Biomedical subjects

V Daniel Castracane

Publications and source records attributed to V Daniel Castracane.

25 records · Page 2Linked to original sources

PubMed2003

Adiponectin responses to continuous and progressively intense intermittent exercise.

PURPOSE: Adiponectin is a recently discovered adipocyte protein that is lower in patients with coronary artery disease and in Type II diabetics who have insulin resistance. Regular exercise is known to be a preventative factor in the development of atherosclerosis and Type II diabetes. Acute exercise increases insulin sensitivity; however, it also increases beta-adrenergic and glucocorticoid activities that may suppress adiponectin expression. Two experiments were conducted to determine whether acute exercise affects adiponectin concentrations. METHODS: In the first experiment, six healthy male subjects completed 30 min of heavy continuous running exercise at 79% of VO (2max). In the second experiment, well-trained runners completed strenuous intermittent exercise consisting of treadmill running at 60, 75, 90, and 100% VO (2max). A resting control trial for the second experiment was also conducted. RESULTS: Glucose and insulin were not altered significantly in the first experiment, but both increased significantly (P < 0.05) in the second experiment. A significant increase (P < 0.05) in adiponectin in the first experiment was no longer significant after correction for plasma volumes shifts. In the second experiment, there were significant (P < 0.05) changes in adiponectin concentrations over time but not a significant difference between adiponectin responses in exercise and control trials. CONCLUSIONS: The data suggest that 30 min of heavy continuous running or more strenuous intermittent running does not stimulate an increase in production and release of adiponectin, and small increases in adiponectin concentrations resulting from the exercise may be attributed to normal plasma volume shifts.

Adiponectin↗

PubMed2003

Effects of high-intensity exercise on leptin and testosterone concentrations in well-trained males.

OBJECTIVE: A number of investigations have examined the effect of exercise on leptin concentrations, because leptin is associated with obesity, satiety, and reproductive function. High-intensity exercise is known to increase testosterone, an inhibitor of leptin. The objective of the study was to determine whether the leptin responses to a progressive, intermittent exercise protocol were related to serum testosterone concentrations. Most previous studies have examined leptin responses to low or moderately high exercise intensities. A second objective was to determine whether leptin responses were different than previous experiments using intermittent moderate and high-intensity exercise. METHODS: Well-trained runners completed strenuous intermittent exercise consisting of treadmill running at 60, 75, 90, and 100% VO(2 max) and a subsequent resting control trial was also conducted. RESULTS: There were significant increases in mean serum levels of leptin and testosterone with both quickly returning to baseline during recovery, but no relationship between the two hormones was found. After examining individual data for both hormones, it was discovered that subjects could be classified as leptin responders or nonresponders, whereas testosterone increased in all subjects. Responders had elevated serum leptin levels at baseline and exhibited increases after high-intensity exercise, whereas nonresponders did not show changes in leptin during exercise. CONCLUSIONS: Data suggest testosterone levels do not acutely affect leptin responses to exercise or 1-h of recovery. Moreover, varied leptin responses to intense exercise in comparable well-trained runners was observed and was associated with baseline leptin concentrations.

Adult↗

PubMed2002

Substrate utilization during exercise in postmenopausal women on hormone replacement therapy.

