Number needed to treat is a simple measure of treatment efficacy for clinicians.
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Humans↗
Biomedical subjects
A B Gustafson
Publications and source records attributed to A B Gustafson.
Drug-induced disorders of glucose tolerance.
PURPOSE: To review the medications that influence glucose metabolism and to examine the mechanisms of these medications on glucose metabolism. DATA SOURCES: Data were obtained from a MEDLINE search back to 1966 and included animal and human studies published in the English language. STUDY SELECTION: Approximately 80% of original publications were included after review by the authors. Case reports were included if they provided additional information. DATE EXTRACTION: The original data from the literature were included on the basis of independent extraction by the authors. DATA SYNTHESIS: Many common therapeutic agents influence glucose metabolism. Multiple mechanisms of action on glucose metabolism exist through pancreatic, hepatic, and peripheral effects. Based on circumstances at the time of use, a drug may cause both hyper- and hypoglycemia in a patient. The patient's previous pancreatic reserve, nutritional state, use of other medication, or exposure to alcohol may influence the direction of the plasma glucose alterations. CONCLUSION: Hyperinsulinemia and insulin resistance form an intrinsic component of diabetes, hyperlipidemia, and atherosclerotic vascular disease (syndrome X). The induction of hyperinsulinemia and insulin resistance by medication may therefore counteract intended benefits. An extensive review of recent medication in patients with disorders of glucose tolerance and the avoidance of polypharmacy are recommended. It is prudent to monitor plasma glucose values when it is not possible to avoid prescription of medication with known effects on carbohydrate metabolism.
Animals↗
Relationship of regional fat distribution and obesity to electrocardiographic parameters in healthy premenopausal women.
Abdominal obesity is an independent cardiovascular risk factor. The coexistence of abdominal obesity and electrocardiographic abnormalities may facilitate the development of cardiac arrhythmias and sudden death. We determined the relationship of body fat distribution and obesity to ECG indices in 27 obese premenopausal women on an isocaloric diet. Intra-abdominal fat distribution was assessed by computerized tomography, and obesity was assessed by hydrostatic weighing. The PR, QRS, and QTc intervals, the P and QRS axes, and the P-QRS angle were determined from a resting electrocardiogram. Cardiovascular risk profile was assessed by systolic and diastolic blood pressure and plasma cholesterol and triglyceride levels. Increased deposition of intra-abdominal fat was significantly associated with prolongation of the QTc interval independent of obesity and other cardiovascular risk factors. The prolongation of the QTc interval seen with increasing intra-abdominal fat distribution may enhance susceptibility to cardiac arrhythmias. These subjects should have electrocardiographic monitoring during periods of weight loss achieved by intensive regimens.
Abdomen↗
Impaired plasma catecholamine response to submaximal treadmill exercise in obese women.
After an overnight fast, blood samples were obtained from seven obese women (50% +/- 3% body fat) and from seven control women (25% +/- 1% body fat) before, during, and after 10 minutes of treadmill exercise at 70% of each individual's maximal oxygen uptake (VO2max). During exercise, peak plasma epinephrine (E), norepinephrine (NE), and glucagon concentrations in the control group significantly exceeded corresponding peak values in the obese group by 1.4-fold to twofold, whereas lactate responses did not differ. After 5 minutes of rest, peak plasma glucose, free fatty acid (FFA), and growth hormone (GH) concentrations in the control group also were significantly higher than in the obese women, but the plasma cortisol responses were comparable. Although plasma insulin concentrations decreased during exercise and rose to maximum values at 5-minute recovery in all individuals, levels were more than 3.5-fold higher in the obese group throughout the study. We conclude that the combination of heightened plasma insulin and diminished catecholamine and other counterregulatory hormone responses may account for subnormal plasma substrate increments that distinguish obese from non-obese women during exercise at comparable work intensities.
3-Hydroxybutyric Acid↗
Plasma free and sulfoconjugated catecholamines during sustained exercise.
