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David R Brown

Publications and source records attributed to David R Brown.

At least 55 records · Page 3Linked to original sources
PubMed2004

Astrocytic regulation of NMDA receptor subunit composition modulates the toxicity of prion peptide PrP106-126.

Prion diseases are neurodegenerative conditions. The main pathological alterations common to these diseases include the loss of neurones, gliosis and the deposition of an abnormal isoform of the prion protein in aggregates in the nervous tissue. Prevention of the devastating effects of prion disease requires prevention of neuronal death. Therefore, understanding the mechanism by which this occurs is essential. Cell culture studies using the synthetic peptide PrP106-126 have been central to developing a model of this mechanism. Using a coculture system, we have shown that PrP106-126 caused neuronal death mediated by glutamate. This neuronal death resulted from modification of the expression of NMDA receptor subtypes stimulated by the exposure of neurones to the combination of astrocytic factors, elevated Cu and PrP106-126. The results of these experiments suggest neuronal death in prion disease might be reduced by the use of NMDA receptor antagonists such as MK801 or inhibitors of the arachidonic acid metabolism pathway.

Animals↗
PubMed2004

Role of the prion protein in copper turnover in astrocytes.

The prion protein (PrP(c)) is a glycoprotein that is not only expressed predominantly by neurones but also by other cells, including astrocytes. The recent identification of PrP(c) as a Cu-binding protein has opened the way to investigating its function in a cellular context. Experiments with recombinant PrP showed that the protein could block copper (Cu) toxicity to neurones. This inhibition was due to the protein's Cu-binding capacity. Astrocytes expressing PrP(c) were also able to block Cu toxicity. Analysis of PrP(c) expression by astrocytes showed that the level of extracellular Cu modulates both the level of expression of PrP(c) and its turnover. This in turn modulates the level of Cu stored within astrocytes. Experiments with radioactive Cu suggest that astrocytes may have an important role in uptake and clearance of Cu dependent upon PrP(c) expression. In addition, it was found that astrocytes clear Cu released by neurones. Astrocytes were also shown to take up PrP(c) released from neurones. As PrP(c) is a Cu-binding protein, it is possible that PrP(c) collects Cu from the extracellular environment and shuttles it to astrocytes, where Cu can be stored or exported in proteins such as ceruloplasmin. These results indicate that PrP(c) plays a role in the regulation of Cu taken up by astrocytes and potentially protects neurones from Cu toxicity by this mechanism.

Animals↗
PubMed2004

Metallic prions.

Prion diseases, also referred to as transmissible spongiform encephalopathies, are characterized by the deposition of an abnormal isoform of the prion protein in the brain. However, this aggregated, fibrillar, amyloid protein, termed PrPSc, is an altered conformer of a normal brain glycoprotein, PrPc. Understanding the nature of the normal cellular isoform of the prion protein is considered essential to understanding the conversion process that generates PrPSc. To this end much work has focused on elucidation of the normal function and activity of PrPc. Substantial evidence supports the notion that PrPc is a copper-binding protein. In conversion to the abnormal isoform, this Cu-binding activity is lost. Instead, there are some suggestions that the protein might bind other metals such as Mn or Zn. PrPc functions currently under investigation include the possibility that the protein is involved in signal transduction, cell adhesion, Cu transport and resistance to oxidative stress. Of these possibilities, only a role in Cu transport and its action as an antioxidant take into consideration PrPc's Cu-binding capacity. There are also more published data supporting these two functions. There is strong evidence that during the course of prion disease, there is a loss of function of the prion protein. This manifests as a change in metal balance in the brain and other organs and substantial oxidative damage throughout the brain. Thus prions and metals have become tightly linked in the quest to understand the nature of transmissible spongiform encephalopathies.

Animals↗
PubMed2004

Adrenergic modulation of Escherichia coli O157:H7 adherence to the colonic mucosa.

