Biomedical subjects

W T Donahoo

Publications and source records attributed to W T Donahoo.

8 recordsLinked to original sources

PubMed2003

Relation between calcium intake and fat oxidation in adult humans.

OBJECTIVE: To determine if total calcium (Ca(2+)) intake and intake of Ca(2+) from dairy sources are related to whole-body fat oxidation. DESIGN: : Cross-sectional study. SUBJECTS: A total of 35 (21 m, 14 f) non-obese, healthy adults (mean+/-s.d., age: 31+/-6 y; weight: 71.2+/-12.3 kg; BMI: 23.7+/-2.9 kg m(-2); body fat: 21.4+/-5.4%). MEASUREMENTS: Daily (24 h) energy expenditure (EE) and macronutrient oxidation using whole-room indirect calorimetry; habitual Ca(2+) intake estimated from analysis of 4-day food records; acute Ca(2+) intake estimated from measured food intake during a 24-h stay in a room calorimeter. RESULTS: Acute Ca(2+) intake (mg. kcal(-1)) was positively correlated with fat oxidation over 24 h (r=0.38, P=0.03), during sleep (r=0.36, P=0.04), and during light physical activity (r=0.32, P=0.07). Acute Ca(2+) intake was inversely correlated with 24-h respiratory quotient (RQ) (r=-0.36, P=0.04) and RQ during sleep (r=-0.31, P=0.07). After adjustment for fat mass, fat-free mass, energy balance, acute fat intake, and habitual fat intake, acute Ca(2+) intake explained approximately 10% of the variance in 24-h fat oxidation. Habitual Ca(2+) intake was not significantly correlated to fat oxidation or RQ. Total Ca(2+) intake and Ca(2+) intake from dairy sources were similarly correlated with fat oxidation. In backwards stepwise models, total Ca(2+) intake was a stronger predictor of 24 h fat oxidation than dairy Ca(2+) intake. CONCLUSION: Higher acute Ca(2+) intake is associated with higher rates of whole-body fat oxidation. These effects were apparent over 24 h, during sleep and, to a lesser extent, during light physical activity. Calcium intake from dairy sources was not a more important predictor of fat oxidation than total Ca(2+) intake.

Adult↗

PubMed2002

From instinct to intellect: the challenge of maintaining healthy weight in the modern world.

The global obesity epidemic is being driven in large part by a mismatch between our environment and our metabolism. Human physiology developed to function within an environment where high levels of physical activity were needed in daily life and food was inconsistently available. For most of mankind's history, physical activity has 'pulled' appetite so that the primary challenge to the physiological system for body weight control was to obtain sufficient energy intake to prevent negative energy balance and body energy loss. The current environment is characterized by a situation whereby minimal physical activity is required for daily life and food is abundant, inexpensive, high in energy density and widely available. Within this environment, food intake 'pushes' the system, and the challenge to the control system becomes to increase physical activity sufficiently to prevent positive energy balance. There does not appear to be a strong drive to increase physical activity in response to excess energy intake and there appears to be only a weak adaptive increase in resting energy expenditure in response to excess energy intake. In the modern world, the prevailing environment constitutes a constant background pressure that promotes weight gain. We propose that the modern environment has taken body weight control from an instinctual (unconscious) process to one that requires substantial cognitive effort. In the current environment, people who are not devoting substantial conscious effort to managing body weight are probably gaining weight. It is unlikely that we would be able to build the political will to undo our modern lifestyle, to change the environment back to one in which body weight control again becomes instinctual. In order to combat the growing epidemic we should focus our efforts on providing the knowledge, cognitive skills and incentives for controlling body weight and at the same time begin creating a supportive environment to allow better management of body weight.

Biological Evolution↗

PubMed2000

Percent body fat and lean mass explain the gender difference in leptin: analysis and interpretation of leptin in Hispanic and non-Hispanic white adults.