Previous research established a relationship between circulating sulfoconjugated norepinephrine (NE-SO4) and oxygen consumption at various exercise intensities. In this study, the stability of the NE-SO4 response was examined during sustained exercise at a constant relative intensity. Seven trained men bicycled at 78 +/- 3% of their maximal O2 consumption for 28 min and then rested on the ergometer for a comparable duration. After a 30-min rest, plasma samples were collected through an indwelling catheter at 7-min intervals during the exercise and recovery periods. Free NE and epinephrine increased sixfold during exercise. These changes were accompanied by increases in sulfoconjugated catecholamines, but only NE-SO4 achieved statistical significance (rest, 712 +/- 602; exercise, 1,329 +/- 1,163 pg/ml). This occurred at three collection periods (14, 21, and 28 min). Approximately 35, 52, and 95% of NE, epinephrine, and dopamine, respectively, existed as sulfoconjugated during exercise. Subject variation was present in the sulfoconjugated catecholamine response that could not be attributed to corresponding differences in circulating free catecholamine release. These findings implicate blood flow as a factor in the sulfoconjugation of NE, but not epinephrine or dopamine.
Adult↗
Adiposity, fat distribution, and cardiovascular risk.
STUDY OBJECTIVE: To determine the relative importance of adiposity and fat distribution to cardiovascular risk profile. DESIGN: A cross-sectional study. SETTING: Clinical research center funded by the National Institutes of Health. PATIENTS: Convenience sample of 33 healthy premenopausal women with a wide range of body weight who did not have diabetes mellitus, hirsutism and virilism, gynecologic disorder, cardiac disease, or hypertension. Women participating in exercise or dietary programs or taking medication were excluded. All subjects completed the study. INTERVENTIONS: Total body fat mass was determined by hydrostatic weighting, and fat distribution was assessed by subscapular skinfold thickness, subscapular-to-triceps skinfold ratio, the waist-to-hip ratio, and computed tomography. Cardiovascular risk was assessed by the serum insulin response during oral glucose stimulation; levels of triglycerides and total cholesterol; high-density lipoprotein cholesterol to total cholesterol concentrations; and systolic and diastolic blood pressures. MEASUREMENTS AND MAIN RESULTS: The anthropometric parameters chosen were significantly associated with the cardiovascular risk profile (P less than 0.001). Visceral fat distribution assessed by computed tomography accounted for a significantly greater degree of variance in the cardiovascular risk factors than the total body fat mass (P less than 0.05). The cumulative insulin response was the primary metabolic variable relating the anthropometric indices to cardiovascular risk. CONCLUSIONS: Intra-abdominal fat deposition constitutes a greater cardiovascular risk than obesity alone. Hyperinsulinemia may constitute an important component of the increased cardiovascular risk of abdominal obesity.
Adipose Tissue↗
Relative contribution of obesity and body fat distribution to alterations in glucose insulin homeostasis: predictive values of selected indices in premenopausal women.
Obesity and fat topography are risk factors for hyperinsulinemia, insulin resistance, and diabetes mellitus. The relative contribution of obesity and body fat distribution indices to fasting and oral glucose-stimulated C peptide, insulin, and glucose concentrations were determined in 33 healthy premenopausal women. Obesity level was assessed by hydrostatic weighing and fat topography by computerized tomography-derived intraabdominal fat area, waist to hip ratio, subscapular skinfold thickness and the ratio of subscapular to triceps skinfold thickness. Both fat mass and regional fat distribution indices were associated closely with changes in insulin secretion. Fat topography indices were more closely correlated (p less than 0.001) to insulin response than were fat mass indices (p less than 0.01). The subscapular skinfold thickness had the greatest integrity for reflecting fat mass and fat distribution as they relate to the metabolic profile. The subscapular skinfold thickness may help identify individuals at risk for noninsulin dependent diabetes mellitus.
Adipose Tissue↗
Cardiovascular fitness and selected adrenal hormone responses to cognitive stress.
Individuals manifesting high maximal oxygen consumption (VO2max) have augmented adrenal responsivity to physical stress. We subjected 17 males representing a wide range of VO2max to cognitive stress and measured their forearm venous plasma epinephrine, norepinephrine, and cortisol responses. Six repeated blood samples were collected at resting, stress, and recovery intervals. Significant increases were observed for epinephrine (X +/- SD; rest, 50 +/- 30; stress, 81 +/- 77 pg/ml; p less than or equal to 0.05) and norepinephrine (rest, 404 +/- 235; stress, 481 +/- 314 pg/ml; p less than or equal to 0.05). Cortisol changes were not significant. A positive association (r = 0.54; p less than or equal to 0.05) was observed between epinephrine and VO2max during the first collection of the stress period. An inverse association (r = 0.49; p less than or equal to 0.05) was present between VO2max and norepinephrine. No significant correlations occurred with cortisol. These results indicate that enhanced cardiovascular fitness is characterized by augmented epinephrine responsivity to cognitive stress. This association exists in the presence of an inverse relationship between plasma free norepinephrine response and VO2max.
