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Biomedical subjects

C Bogardus

Publications and source records attributed to C Bogardus.

At least 145 records · Page 8Linked to original sources
PubMed1991

Billing tactics. Advantages of a professional billing service in radiation oncology.

An efficient billing system for your professional services must include the following items: 1. A significant amount of personal involvement by the physician in the origination of the patients' charges. 2. Friendly, courteous, and helpful personnel for patient interaction. 3. Timely and accurately posting of accounts. 4. An absolute separation of receipt of payments and account reconciliation. 5. A personal interest by the physician in the accounts receivable balance as well as monthly financial summaries of the ongoing business of your practice. 6. Knowledge of the patient's credit history and ability to pay for services. 7. Dedication to serving you in the most efficient cost-effective manner. 8. A method for remaining absolutely current on any changes occurring in the healthcare reimbursement sector. 9. Frequent meetings between the radiation oncologist and the service responsible for professional billing. 10. Timely review and management of all past due accounts making decisions toward collection or adjustment. 11. A method for tracking referral physician identification and disease categories which are now a part of Medicare billing requirements and should allow you to be able to graphically demonstrate trends in your practice referrals.

Commerce↗
PubMed1990

Low urinary chiro-inositol excretion in non-insulin-dependent diabetes mellitus.

BACKGROUND AND METHODS: Inositol is a major component of the intracellular mediators of insulin action. To investigate the possible role of altered inositol metabolism in non-insulin-dependent diabetes mellitus (NIDDM), we used gas chromatography and mass spectrometry to measure the myo-inositol and chiro-inositol content of urine specimens from normal subjects and patients with NIDDM: The study subjects were whites, blacks, and Pima Indians. The type of inositol and its concentration in insulin-mediator preparations from muscle-biopsy specimens from normal subjects and diabetic patients were also determined. RESULTS: The urinary excretion of chiro-inositol was much lower in the patients with NIDDM (mean [+/- SE], 1.8 +/- 0.8 mumol per day) than in the normal subjects (mean, 84.9 +/- 26.9 mumol per day; P less than 0.01). In contrast, the mean urinary myo-inositol excretion was higher in the diabetic patients than in the normal subjects (444 +/- 135 vs. 176 +/- 46 mumol per day; P less than 0.05). There was no correlation between chiro-inositol excretion and the age, sex, or weight of the diabetic patients, nor was there any correlation between urinary chiro-inositol and myo-inositol excretion in either group. The results were similar in a primate model of NIDDM, and chiro-inositol excretion was decreased to a lesser extent in animals with prediabetic insulin resistance. chiro-Inositol was undetectable in insulin-mediator preparations from muscle-biopsy samples obtained from patients with NIDDM: Similar preparations from normal subjects contained substantial amounts of chiro-inositol. Furthermore, the chiro-inositol content of such preparations increased after the administration of insulin during euglycemic-hyperinsulinemic-clamp studies in normal subjects but not in patients with NIDDM: CONCLUSIONS: NIDDM is associated with decreased chiro-inositol excretion and decreased chiro-inositol content in muscle. These abnormalities seem to reflect the presence of insulin resistance in NIDDM:

Age Factors↗
PubMed1990

Skeletal muscle glycogen synthase activity in subjects with non-insulin-dependent diabetes mellitus after glyburide therapy.

Sulfonylureas are used in the treatment of non-insulin-dependent diabetes mellitus (NIDDM) largely because of their ability to enhance insulin secretion and possibly to potentiate insulin action. In this study, we investigated the effects of chronic glyburide treatment on glycogen synthase activity determined in skeletal muscle biopsies taken during euglycemic hyperinsulinemic clamps in nine Pima Indians with NIDDM. Insulin was infused at the rate of 40 mU/m2/min (low dose) followed by 400 mU/m2/min (high dose). Compared with the fasting value, the mean glycogen synthase activity assayed at low glucose-6-phosphate (G6P) concentration (active glycogen synthase) showed no significant changes during insulin infusion before glyburide treatment. After glyburide treatment, the mean active glycogen synthase increased by 39% (P less than .05) above the fasting value during the high-dose insulin infusion. Total glycogen synthase activity assayed at high G6P concentration did not change after glyburide treatment. Changes of insulin-stimulated active glycogen synthase associated with glyburide treatment correlated with changes in total body glucose disposal rates (r = .70, P less than .05) during euglycemic clamps. We conclude that glyburide treatment of subjects with NIDDM is associated with an increase in insulin action in vivo and concomitantly with improved insulin action on skeletal muscle glycogen synthase.