Enteric neurotransmitters can modulate the biodefensive functions of the intestinal mucosa, but their role in mucosal interactions with enteropathogens is not well defined. Here we tested the hypothesis that norepinephrine (NE) modulates interactions between enterohemorrhagic Escherichia coli O157:H7 (EHEC) and the colonic epithelium. Mucosal sheets from porcine distal colon were mounted in Ussing chambers. Drugs and an inoculum of either Shiga toxin-negative or -positive EHEC were added to the contraluminal and luminal bathing medium, respectively. After 90 min, adherent bacteria were quantified by an adherence assay and by immunohistochemical methods; short-circuit current (I(sc)) was measured continuously to assess changes in active ion transport. NE-treated tissues exhibited concentration-dependent increases in I(sc) and EHEC adherence. NE did not alter adherence of a rodent-adapted, noninfectious E. coli strain or two porcine-adapted non-O157 E. coli strains. The actions of NE on EHEC adherence but not I(sc) were prevented by the alpha-adrenergic antagonist yohimbine and the PKA activator Sp-8-bromoadenosine-3',5'-cyclic monophosphorothioate. Like NE, the PKA inhibitor Rp-8-bromoadenosine-3',5'-cyclic monophosphorothioate or indirectly acting sympathomimetic agents increased EHEC adherence. Nerve fibers immunoreactive for the NE-synthesizing enzymes tyrosine hydroxylase and dopamine beta-hydroxylase appeared to innervate the colonic epithelium. EHEC-like immunoreactivity on the colonic surface had the appearance of bacterial microcolonies and increased after NE treatment by a phentolamine-sensitive mechanism. Through interactions with alpha(2)-adrenergic receptors, NE appears to increase EHEC adherence to the colonic mucosa. Changes in sympathetic neural outflow may alter intestinal susceptibility to infection.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2004

Associations between physical activity dose and health-related quality of life.

PURPOSE: Although the beneficial effects of participation in regular physical activity (PA) are widely accepted, dose-response relationships between PA and health-related quality of life (HRQOL) remain unclear. METHODS: We examined relationships between frequency, duration, and intensity of PA and HRQOL among 175,850 adults using data from the 2001 BRFSS. Logistic regression was used to obtain odds ratios (OR) and 95% confidence intervals (CI) adjusted for age, gender, race/ethnicity, education, smoking status, and body mass index. RESULTS: The age-standardized prevalence (standard error) of 14 or more unhealthy (physical or mental) days during the previous 30 d was 28.4% (0.50) among physically inactive adults, 16.7% (0.27) among those with insufficient levels of PA, and 14.7% (0.22) among adults who met recommended levels. Overall, participation in no moderate PA (OR: 2.02; 95% CI: 1.85-2.21) was associated with an increased likelihood of having 14 or more unhealthy days. Also for moderate PA, participation every day of the week (5-6 d x wk as referent) (OR: 1.35; 1.26-1.46) was associated with an increased likelihood of 14 or more unhealthy days, as was participation for periods < 20 min (OR: 1.43; 95% CI: 1.30-1.58) or > or = 90 min (OR: 1.22; 95% CI: 1.14-1.31) per day (30-59 min x d as referent). Similar associations were observed for participation in vigorous PA. CONCLUSION: Persons achieving recommended levels of PA were more likely to report fewer unhealthy days compared with inactive and insufficiently active persons; however, participation in daily moderate or vigorous PA and participation in very short (< 20 min x d) or extended ( > or = 90 min x d) periods of PA was associated with poorer HRQOL. Further research examining the relationship between the dose of PA and HRQOL as well as other health outcomes is needed.

Adolescent↗
PubMed2004

Centrifuge training increases presyncopal orthostatic tolerance in ambulatory men.

INTRODUCTION: Exposure to spaceflight or simulations of microgravity reduce human postflight orthostatic tolerance. Exercise training and volume loading can reduce associated losses of plasma volume and muscle strength, but are not successful in maintaining postflight orthostatic tolerance. A preliminary study (16) indicated that short bouts of artificial gravity (AG) training on a centrifuge could increase orthostatic tolerance in healthy, ambulatory volunteers. We tested the same AG protocol for its tolerance effect on 14 men who underwent a 3-wk exposure to Gz acceleration training on NASA-Ames' (Moffet Field, CA) human-powered centrifuge. METHODS: Subjects trained supine (head near the center of rotation) and in pairs (one subject rode passively while the other provided power to operate the 1.9-m centrifuge). The acceleration profile consisted of 7 min at 1 Gz before alternating between 1 and 2.5 Gz at 2-min intervals for 28 min. Each subject's presyncopal orthostatic tolerance limit (to a combination of 70 degrees head-up tilt and increasing lower body negative pressure) was determined before and after training. RESULTS: There were no significant differences between training groups, but presyncopal orthostatic tolerance time was improved 17 +/- 10% (p < 0.05) for the combined groups. Mechanisms associated with increased tolerance included: increased cardiac output (p < 0.04), stroke volume (p < 0.01) and low-frequency spectral power of arterial pressure (p < 0.006), and decreased arterial pressure (p < 0.05) and vascular resistance (p < 0.04). Artificial gravity training in this group of men appears to increase orthostatic tolerance through a combination of decreased vascular resistance and enhanced cardiac function.