Adult↗
Hemodynamic and hormonal abnormalities in canine aortic coarctation at rest and during exercise.
This study was designed to determine the hemodynamic and hormonal consequences of aortic coarctation at rest and during treadmill exercise. Twelve normal adult dogs served as controls. In eight dogs coarctation was created within 1 week of birth by banding the aorta just proximal to the ductus ligament, thereby fixing luminal diameter at 1 to 2 mm. Studies were performed 18 months after operation. Vascular pressures were monitored proximal and distal to the coarctation, cardiac output and regional blood flow were evaluated with radioactive microspheres and blood samples were collected for determination of hormone levels and blood gases. At rest, systolic pressure in the proximal aorta was 130 +/- 12 mm Hg (mean +/- SD) in the control group and 167 +/- 16 mm Hg in dogs with coarctation (p less than 0.01). During exercise at a level that doubled heart rate and cardiac index, mean aortic pressure increased by 11 and 31% (p less than 0.01) in the control and the coarctation group, respectively. Mean distal aortic pressure increased by 8% during exercise in control dogs but decreased by 29% in dogs with coarctation. Exercise decreased flow to the kidneys and the large intestine in the coarctation group. Plasma norepinephrine concentrations were greater in the coarctation group than in control dogs at rest; during exercise, plasma norepinephrine, epinephrine and renin activity increased in both groups, but to a greater degree in the group with coarctation. These results confirm an abnormality in renal and gut perfusion in experimental coarctation and suggest that this may be related to a decline in perfusion pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Comparison of discrete cardiovascular fitness groups on plasma catecholamine and selected behavioral responses to psychological stress.
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Adult↗
Plasma free and sulfoconjugated catecholamine responses to varying exercise intensity.
Plasma free catecholamines rise during exercise, but sulfoconjugated catecholamines reportedly fall. This study examined the relationship between exercise intensity and circulating levels of sulfoconjugated norepinephrine, epinephrine, and dopamine. Seven exercise-trained men biked at approximately 30, 60, and 90% of their individual maximal oxygen consumption (VO2max) for 8 min. The 90% VO2max period resulted in significantly increased plasma free norepinephrine (rest, 219 +/- 85; exercise, 2,738 +/- 1,149 pg/ml; P less than or equal to 0.01) and epinephrine (rest, 49 +/- 49; exercise, 555 +/- 516 pg/ml; P less than or equal to 0.05). These changes were accompanied by consistent increases in sulfoconjugated norepinephrine at both the 60% (rest, 852 +/- 292; exercise, 1,431 +/- 639; P less than or equal to 0.05) and 90% (rest, 859 +/- 311; exercise, 2,223 +/- 1,015; P less than or equal to 0.05) VO2max periods. Plasma sulfoconjugated epinephrine and dopamine displayed erratic changes at the three exercise intensities. These findings suggest that sulfoconjugated norepinephrine rises during high-intensity exercise.
Adult↗
Enkephalins, catecholamines, and psychological mood alterations: effects of prolonged exercise.
Seven healthy trained men were studied to determine if running at various relative intensities [percent maximal oxygen consumption (VO2max)] alters peripheral venous levels of leucine enkephalin-like material. Enkephalins were measured using a radio-receptor assay (Leu-Enk RRA). Subjects ran for 80 min at 40 and 60% VO2max and for 40 min at 80% VO2max. Each session was separated by at least 1 wk. Heart rate, blood pressure, lactic acid, and rectal temperature responses increased in an intensity-dependent manner. Epinephrine increased from resting values of 38.2 +/- 6.8 pg X ml-1, mean +/- SE to 75.0 +/- 13.3 pg X ml-1 during the 40% VO2max run, from 60.2 +/- 15 to 186 +/- 45 pg X ml-1 during the 60% run, and from 33.4 +/- 7.6 to 311 +/- 52 pg X ml-1 at the 40th min of the highest workload (80% VO2max). These increases were significant (P less than 0.05). Plasma Leu-Enk RRA was between 3.8 and 6.2 pmol X ml-1 prior to each run and did not change significantly as a result of exercise. Levels of Leu-Enk RRA also did not change during 30 min of supine recovery. Perception of effort increased (P less than 0.05) with increases in exercise intensity, and effort sense was unrelated to plasma Leu-Enk RRA. Psychological tension decreased significantly (P less than 0.05) following exercise at 60 and 80% of VO2max, but the decrease following the 40% run was not significant (P greater than 0.05). Reduced tension following exercise was not related to Leu-Enk RRA.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Influence of endogenous opioids on the response of selected hormones to exercise in humans.