Adult↗
PubMed1990

Regulation of plasma lactate concentration in resting human subjects.

We evaluated the relative contributions of glucose, insulin, and the rate of glucose disposal to the regulation of the plasma lactate concentration. Rates of glucose disposal were measured in 88 separate studies in whole body and across the forearm at varying plasma insulin (9, 50, 160, and 1,800 microU/mL) concentrations, and at each insulin concentration at four different glucose concentrations (90, 160, 250, and 400 mg/dL) in healthy male subjects. The rate of glucose disposal was positively correlated with the plasma lactate concentration (r = .83, n = 88, P less than .0001). When the plasma lactate concentration was adjusted for the rate of glucose disposal, plasma glucose or insulin concentrations did not contribute significantly to the residual variation in plasma lactate. When plasma lactate concentrations were compared at matched rates of glucose disposal, the lactate levels were similar regardless of whether glucose disposal was induced by hyperglycemia or hyperinsulinemia. At the lowest glucose and insulin concentrations, forearm tissues released lactate, but at all other glucose and insulin concentrations, no significant net lactate flux was observed. After subtraction of the rate of forearm glucose disposal from whole-body glucose disposal, the plasma lactate concentration correlated with the remaining, extramuscular, rate of glucose disposal (r = .60, P less than .0001). These data suggest that in resting normal subjects the plasma lactate concentration may be determined by the rate of glucose disposal in extramuscular tissues, rather than the ambient glucose or insulin concentration.

Adult↗
PubMed1990

Insulin-mediated increase in glucose 1,6-bisphosphate is attenuated in skeletal muscle of insulin-resistant man.

The purpose of this study was to determine the effect of insulin infusion on the glucose 1,6-bisphosphate (glucose 1,6-P2) content in skeletal muscle of insulin resistant man. Euglycemic (approximately 100 mg/dL) hyperinsulinemic clamps were performed on seven men with chronically elevated fasting plasma glycemia (228 +/- 13 mg/dL, mean +/- SE) who were insulin resistant (HIR) and five men with normal fasting glycemia (115 +/- 5 mg/dL) who were insulin resistant (NIR). Insulin was infused at successive rates of 40 and 400 mU/m2/min, and biopsies were obtained from the quadriceps femoris muscle before and after insulin infusion. The results were compared with those of normoglycemic insulin-sensitive (NIS) men. The insulin-resistant groups had significantly higher percent body fat values than did the NIS group. Glucose 1,6-P2 increased from 70 +/- 6, 49 +/- 9, and 67 +/- 3 mumols/kg dry weight in the basal state to 135 +/- 12 (P less than .001 v basal), 67 +/- 11 (P greater than .05) and 79 +/- 3 (P greater than .05) after 40 mU insulin in NIS, HIR, and NIR, respectively. Glucose 1,6-P2 increased to 147 +/- 12 (P less than .001 v basal), 91 +/- 15 (P less than .01) and 99 +/- 13 (P less than .05) mumols/kg dry weight after 400 mU insulin in NIS, HIR, and NIR, respectively. The increase in glucose 1,6-P2 in response to 40 mU insulin was only 28% and 18% in HIR and NIR, respectively, of that in NIS.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Insulin-sensitive tyrosine kinase: relationship with in vivo insulin action in humans.

To investigate the relationship of insulin receptor kinase with insulin resistance in humans, we studied insulin-sensitive tyrosine kinase activity in muscle biopsies taken from 20 Pima Indians [14 nondiabetics, 6 with non-insulin-dependent mellitus (NIDDM)] during euglycemic clamps, at insulin concentrations of approximately 68 microU/ml (low dose) and approximately 1,170 microU/ml (high dose). In the nondiabetics, the low dose, insulin-induced kinase activation in vivo was 1.5-fold the activity in the fasting state (P less than 0.05), whereas in the diabetics, the kinase activity actually decreased by 40% relative to fasting (P less than 0.05). The difference in delta-kinase in vivo was significant (P less than 0.01) between the two groups. Similarly, the kinase activation in vitro in response to 1 nM insulin was lower in diabetic subjects compared with nondiabetics (P less than 0.01). These data indicate that, in NIDDM, both in vitro and in vivo insulin-stimulated tyrosine kinase activity is impaired. Among nondiabetics, the kinase sensitivity to insulin, calculated as the ratio of the kinase activity at 1 nM insulin in vitro to the kinase activity at 100 nM insulin, was positively correlated with plasma insulin concentrations 2 h after an oral glucose load (r = 0.69, P less than 0.01). Thus, in nondiabetic subjects with insulin resistance, insulin activation of the kinase is not reduced, but the kinase sensitivity to insulin increases with increasing plasma insulin levels. Therefore, the site of insulin resistance in nondiabetic subjects is distal to the insulin receptor kinase. Furthermore, it is possible that circulating insulin, by increasing the kinase sensitivity to insulin, is a determinant of the receptor kinase activity.