Adaptation, Physiological↗
PubMed2003

Characterization of specific delta-opioid binding sites in the distal small intestine of swine.

Delta-opioid receptors modulate neurogenic smooth muscle contractions and mucosal ion transport in the porcine distal small intestine. We compared specific delta-opioid binding sites in neuronal membranes isolated from the inner submucosal plexus and myenteric plexus of this gut region. In both preparations, the delta-opioid receptor antagonist naltrindole displaced [3H]diprenorphine from two binding sites. [3H]Naltrindole bound specifically to a single high-affinity site that was displaced by delta-opioid receptor ligands with the rank order of affinity: naltriben >7-benzylidenenaltrexone>deltorphin II>[D-Pen(2), D-Pen(5)] enkephalin. Relative decreases in delta-opioid receptor agonist affinity in the presence of Na(+) and other ions differed in submucosal and myenteric membranes. The kappa-opioid receptor antagonist norbinaltorphimine displaced [3H]naltrindole binding in myenteric membranes (K(i)=7.2 nM). Delta-opioid receptors in submucosal and myenteric plexuses of porcine ileum appear to differ in some respects.

Animals↗
PubMed2003

Characterization of specific opioid binding sites in neural membranes from the myenteric plexus of porcine small intestine.

Delta- and kappa-opioid receptors (OPRs), but not micro-OPRs, are expressed in the myenteric plexus of the porcine distal small intestine. In a subpopulation of myenteric neurons, delta- and kappa-OPRs seem to be colocalized and may functionally interact. In this study, radioligand binding was used to characterize myenteric OPR populations in detail. The nonselective OPR antagonist [3H]diprenorphine bound to a single, high-affinity site in myenteric neural membrane homogenates. Naloxone displaced 65 and 59% of [3H]diprenorphine binding from this site in Na(+)-free Tris and Krebs-HEPES buffers, respectively. Naltrexone-derived delta- and kappa-OPR antagonists, including naltriben, 7-benzylidenenaltrexone, nor-binaltorphimine, and 5'-guanidinonaltrindole, displaced [3H]diprenorphine from two distinct binding sites to levels similar to that of naloxone. The selective delta-OPR ligands Tyr-1,2,3,4-tetrahydroisoquinoline-Phe-Phe-OH (TIPP), [D-Pen2,D-Pen5]enkephalin (DPDPE), [D-Ala2, Glu4]deltorphin II, and (+)-4-[(alphaR)-alpha((2S,5R)-4-allyl-2,5-dimethyl-1-piperazinyl-3-methoxybenzyl)-N,N-diethylbenzamide (SNC-80) and the kappa-OPR agonist (D-(5alpha,7alpha,8beta)-(-)-N-methyl-N-(7-(1-pyrrolidinyl)-1-oxoaspiro-(4,5)dec-8-yl) benzeneacetamide (U-69,593) displaced [3H]diprenorphine from three independent binding sites; these included high-affinity delta- and kappa-OPR sites, and a residual binding site. Residual [3H]diprenorphine binding was displaced by the selective kappa-OPR antagonist nor-binaltorphimine after saturation of delta and kappa sites, respectively, with DPDPE and U-69,593. The residual binding site displayed low affinity for delta- and kappa-OPR agonists and TIPP, as well as moderate affinity for naltrexone-derived ligands, properties reminiscent of delta-/kappa-OPR heterodimers.

Animals↗
PubMed2003

Copper chelation delays the onset of prion disease.

