic glycogen repletion by inhibition at at least two distinct sites, namely (a) intestinal glucose absorption and (b) hepatic gluconeogenic flux.
Behavior change through psychotherapy is frequently accomplished through the use of homework assignments conducted by patients between treatment sessions. There has been little attention directed at adherence to such behavioral prescriptions. This study compares the effects of Verbal versus Written behavioral prescriptions on recall of self-reported adherence to therapeutic homework assignments. Thirty subjects were randomly assigned to the Verbal and Written conditions in a counterbalanced, within-subjects, crossover design. Written prescriptions led to significantly better recall of and adherence to homework assignments.
Self-management of insulin-dependent diabetes mellitus (IDDM) is dependent on a negative feedback loop of blood glucose (BG) fluctuations, which in turn directs treatment decisions to maintain normal BG. Although this feedback is typically accomplished by self-monitoring of blood glucose (SMBG), SMBG has limitations, and patients often rely on what their BG "feels" like. Two studies were performed to evaluate whether patients could learn to more accurately "feel"/discriminate their BG on the basis of internal cues or internal plus external BG cues. In Study I, BG Awareness Training significantly improved pre- to posttreatment BG estimation accuracy, relative to a control group. Study II replicated BG Awareness Training efficacy in improving BG estimation accuracy. Improvement in estimation accuracy was related only to initial accuracy; those who were initially less accurate improved the most. This improvement was represented in a 31% reduction in dangerous BG estimation errors and a 9% increase in accurate estimates. Resulting estimations were, however, still significantly less accurate than SMBG at the end of training.
This study was designed to see whether the high vs low serum level of imipramine influenced the outcome of in vivo exposure therapy on patients with agoraphobia. Thirty-six subjects completed the Hopkins Symptom Checklist-90 one week before treatment and weekly throughout treatment. Both groups demonstrated equal improvement. It was noted that the rate of improvement differed for different symptom subscales: (1) Hostility, Paranoia and Psychotic symptom ratings improved over the first three weeks of treatment, (2) Interpersonal Sensitivity, Anxiety and Depression ratings improved throughout the first seven weeks of treatment and (3) Phobic Anxiety, Somatization and Obsessive Compulsure symptom ratings continued to improve throughout the entire 12 week course of treatment. Responsive vs nonresponsive subjects could be significantly differentiated after one week of treatment on the basis of their responses to the Psychoticism subscale.
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Eighteen insulin-dependent diabetic subjects [age (mean +/- SD) 33.2 +/- 10.6 yr] participated in a study designed to determine the metabolic and cutaneous parameters associated with activation of the nocturnal hypoglycemia monitor Sleep Sentry. Plasma glucose, glucagon, epinephrine, norepinephrine, and pancreatic polypeptide concentrations were determined every 10 min during a 2-h constant intravenous insulin infusion (40 mU.kg-1.h-1). In addition, skin temperature and electrical conductance were monitored at the same time intervals, and subjects were asked to rate the degree to which they felt cold and/or sweaty. Ten of the subjects (alarmers) activated the device with a mean plasma glucose nadir of 52.8 +/- 13.8 mg/dl, whereas eight (nonalarmers) failed to do so despite a mean plasma glucose nadir of 50.5 +/- 8.2 mg/dl. There were no significant differences between alarmers and nonalarmers with respect to initial or nadir plasma glucose levels, rate of fall of plasma glucose, or changes in plasma epinephrine, norepinephrine, or pancreatic polypeptide concentrations. In addition, changes in skin temperature and conductance were similar in both groups as were descriptive variables including age, disease duration, gender, and level of glucose control. No subject reported an increase in coldness, whereas 80% of both groups reported an increase in sweatiness. Three subjects studied on more than one occasion over a year failed to exhibit consistent activation of the alarm. This study suggests that it may not be possible to identify patients for whom the Sleep Sentry would be a reliable addition to their self-management regimen and that physicians should exercise caution in recommending its use.
In mice, the response of carcass glycogen to glucose re-feeding after starvation is biphasic. The initial repletive phase is followed by partial (greater than 50%) glycogen mobilization. This turnover of carcass glycogen in response to carbohydrate re-feeding may play an important role in the provision of C3 precursors for hepatic glycogen synthesis.