Adult↗
PubMed1990

Low ratio of fat to carbohydrate oxidation as predictor of weight gain: study of 24-h RQ.

Reduced oxidation of fat leading to a positive fat balance could be a factor in the development of obesity. Twenty-four-hour respiratory quotient (RQ) was measured in 152 nondiabetic Pima Indians fed a weight-maintenance diet [87 males and 65 females; 27 +/- 6 yr (mean +/- SD); 93.9 +/- 22.9 kg; 32 +/- 9% fat]. Twenty-four-hour RQ varied from 0.799 to 0.903. Prior change in body weight, 24-h energy balance, sex, and percent body fat explained 18% of the variance in 24-h RQ (P less than 0.001). In a subgroup of 66 siblings from 28 families, family membership explained 28% of the remaining variance in 24-h RQ (P less than 0.05). In 111 subjects for whom follow-up data (25 +/- 11 mo) were available, 24-h RQ was correlated with subsequent changes in body weight and fat mass (r = 0.27, P less than 0.01 and r = 0.19, P less than 0.05, respectively). Subjects with higher 24-h RQ (90th percentile) independent of 24-h energy expenditure were at 2.5 times higher risk of gaining greater than or equal to 5 kg body weight than those with lower 24-h RQ (10th percentile). We conclude that in Pima Indians fed a standard diet 1) family membership is the principal determinant of the ratio of fat to carbohydrate oxidation, and 2) a low ratio of fat to carbohydrate oxidation is associated with subsequent weight gain independent of low energy expenditure and may contribute to the familial aggregation of obesity.

Adult↗
PubMed1990

Energy expenditure in the obese: is there a thrifty gene?

Seven to eight thousand Pima Indians are presently living in the southwestern desert of Arizona. The prevalence of type II diabetes in this population exceeds 45% and more than 75% of the Pimas are obese. In 1962, Neel proposed that obesity in populations like the Pima Indians might be the expression of a "thrifty gene" which becomes detrimental with progress. Since 1982, longitudinal studies have been conducted including measurements of metabolic rate in 200 non-diabetic Pima Indians and have shown that 1) at any given body weight and body composition, there is quite a large variability in the resting metabolic rate which is not accounted for by intra-individual variability or errors of the methods; 2) metabolic rate after adjustment for body composition and body weight is a familial trait; 3) a low metabolic rate is a risk factor for body weight gain; 4) in response to body weight gain, there is a "normalization" of the resting metabolic rate. These studies are the first showing that a "thrifty" metabolic rate can play a role in the development of obesity.

Arizona↗
PubMed1990

Insulin resistance is associated with reduced fasting and insulin-stimulated glycogen synthase phosphatase activity in human skeletal muscle.

Insulin-stimulated glycogen synthase activity in human skeletal muscle correlates with insulin-mediated glucose disposal rate (M) and is reduced in insulin-resistant subjects. We have previously reported reduced insulin-stimulated glycogen synthase activity associated with reduced fasting glycogen synthase phosphatase activity in skeletal muscle of insulin-resistant Pima Indians. In this study we investigated the time course for insulin stimulation of glycogen synthase and synthase phosphatase during a 2-h high-dose insulin infusion (600 mU/min per m2) in six insulin-sensitive caucasians (group S) and in five insulin-resistant Pima Indians (group R). Percutaneous muscle biopsies were obtained from the quadriceps femoris muscle after insulin infusion for 0, 10, 20, 40, and 120 min. In group S, insulin-stimulated glycogen synthase activity increased with time and was significantly higher than in group R. In group S, synthase phosphatase activity increased significantly by 25% at 10 min and then decreased gradually. No significant change in synthase phosphatase was seen in group R and activity was lower than group S at 0 to 20 min. These data suggest that a low basal synthase phosphatase activity and a defect in its response to insulin explain, at least in part, reduced insulin stimulation of skeletal muscle glycogen synthase associated with insulin resistance.

Adenosine Triphosphate↗
PubMed1990

Skeletal muscle metabolism is a major determinant of resting energy expenditure.