The prion protein (PrP) binds copper and under some conditions copper can facilitate its folding into a more protease resistant form. Hence, copper levels may influence the infectivity of the scrapie form of prion protein (PrPSc). To determine the feasibility of copper-targeted therapy for prion disease, we treated mice with a copper chelator, D-(-)-penicillamine (D-PEN), starting immediately following intraperitoneal scrapie inoculation. D-PEN delayed the onset of prion disease in the mice by about 11 days (p = 0.002), and reduced copper levels in brain by 29% (p < 0.01) and in blood by 22% (p = 0.03) compared with control animals. Levels of other metals were not significantly altered in the blood or brain. Modest correlation was observed between incubation period and levels of copper in brain (p = 0.08) or blood (p = 0.04), indicating that copper levels are only one of many factors that influence the rate of progression of prion disease. In vitro, copper dose-dependently enhanced the proteinase K resistance of the prion protein, and this effect was counteracted in a dose-dependent manner by co-incubation with D-PEN. Overall, these findings indicate that copper levels can influence the conformational state of PrP, thereby enhancing its infectivity, and this effect can be attenuated by chelator-based therapy.

Animals↗
PubMed2003

Quinacrine acts as an antioxidant and reduces the toxicity of the prion peptide PrP106-126.

The accumulation of protein aggregates in the brain is a central feature of several different neurodegenerative diseases. We have recently shown that Abeta and alpha-synuclein, associated with Alzheimer's disease, Parkinson's disease and related disorders, can both induce the formation of hydroxyl radicals following incubation in solution, upon addition of Fe(II). PrP106-126, a model peptide for the study of prion protein-mediated cell death, shares the same property. In this study we show that quinacrine (an anti-malarial drug and inhibitor of prion replication) acts as an effective antioxidant, readily scavenging hydroxyl radicals formed from hydrogen peroxide via the Fenton reaction or generated during incubation of the PrP106-126 peptide. Furthermore, the toxicity of PrP106-126 to cultured cells was significantly inhibited by quinacrine.

Animals↗
PubMed2003

Interactions within the intrinsic cardiac nervous system contribute to chronotropic regulation.

The objective of this study was to determine how neurons within the right atrial ganglionated plexus (RAGP) and posterior atrial ganglionated plexus (PAGP) interact to modulate right atrial chronotropic, dromotropic, and inotropic function, particularly with respect to their extracardiac vagal and sympathetic efferent neuronal inputs. Surgical ablation of the PAGP (PAGPx) attenuated vagally mediated bradycardia by 26%; it reduced heart rate slowing evoked by vagal stimulation superimposed on sympathetically mediated tachycardia by 36%. RAGP ablation (RAGPx) eliminated vagally mediated bradycardia, while retaining the vagally induced suppression of sympathetic-mediated tachycardia (-83%). After combined RAGPx and PAGPx, vagal stimulation still reduced sympathetic-mediated tachycardia (-47%). After RAGPx alone and after PAGPx alone, stimulation of the vagi still produced negative dromotropic effects, although these changes were attenuated compared with the intact state. Negative dromotropic responses to vagal stimulation were further attenuated after combined ablation, but parasympathetic inhibition of atrioventricular nodal conduction was still demonstrable in most animals. Finally, neither RAGPx nor PAGPx altered autonomic regulation of right atrial inotropic function. These data indicate that multiple aggregates of neurons within the intrinsic cardiac nervous system are involved in sinoatrial nodal regulation. Whereas parasympathetic efferent neurons regulating the right atrium, including the sinoatrial node, are primarily located within the RAGP, prejunctional parasympathetic-sympathetic interactions regulating right atrial function also involve neurons within the PAGP.

Animals↗
PubMed2003

Generation of hydrogen peroxide from mutant forms of the prion protein fragment PrP121-231.

By means of electron spin resonance spectroscopy, in conjunction with the spin trapping technique, we have shown previously that Abeta and alpha-synuclein (aggregating proteins that accumulate in the brain in Alzheimer's disease, Parkinson's disease, and related disorders) both induce the formation of hydroxyl radicals following incubation in solution, upon addition of Fe(II). These hydroxyl radicals are apparently formed from hydrogen peroxide, via Fenton's reaction. An N-terminally truncated fragment of the mouse prion protein (termed PrP121-231) is toxic to cerebellar cells in culture, and certain human mutations, responsible for inherited prion disease, enhance this toxicity. Here we report that PrP121-231 containing three such mutations (E200K, D178N, and F198S) also generated hydroxyl radicals, upon addition of Fe(II). The formation of these radicals was blocked by catalase, or by metal chelators, each of which also reduced the toxicity of the PrP121-231 fragments to cultured normal mouse cerebellar cells. Wild-type PrP121-231, full-length cellular PrP, and its homologue doppel did not generate any detectable hydroxyl radicals. We conclude that the additional cytotoxic effects of the mutant forms of PrP121-231 could be due to their ability to generate hydrogen peroxide, by a metal-dependent mechanism. Thus, one effect of these (and possibly other) prion mutations could be production of a particularly toxic form of the prion protein, with an enhanced capacity to induce oxidative damage, neurodegeneration, and cell loss.