The enzymic determination of D-3-hydroxybutyrate and acetoacetate normally involves the use of 3-hydroxybutyrate dehydrogenase (HBDH, EC 1.1.1.30) of bacterial origin. We show that HBDH from Rhodopseudomonas spheroides (BCL, grade II) contains a 3-hydroxyisobutyrate dehydrogenase (HIBDH) activity: activity with 3-hydroxyisobutyrate as substrate was greater than 10% of that with 3-hydroxybutyrate. However, HBDH could be prepared essentially free of HIBDH activity by incubation at 37 degrees C in the presence of 1 mM-CaCl2, to produce an enzyme preparation that may be used for the specific determination of 3-hydroxybutyrate. Use of the purified enzyme preparations indicated that a major product of valine metabolism in hemidiaphragms from 40 h-starved rats was 3-hydroxyisobutyrate rather than 3-hydroxybutyrate.
The purpose of the present study was to address the question of whether environmental stress affects the age of onset and incidence of overt insulin-dependent diabetes mellitus in an animal model of human Type 1 (insulin-dependent) diabetes. Thirty-five diabetes prone BB rats of both sexes were divided into two groups: experimental animals were exposed to multiple, concurrent, and unpredictable environmental stressors, while littermate controls were exposed to a standard lab environment. Groups were housed in two separate, sound attenuated, independently ventilated, and restricted rooms. By age 150 days, experimental group animals had developed overt diabetes at a significantly earlier age.
Recent findings demonstrate that, in rats, posttraining injections of glucose can enhance subsequent memory performance. The purpose of this study was to extend these findings to an elderly human population by testing the hypothesis that acute increases in peripheral blood glucose levels would enhance performance on memory tasks. Eleven subjects ranging in age from 58 to 76 years participated in the study. A within-subject, repeated-measures design was used in which each subject was tested under two different glycemic conditions: with fasting blood glucose levels and with increased blood glucose levels. Blood glucose was manipulated via consumption of beverages sweetened with either saccharin or glucose powder. After beverage consumption, subjects took four tests from the Wechsler Memory Scale. Comparisons of performance under the two glycemic conditions showed that scores were higher after the glucose beverage on narrative memory tests and the total Wechsler Scale. Nine of the eleven subjects had higher total Wechsler Scale scores. These results contribute to the growing evidence that glucose metabolism should be considered in the study of memory processes. The implications of such relationships for age-related memory deficits are discussed.
Both diabetic patients and health care practitioners often assume that the subjective symptoms of extreme low and high blood glucose (BG) levels are easily recognized. This study tested the accuracy of BG symptom beliefs in a group of 26 insulin-dependent diabetic patients. A within-subject, repeated measures design was used to identify symptoms related to low and high glucose levels for individual subjects. On three occasions over a 1-year period, subjects completed symptom checklists just prior to 40 consecutive self-measurements of BG (an average of four times per day for 10 days). At the end of the year, subjects reported which symptoms they believed were related to their own low and high glucose levels. After determining whether each checklist item was empirically related to glucose levels and believed to relate to glucose levels, symptom beliefs were categorized as hits, false alarms, misses, or correct rejections. Across subjects, the frequency of accurate beliefs (hits and correct rejections) was higher than the frequency of inaccurate beliefs (false alarms and misses). Symptom belief accuracy differed greatly for individual subjects, however, and every subject had at least one inaccurate belief. False alarm beliefs were the more common type of error. Female subjects' symptom beliefs yielded more hits, as well as more false alarms. Males missed more symptoms, especially low BG symptoms, than females. Symptom belief accuracy was greater if symptom-glucose relationships remained stable across time.
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In quarter-diaphragms from 40 h-starved rats the rate of glycogen mobilization is sufficient to account for the rate of lactate+pyruvate+alanine production. It is concluded, therefore, that alanine derives its carbon skeleton predominantly via glycolysis and not via synthesis de novo from tricarboxylic acid-cycle intermediates and related amino acids.