Energy expenditure varies among people, independent of body size and composition, and persons with a "low" metabolic rate seem to be at higher risk of gaining weight. To assess the importance of skeletal muscle metabolism as a determinant of metabolic rate, 24-h energy expenditure, basal metabolic rate (BMR), and sleeping metabolic rate (SMR) were measured by indirect calorimetry in 14 subjects (7 males, 7 females; 30 +/- 6 yr [mean +/- SD]; 79.1 +/- 17.3 kg; 22 +/- 7% body fat), and compared to forearm oxygen uptake. Values of energy expenditure were adjusted for individual differences in fat-free mass, fat mass, age, and sex. Adjusted BMR and SMR, expressed as deviations from predicted values, correlated with forearm resting oxygen uptake (ml O2/liter forearm) (r = 0.72, P less than 0.005 and r = 0.53, P = 0.05, respectively). These findings suggest that differences in resting muscle metabolism account for part of the variance in metabolic rate among individuals and may play a role in the pathogenesis of obesity.

Adult↗
PubMed1989

Euglycemic hyperinsulinemia increases glucose 1,6-bisphosphate in human skeletal muscle.

1. The effects of physiologic concentrations of insulin on the contents of glucose 1,6-bisphosphate (glucose 1,6-P2) and regulators of glucose 1,6-P2 synthase in intact human skeletal muscle have been investigated. 2. Insulin increased glucose 1,6-P2 from a basal value of 70 +/- 6 to 135 +/- 12 mumol/kg dry wt (P less than 0.001). 3. Activation of synthase could not be associated with changes in its inhibitors (fructose 1,6-P2, Pi, citrate) or its substrate glucose 6-P.

Analysis of Variance↗
PubMed1989

The effect of propranolol on free fatty acid mobilization and resting metabolic rate.

The role of the sympathetic nervous system in free fatty acid (FFA) mobilization was assessed in this study. FFA turnover rate using 1-14C-palmitic acid and metabolic rate by using indirect calorimetry were measured in ten white and 12 Pima Indian males after an overnight fast and during propranolol infusion (120 micrograms/kg fat-free mass [FFM] bolus and 1.2 micrograms/kg FFM/min). Baseline FFA turnovers were similar in both racial groups and decreased similarly following propranolol infusion (-16% +/- 4%; P less than .001, n = 22). This decrease was greater in more obese subjects (decrease in FFA turnover v % body fat, r = -.59, P less than .01, n = 22). Propranolol also induced an increase in lipid oxidation, which was more marked in the subjects with a high ratio of abdomen to thigh circumference (A/T ratio) (r = .63, P less than .01, n = 22). On average the resting metabolic rate (RMR) was unchanged during propranolol infusion, but individuals with lower A/T ratio had greater decreases in RMR than subjects with higher A/T ratio (r = .48, P less than .05). Assuming that the change in FFA turnover following beta-blockade is proportional to the role that the catecholamines (and therefore the sympathetic nervous system) play in mobilization of FFA, the greater fall in FFA turnover after propranolol infusion in more obese subjects suggests that they have a higher basal sympathetic activity. Furthermore, the lack of decrease in metabolic rate in response to beta-blockade in persons with a high A/T ratio could be the reflection of an even greater SNS activity in individuals with central obesity.

Basal Metabolism↗
PubMed1989

Energy expenditure during normo- and overfeeding in peripubertal children of lean and obese Pima Indians.

We investigated the hypothesis that peripubertal children born to obese parents have a lower 24-h energy expenditure during "weight maintenance" and/or in response to overfeeding when compared with children born to normal-weight parents. Sixteen Southwestern American Indians (12.4 +/- 1.4 yr, 55.5 +/- 14.1 kg, 30 +/- 8% body fat), eight offspring from obese parents [body mass index (BMI) = 40 +/- 6 kg/m2], and eight offspring from thin parents (BMI = 24 +/- 3 kg/m2) were admitted for 8 days to our metabolic ward. The 24-h energy expenditure was measured under eucaloric conditions and on the 3rd day of progressive overfeeding of a mixed diet, i.e., 150, 200, and 200% of weight maintenance on day 1, 2, and 3 of overfeeding. At base line, offspring of obese parents were heavier (64 +/- 15 vs. 47 +/- 6 kg, P less than 0.05) and tended to be fatter (34 +/- 8 vs. 26 +/- 9% body fat, P = 0.07), with a higher absolute fat mass (22 +/- 9 vs. 13 +/- 4 kg body fat, P less than 0.05) when compared with offspring of thin parents. During both normo- and over-feeding, the larger part of the variance in 24-h energy expenditure in the conditions of a respiratory chamber was accounted for by differences in fat-free body mass (54 and 68%, respectively), whereas differences in the level of spontaneous physical activity accounted for another 19 and 21%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