Animals↗
PubMed2003

Detection of bovine spongiform encephalopathy, ovine scrapie prion-related protein (PrPSc) and normal PrPc by monoclonal antibodies raised to copper-refolded prion protein.

Prion-related protein (PrP) is a glycosylphosphatidylinositol-linked cell-surface protein expressed by a wide variety of cells, including those of the nervous system and the immune system. Several functions of normal cellular PrP (PrPc) have been proposed that may be associated with the capacity of this protein to bind copper. In the present study, we describe the generation of a panel of monoclonal antibodies raised to copper-refolded PrP, which may be used to analyse the normal and disease-associated forms of this protein. The anti-PrP monoclonal antibodies were reactive by Western blot and ELISA with recombinant murine PrPc refolded in the presence or absence of either copper or manganese, and with the disease-susceptible allelic form V136R154Q171 ('VRQ'; where single-letter amino-acid notation has been used) and disease-resistant allelic form A136R154R171 ('ARR') of recombinant ovine PrPc. FACS analysis of lymphoid cells using these monoclonal antibodies showed that wild-type non-activated mouse lymphocytes expressed little, if any, PrPc. These monoclonal antibodies were shown to react with the unglycosylated and monoglycosylated forms of PrPSc (abnormal disease-specific conformation of PrP) in prion-infected tissue samples from all of the different species tested by Western blot. In addition, this analysis allowed one to make a distinction between bovine spongiform encephalopathy ('BSE') and scrapie PrPSc) isolates from experimentally infected sheep on the basis of their different electrophoretic mobilities.

Animals↗
PubMed2003

Kinin-induced anion-dependent secretion in porcine ileum: characterization and involvement of opioid- and cannabinoid-sensitive enteric neural circuits.

The intestinal secretory actions of the proinflammatory peptide kallidin (lysyl-bradykinin) are mediated partially by enteric neurons. We hypothesized that kallidin produces neurogenic anion secretion through opioid- and cannabinoid-sensitive enteric neural pathways. Changes in short-circuit current (I(sc)) across sheets of porcine ileal mucosa-submucosa mounted in Ussing chambers were measured in response to kallidin (1 microM) or drugs added to the contraluminal bathing medium. Kallidin transiently increased I(sc), an effect reduced after inhibition of neuronal conduction by 0.1 microM saxitoxin, cyclooxygenase inhibition by 10 microM indomethacin, or kinin B(2) receptor blockade by 1 microM d-arginyl-l-arginyl-l-prolyl-trans-4-hydroxy-l-prolylglycyl-3-(2-thienyl)-l-alanyl-l-seryl-d-1,2,3,4-tetrahydro-3-isoquinolinecarbonyl-l-(2alpha,3beta,7alphabeta)-octahydro-1H-indole-2-carbonyl-l-arginine (HOE-140). Its action was dependent upon extracellular Cl(-) or HCO(3)(-) ions, but was resistant to 10 microM bumetanide or 0.3 mM 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid, and seemed to involve luminal alkalinization as measured by pH-stat titration. Kallidin-induced I(sc) elevations were sensitive to saxitoxin in tissues bathed in Cl(-)-, but not HCO(3)(-)-deficient media. Tissues pretreated with 0.1 microM [d-Pen(2,5)]-enkephalin, a selective delta-opioid agonist, displayed reduced I(sc) responses to kallidin; this effect was prevented by the delta-opioid antagonist naltrindole. At a contraluminal concentration of 1 microM, the cannabinoid receptor agonist (6aR)-trans-3-(1,1-dimethylheptyl)-6a,7,10,10a-tetrahydro-1-hydroxy-6,6-dimethyl-6H-dibenzo[b,d]pyran-9-methanol (HU-210) also attenuated responses to kallidin. Proinflammatory kinins seem to stimulate neurogenic anion secretion in porcine ileum by activating enteric neural circuits expressing inhibitory opioid and possibly cannabinoid receptors.