OBJECTIVE: To reassess the relationship between body fat and fasting leptin concentrations comparing plasma vs. serum assessments of leptin; ratios vs. regression adjustment for body composition; fat and lean mass vs. percent body fat; and gender-, ethnic-, and age-related variations. RESEARCH METHODS AND PROCEDURES: Subjects included 766 adults from the nondiabetic cohort of the San Luis Valley Diabetes Study examined at follow up (1997 to 1998). Body composition was determined by dual energy X-ray absorptiometry. Leptin concentrations were determined after an overnight fast. RESULTS: Fasting serum and plasma assessments of leptin were correlated with percent body fat to the same degree. Women had significantly higher serum leptin concentrations than men when leptin concentrations were divided by body mass index, fat mass in kilograms or percent body fat. The methodological problem inherent in interpreting these ratio measures is pictorially demonstrated. In regression analysis, fat mass alone did not explain the gender difference. However, lean body mass was inversely related to leptin concentrations (p < 0.0001) and explained 71% of the gender difference at a given fat mass. Percent body fat explained all of the gender difference in leptin concentrations in both Hispanics and non-Hispanic whites. Similar to findings about gender differences, ethnic- and age-related variations in the leptin-body fat association were minimized when percent body fat was employed as the body fat measure. DISCUSSION: Regression analysis and percent body fat measured with dual energy X-ray absorptiometry are recommended when assessing the relationship between leptin and body fat. Gender differences in leptin concentrations were accounted for by percent body fat in free living (no diet control), Hispanic and non-Hispanic white adults.

Absorptiometry, Photon↗

PubMed2000

Comparison of risk factors for obesity in young, nonobese African-American and Caucasian women.

OBJECTIVE: To determine whether specific risk factors for obesity were more evident in young, normal-weight African-American (AA) compared to Caucasian-American (CA) women. DESIGN: Cross-sectional age-matched study. SUBJECTS: Young, nonobese, sedentary AA (n= 13, 22.5y of age, 23.6% body fat) and CA women (n = 11, 21.5y of age, 24.0% body fat). MEASUREMENTS: Aerobic physical fitness (peak VO2), resting metabolic rate (RMR), resting and submaximal exercise fat oxidation rates, total daily energy expenditure (TDEE) by the doubly-labeled water method, physical activity energy expenditure (PAEE), skeletal muscle glycolytic (phosphofructokinase activity (PFK)) and beta-oxidative (beta-hydroxy-acyl CoA dehydrogenase (beta-HADH)) activity, and insulin sensitivity estimated by the insulin-augmented frequently sampled intravenous glucose tolerance test. RESULTS: The AA and CA subjects were similar in age, body mass index and body composition, but the AA women exhibited lower peak VO2. There were no group differences in RMR adjusted for body composition, or in the rates of submaximal exercise energy expenditure or fat oxidation, and no difference in skeletal muscle beta-HADH or PFK activity. The AA women exhibited lower insulin sensitivity and greater acute insulin response to glucose. The mean TDEE for the AA women was only 74% that of the CA women, primarily due to a lower physical activity energy expenditure (AA group: xPAEE = 1,246+/-438 kJ/day; CA group: x= 3,310+/-466 kJ/day. CONCLUSION: These data indicate that PAEE and its correlates of peak aerobic capacity and insulin sensitivity are lower in young, nonobese AA women compared to their CA counterparts.

Adolescent↗

PubMed2000

Seasonal variation in lipoprotein lipase and plasma lipids in physically active, normal weight humans.

Adipose tissue lipoprotein lipase (ATLPL) provides free fatty acids (FFA) for storage in adipocytes, whereas in skeletal muscle LPL (SMLPL) provides FFA for oxidation. In hibernating animals, the level of SMLPL is relatively higher in summer than winter (promoting fat oxidation), whereas the opposite is seen with ATLPL. A patient-controlled study was designed to determine whether such seasonal variation occurs in normal weight humans. Eighteen subjects were studied in the summer and winter. After 2 days of a standardized diet, they underwent muscle and adipose biopsies for LPL activity, assessment of fitness by VO2 max, and determination of body composition by hydrostatic weighing. The percentages of body fat, body mass index, VO2 max, insulin, glucose, FFA, glycerol, and leptin were not affected by the season. Total cholesterol was higher in the winter than in the summer (157 +/- 5.5 vs. 148 +/- 4.2 mg/dL respectively; P = 0.03). The ATLPL activity was also higher in the winter than in the summer (4.4 +/- 0.8 vs. 2.3 +/- 0.6 nmol FFA/10(6) cells-min; P = 0.04). SMLPL activity trended to be higher in the winter than in the summer (1.9 +/- 0.5 vs. 1.0 +/- 0.1 nmol FFA/g x min; P = 0.06). In summary, ATLPL is seasonally regulated. It appears that SMLPL is similarly regulated by season. For physically active lean subjects, this increase in SMLPL may be a compensatory mechanism to help protect from seasonal weight gain.