To examine the influence of endogenous opioids on the hormonal response to isotonic exercise, eight males were studied 2 h after oral administration of placebo or 50 mg naltrexone, a long-lasting opioid antagonist. Venous blood samples were obtained before, during, and after 30 min of bicycle exercise at 70% VO2max. Naltrexone had no effect on resting cardiovascular, endocrine, or serum variables. During exercise epinephrine was higher [mean 433 +/- 100 (SE) pg/ml] at 30 min with naltrexone than during placebo (207 +/- 26 pg/ml, P less than 0.05). Plasma norepinephrine showed the same trend but the difference (2,012 +/- 340 pg/ml with naltrexone and 1,562 +/- 241 pg/ml with placebo) was not significant. Plasma glucose was higher at all times with naltrexone. However, the difference was significant only 10 min into recovery from exercise (104.7 +/- 4.7 vs. 94.5 +/- 2.8 mg/dl). Plasma growth hormone and cortisol increased during recovery and these elevations were significantly (P less than 0.05) augmented by naltrexone. Plasma vasopressin and prolactin increased with exercise as did heart rate, blood pressure, lactic acid, and several serum components; these increases were not affected by naltrexone. Psychological tension or anxiety was lower after exercise compared with before and this improved psychological state was not influenced by the naltrexone treatment. These data suggest that exercise-induced activation of the endogenous opioid system may serve to regulate the secretion of several important hormones (i.e., epinephrine) during and after exercise.
Adult↗
Elevated plasma vasopressin (AVP) levels during resection of pheochromocytomas.
During the evaluation of epidural blockade with light general anesthesia for pheochromocytoma resection, increases in plasma arginine vasopressin (AVP) concentrations were noted. We measured AVP levels in conjunction with plasma catecholamines during perioperative maneuvers in eight consecutive patients undergoing resection of pheochromocytomas. Hormonal responses (mean +/- SE) for preoperative baseline and peak values during tumor manipulation were as follows: AVP, 5 microgram/ml or picogram/ml (+/- 1.7) to a peak of 129 pg/ml (+/- 44) pg/ml; norepinephrine, 5,834 pg/ml (+/- 2,564) to 72,422 (+/- 31,433) pg/ml; epinephrine, 1,033 pg/ml (+/- 405) to 56,444 (+/- 23,542) pg/ml; and dopamine, 165 pg/ml (+/- 35) to 4,231 (+/- 1,318) pg/ml. Maximal AVP values occurred with tumor manipulation and remained elevated for 24 hours postoperatively. Neither epidural placement, induction of anesthesia, nor epidural narcotics used for postoperative pain control had any effect on AVP or catecholamine levels. These extraordinarily high concentrations of plasma AVP found during tumor manipulation may contribute to hemodynamic lability and fluid problems in patients undergoing surgery for the treatment of pheochromocytoma.
Adolescent↗
Transient laryngeal nerve paralysis accompanying Hashimoto's thyroiditis.
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Adult↗
Assessment of methods for assigning treadmill exercise workloads for lean and obese women.
The use of relative oxygen consumption (% VO2 max) to equate workloads between trained and untrained subjects is considered appropriate. Whether this method (% VO2 max) is correct when testing lean versus obese subjects has not been studied. Using three experimental sessions separated by at least one week we studied seven obese, nondiabetic women weighting 140 +/- 21 kg (mean +/- s.d.) and 10 lean women of similar age weighing 51 +/- 5 kg during treadmill walking. Body fat determined by hydrostatic weighing was 50 +/- 7 and 23 +/- 7 percent in obese and lean groups, respectively (P less than 0.05). Absolute maximal VO2 (VO2 max) in obese women (3.18 +/- 0.28 l/min) significantly exceeded VO2 max for lean women (2.45 +/- 0.31 l/min, P less than 0.05). However, in obese women VO2 max relative to total body weight (TBW) was lower (P less than 0.05) while VO2 max relative to fat-free weight (FFW) was similar to corresponding values for lean women. Submaximal treadmill exercise at 75m/min with 0, 5 and 10 percent inclines resulted in higher VO2 (l/min) and heart rate (HR) in the obese group (P less than 0.05). At each incline VO2 relative to BW was significantly lower in the obese (P less than 0.05) yet significantly higher when expressed relative to FFW (P less than 0.05). The relationship between HR and %VO2 max was similar for lean and obese. Ten minutes of walking at 70% VO2 max resulted in no significant differences between the groups in the 10 min values for HR, total work done, rise in rectal temperature, plasma lactic acid, perceived exertion and oxygen consumption relative to FFW. We conclude that either fixed absolute workloads or fixed oxygen consumption (absolute or relative to BW or FFW) are inappropriate methods for equating workloads when lean and obese subjects are compared. Relative VO2 accurately defines physiologically comparable exercise intensities for these groups and this should be the method of preference when studies are designed to investigate metabolic, endocrine or cardiovascular similarities and/or differences between these groups.