It has been suggested that due to the slight direct or indirect effect of estrogen on lipolytic activity, the age-related decrease in production associated with the menopause may heighten the risk of cardiovascular and metabolic disease in women. While hormone replacement therapy (HRT) alone may have little or no effect on body mass in postmenopausal women, data suggest it can alter the shift toward abdominal adiposity. Furthermore, estrogen may have a synergistic effect on exercise-induced reduction in fat mass. Accordingly, the purpose of this investigation was to examine the potential influence of HRT on substrate utilization during 30 min of treadmill exercise at approximately 80% maximal oxygen uptake (VO(2max)) in postmenopausal women. Eight women were receiving HRT and nine women were not (NHRT). No significant differences between the HRT and NHRT groups were noted for age, body mass, body fat, VO(2max) or the percentage of VO(2max) maintained during exercise. Expired gas samples were analyzed every 30 s to determine respiratory exchange ratio (R) and % VO(2max). The R, total energy expended and percentage contributions from fats and carbohydrate were averaged over three periods during the exercise (min 1-10, 11-20, and 21-30). There was no effect of HRT on R, total energy expended or substrate contribution. Thus, treatment of postmenopausal women using HRT (primarily conjugated equine estrogens in doses of 0.625-1.25 mg x day(-1)) did not appear to affect the percentages of fat and carbohydrate utilized during 30 min of treadmill exercise at 80% of VO(2max). However, the exercise responses in this group of menopausal women were consistent with a duration-dependent increased reliance on fat as an energy source during exercise of moderate to vigorous intensity as has been demonstrated in younger populations.

Aged↗

PubMed2002

When did leptin become a reproductive hormone?

Almost 50 years ago the obese mouse model was identified, and parabiosis studies were able to demonstrate that some humoral factor was involved in adiposity, so that the genetics and endocrine nature of this process have been apparent for many years. With the discovery of leptin just a few years ago, early studies validated the role of this protein product of the obese gene. Early studies in the obese mouse model ( ob/ob mouse) demonstrated that the genetic basis was truly a deficiency in leptin. Coincidentally, the relationship to fertility was also associated with leptin. These early studies were also able to demonstrate a relationship to puberty and the time of pubertal development. Very quickly, the recognition that the placenta was a source of leptin and that leptin levels were elevated in pregnancy in a number of species also broadened our appreciation of the relationship to reproductive functions. These many rapidly elucidated relationships to leptin were reported soon after the identification and availability of leptin as a research reagent and have firmly put leptin into the area of reproductive physiology in addition to establishing roles in metabolism, satiety, and energy metabolism. Subsequent studies have expanded all of these situations. Species beyond the rodent model, including the human, have now introduced these physiologic studies into the clinical arena and the role of leptin in fertility, puberty, pregnancy, and genetics. In this issue, all of these topics are reviewed to bring the reader up to date with leptin and its role in reproductive function, many of which overlap with the control of obesity.

Animals↗

PubMed2002

Leptin: roles and regulation in primate pregnancy.

Leptin, a hormone produced by adipose tissue and the placenta, is enhanced in the maternal circulation throughout pregnancy in both the human and the baboon ( Papio sp.), a proven nonhuman primate model for the study of human pregnancy. The presence of both leptin and its receptor in the fetus implies a role for the polypeptide as a regulator of in utero development, although localization in the placental trophoblast may relate to autocrine and/or paracrine regulatory functions in this important endocrine tissue. Although regulatory mechanisms remain incompletely defined, it has been suggested that cross talk occurs between the fetus, placenta, and maternal adipose stores. Placental estrogen, which is present in increasing concentrations with advancing gestation, is suggested to influence leptin synthesis in a tissue- and cell type-specific fashion. In this capacity, cellular hypoxia, diabetes, and preeclampsia are conditions that appear to be intimately linked to leptin dynamics. A better understanding of regulatory mechanisms will have direct clinical significance, as leptin has been proposed to impact on those causes of human perinatal morbidity and mortality that are associated with anomalies of fetal maturity and development, general conceptus growth, trophoblast endocrinology, and placental sufficiency.

Animals↗

PubMed2002

Polycystic ovarian syndrome and insulin resistance in white and Mexican American women: a comparison of two distinct populations.