Adipose Tissue↗

PubMed1999

Leptin levels in restricting and purging anorectics.

Patients with anorexia nervosa of the restricting (AN-R) and purging (AN-P) subtypes were studied to determine if there was a differential effect on leptin levels. It was hypothesized that the AN-P subgroup would have elevated leptin compared to the AN-R subgroup. Fasting plasma and anthropormorphic measurements were collected from 8 women with AN-R and 5 with AN-P. Eleven women served as controls. Overall, the plasma leptin correlated with body mass index (BMI; R = 0.432, p < .05). The AN-P subgroup had elevated leptin compared to the AN-R subgroup (3.8 +/- 0.8 vs. 1.5 +/- 0.2 ng/ml, p < .05) despite similar BMI (16.0 +/- 0.5 vs. 14.8 +/- 0.8 kg/m2). Additionally, the AN-P subgroup had similar plasma leptins as controls (3.8 +/- 0.8 vs. 3.6 +/- 0.1) despite different BMI (16.0 +/- 0.5 vs. 20.2 +/- 0.2, p < .001). Cortisol in the AN-P subgroup trended to be higher than in the restricting anorectics (21.8 +/- 3.0 vs. 15.6 +/- 1.3, p = .06). In AN, leptin was elevated in AN-P vs. AN. This may be due to increased glucocorticoid stimulation of leptin.

Adolescent↗

PubMed1998

Drugs causing dyslipoproteinemia.

Diuretics and beta-blockers have a strong tendency to affect serum lipids adversely, whereas the peripherally acting alpha-blocking agents consistently result in beneficial effects. Most of the other antihypertensive agents (calcium channel blockers, ACE inhibitors, angiotensin II receptor antagonists, and drugs that act centrally) are lipid neutral. The effect of steroid hormones varies with the drug, dose, and route of administration. In general, androgens lower HDL-C and have a variable effect on LDL-C. The effects of progestins vary greatly depending on their androgenicity, and estrogens are beneficial except when hypertriglyceridemia occurs with oral estrogens. Glucocorticoids raise HDL-C and may also increase triglycerides and LDL-C. Retinoids increase triglycerides and LDL-C and also reduce HDL-C. Interferons can cause hypertriglyceridemia. Following organ transplantation, a dyslipidemia often ensues. This is caused in part by the medications used to prevent rejection (glucocorticoids, cyclosporine, and FK-506) and requires close attention and, in some patients, drug therapy to prevent coronary artery disease.

Antihypertensive Agents↗

PubMed1997

Isoproterenol and somatostatin decrease plasma leptin in humans: a novel mechanism regulating leptin secretion.

In cultured adipocytes, leptin is increased by insulin and decreased by cAMP. In animal models, insulin and agents that increase intracellular cAMP have been shown to similarly affect plasma leptin in vivo. This study was undertaken to test the hypothesis that in humans increased cAMP induced by isoproterenol would decrease leptin. Five groups of normal weight subjects were studied; 1) subjects infused with isoproterenol at a rate of 24 ng/kg/min (ISO24); 2) subjects infused with isoproterenol at a rate of 8 ng/kg/min (ISO8); 3) subjects infused with somatostatin/insulin/GH followed by coinfusion with 8 ng/kg/min isoproterenol (ISO8 + SRIH); 4) subjects infused with somatostatin/insulin/GH alone (SRIH); and 5) control subjects infused with saline (NS). ISO24 infusion resulted in a 27% decrease in plasma leptin over 120 min. ISO24 also increased plasma insulin over the infusion. ISO8 resulted in a 16% decrease in leptin. Saline did not change leptin. SRIH alone decreased leptin 19% over the first 120 min, however no additional fall was seen over the next 120 min the SRIH group. Nonetheless, the addition of 8 ng/kg/min ISO during the second 120 min (ISO8 + SRIH) caused a 15% further decline in plasma leptin. Therefore both isoproterenol and somatostatin reduce plasma leptin in humans. The effect of isoproterenol is likely mediated by beta-adrenergic receptors, whereas the effect of somatostatin suggests a novel mechanism for the regulation of leptin.

Adrenergic beta-Agonists↗