Adult↗
Plasma adrenocorticotropin and cortisol responses to submaximal and exhaustive exercise.
Adrenocorticotropic hormone (ACTH) levels were compared before and after submaximal and exhaustive isotonic exercise in six normally active college students (3 men and 3 women). Each subject participated in three experiments conducted at the same morning hour. Venous plasma was obtained before and immediately after 20-min runs at 65 and 80% of maximal O2 consumption (VO2 max) and after a run of gradually increasing work intensity which resulted in exhaustion (100% VO2 max) in 12.6 +/- 1.3 min. ACTH (mean +/- SE) was 48 +/- 15, 57 +/- 12, and 61 +/- 11 pg/ml before the 65, 80, and 100% VO2 max runs, and increased to 61 +/- 15 (NS), 128 +/- 18 (P less than 0.05), and 292 +/- 72 (P less than 0.05) pg/ml, respectively. Plasma glucose, growth hormone, cortisol, and lactic acid concentrations increased in a similar fashion. Cortisol and ACTH levels were significantly correlated at the higher levels of exertion: r = 0.18 (NS) for the 65% VO2 max run, r = 0.65 (P less than 0.05) for the 80% VO2 max run, and r = 0.64 (P less than 0.05) for the run to exhaustion. Both the change in ACTH with exercise and its postrun concentration were significantly related to the change in plasma lactic acid (r = 0.65, P less than 0.05) and the postrun plasma lactic acid (r = 0.64, P less than 0.05). We conclude that exercise-induced increases in plasma ACTH and their correlation with circulating cortisol depend on the intensity of isotonic exercise. Our observations also suggest that plasma lactic acid may influence ACTH release during exercise.
Adrenocorticotropic Hormone↗
Influence of sex and obesity on plasma catecholamine response to isometric exercise.
The effects of obesity and gender on plasma catecholamine levels were studied in 10 lean men, 10 lean women, and 10 obese women. Measurements (mean +/- SE) were obtained sequentially after 30 min of bedrest, 10 min of standing, and 5 min of sustained handgrip, and following 15 min of rest while standing. The supine plasma norepinephrine (NE) levels were comparable among the 3 groups, whereas plasma epinephrine (E) was lowest in obese women (14 +/- 2 pg/ml), intermediate in lean women (19 +/- 2 pg/ml), and highest in lean men (29 +/- 5 pg/ml). Peak plasma levels were reached during handgrip. E values in men (139 +/- 27 pg/ml) exceeded those in lean women (71 +/- 9 pg/ml; P less than 0.05), and both were higher than the E response in obese women (38 +/- 7 pg/ml; P less than 0.01). While peak plasma NE levels in lean women (654 +/- 62 pg/ml) and obese women (524 +/- 46 pg/ml) were comparable, both were significantly lower than the NE response in lean men (1014 +/- 114 pg/ml; P less than 0.02). Increments in plasma FFA during handgrip were 21% and 28% above values during standing (P less than 0.005) in lean men and lean women, respectively, whereas no net increment occurred in obese women. The excursion of plasma beta-hydroxybutyrate in recovery was 59% above the standing concentration for lean women (P less than 0.05), but no net increments were observed in obese women or lean men. We conclude that obesity in women is attended by suppressed plasma E responses to isometric exercise, which may explain subnormal excursions of plasma FFA and beta-hydroxybutyrate during handgrip and recovery, respectively. Lean men have greater plasma elevations of E and NE during isometric exertion than women, suggesting an influence of sex on plasma catecholamine regulation.
3-Hydroxybutyric Acid↗