OBJECTIVES: We sought to determine what differences, if any, existed between white and Mexican American women with polycystic ovary syndrome (PCOS) and whether the same values for fasting insulin, fasting glucose/insulin ratio, and homeostasis model assessment (HOMA) might be applied when screening both ethnic groups for insulin resistance. STUDY DESIGN: Eighty-three consecutive women suspected to have PCOS but who demonstrated absence of other endocrine disorders comprised the study population. Nineteen healthy ovulatory women volunteered as controls. Fasting serum samples were obtained for determination of thyroid-stimulating hormone (TSH), prolactin, glucose, insulin, free and total testosterone, 17-hydroxyprogesterone, and dehydroepiandrosterone sulfate in the early proliferative phase. An oral glucose load was administered, and blood samples for glucose and insulin were drawn at 1, 2, and 3 hours. Those with impaired glucose tolerance or diabetes mellitus were excluded from our final study population. Four different groups were defined: (1) women with PCOS and insulin resistance, (2) women with PCOS without insulin resistance, (3) women with irregular cycles but without PCOS or another identifiable endocrinopathy, and (4) regular, cycling control subjects. Each group was subdivided by ethnicity (white or Mexican American). A total of 65 white and 37 Mexican American women were studied, including control subjects. RESULTS: Among all study participants, Mexican American women with PCOS had significantly higher mean values for body mass index, fasting insulin, and HOMA but lower mean fasting glucose/insulin levels than white women. When group 1 patients (PCOS with insulin resistance) were compared between ethnic groups, mean fasting insulin and HOMA levels were significantly lower and glucose/insulin ratios higher in white than in Mexican American women. A single cutoff value for insulin resistance in PCOS was insensitive when applied to both ethnic groups. A fasting insulin value >20 microU/mL, HOMA value > 3.8, and glucose/insulin value <7.2 were reasonable screening values in our population of white women, whereas a fasting insulin value >23 microU/mL, HOMA value >4.5, and glucose/insulin ratio <4.0 were feasible screening values in Mexican American women. CONCLUSIONS: We conclude that (1) Mexican American women with PCOS are more insulin resistant than white women, (2) the incidence of insulin resistance is higher in Mexican American women with PCOS than in white women, (3) a single "screening" value for PCOS-related insulin resistance screening cannot be applied to both white and Mexican American women, and (4) normative values for insulin resistance screening in the PCOS population should be individualized for different racial or ethnic populations.

Adult↗

PubMed2002

Leptin and exercise.

Short-term exercise (<60 min) studies suggest that leptin concentrations are not acutely affected in healthy males and females. Most reports of reductions in serum leptin may be attributed to circadian rhythms or hemoconcentration. For long-term (> or =60 min) exercise, a reduction in leptin concentrations reported from 1 to 3 hr of running or cycling has been attributed to diurnal reduction in circulating leptin, independent of exercise. Exercise that produces a sufficient energy imbalance (kilocalorie intake versus kilocalorie expenditure) suppresses 24-hr mean and amplitude of the diurnal rhythm of leptin in women. Suppression of leptin concentrations may be counterbalanced by feeding and may explain consistent reports of reductions in leptin concentrations following extreme bouts of exercise such as marathons or ultramarathons. In addition, leptin concentrations are reduced 48 hr after long-term aerobic exercise and long-term resistance exercise is associated with delayed leptin reduction 9 hr postexercise. Training studies have documented that short-term exercise training (< or =12 weeks) does not affect leptin levels, with the exception of patients with type 2 diabetes. Exercise training protocols that result in reduced fat mass will lower leptin concentrations, thus, most investigators have reported leptin concentrations after accounting for fat loss. There are disparate findings concerning long-term (>12 weeks) training studies, with a number of studies finding no effect of training on leptin concentrations other than effects induced by fat loss, and other studies finding reductions in leptin concentrations after accounting for fat loss. Exercise training-induced reductions in leptin levels have been attributed to alterations in energy balance, improvements in insulin sensitivity, alterations in lipid metabolism, and unknown factors. Hormone replacement does not seem to affect leptin adaptations to training. Patients with type 2 diabetes show delayed effects of short-term resistance exercise on leptin concentrations, reduced leptin levels with long-term training, and appear to be more sensitive to training-induced leptin adaptations than other populations.

Energy Metabolism↗