Analgesics, Opioid↗
PubMed2003

Copper-dependent generation of hydrogen peroxide from the toxic prion protein fragment PrP106-126.

Oligomeric forms of many of the aggregating proteins associated with neurodegenerative diseases are toxic to cultured cells. We have shown recently that Abeta and alpha-synuclein can both induce the formation of hydroxyl radicals following incubation in solution, upon the addition of Fe(II). Thus, they appear to generate hydrogen peroxide, which is converted to hydroxyl radicals via the Fenton reaction. Here we show that the widely studied toxic peptide fragment of the prion protein, PrP106-126, has exactly the same property, but only in the presence of copper ions. Since the aggregation and toxicity of PrP106-126 have been reported to be critically dependent on copper binding, our data suggest that the published cytotoxic effects of this peptide could also be due to its ability to generate hydrogen peroxide.

Copper↗
PubMed2003

Effects of nicotine and dietary salt on a learned blood pressure response in Dahl-S rats.

We examined the effects of chronic nicotine exposure and dietary salt on the arterial blood pressure (BP) changes learned in response to an acute behavioral stress in the Dahl salt-sensitive rat. Four groups were tested: low salt + vehicle; low salt + nicotine; high salt + vehicle; and high salt + nicotine. Rats were fed a low-salt (0.08% NaCl) or a high-salt (8% NaCl) diet for 4 wk; 2.4 mg. kg(-1). day(-1) nicotine or vehicle was given via an implanted osmotic minipump for the last 2 wk. All rats were conditioned by following one tone (CS+) with a 0.5-s tail shock; another tone (CS-) was never followed by shock. CS+ in low salt + vehicle and high salt + vehicle-treated rats evoked an initial arterial BP increase (C(1)), a component of the startle response, and an ensuing, smaller, but more sustained, pressor response (C(2)), which is acquired with training. In these rats, both C(1) and C(2) evoked by CS- were significantly smaller than those to CS+, demonstrating that these groups discriminated between the two tests. Conversely, although the low salt + nicotine-treated rats had both the C(1) and C(2) components of the conditional arterial pressure response, they did not discriminate between CS+ and CS-. Finally, the high salt + nicotine group failed to both discriminate between tones and acquire (i.e., learn) the C(2) response. The unconditional response to shock did not differ between groups. We conclude that combined exposure to high salt and to nicotine inhibits the salt-sensitive animal's acquisition of a learned conditional BP response, perhaps because nicotine acts preferentially on those central processes required for associative learning versus those involved in orientating to external stimuli.

Animals↗
PubMed2003

Physical activity and body mass index among US adolescents: youth risk behavior survey, 1999.

OBJECTIVE: To investigate associations of underweight and overweight with physical activity among high school students in the United States. METHODS: A nationally representative sample of 15 349 US high school students participated in the 1999 Youth Risk Behavior Survey; 13 295 were included in these analyses. Five measures of physical activity were examined as dichotomous variables: (1) vigorous-intensity physical activity (>/=3 vs <3 sessions lasting at least 20 minutes each per week); (2) moderate-intensity physical activity (>/=5 vs <5 sessions lasting at least 30 minutes each per week); (3) strength training (>/=3 vs <3 sessions per week); (4) enrollment in physical education (yes or no); and (5) sports participation (yes or no). Using body mass indexes, students were categorized by percentiles as underweight (</=5th percentile), at risk for underweight (>5th to </=15th percentiles), normal weight (>15th to <85th percentiles), at risk for overweight (>/=85th to <95th percentiles), or overweight (>/=95th percentile). Potential associations between physical activity and body mass index were examined using logistic regression. RESULTS: On several measures, adolescent boys who were underweight or overweight were less likely to be physically active than boys of normal weight (eg, odds ratio [OR], 0.23; 95% confidence interval [CI], 0.12-0.45; and OR, 0.75; 95% CI, 0.61-0.93; for boys who were underweight and overweight, respectively, for strength training). Adolescent girls who were overweight or at risk for overweight were less likely (OR, 0.62; 95% CI, 0.50-0.78; and OR, 0.63; 95% CI, 0.46-0.85; respectively) to be involved with sports than girls of normal weight; and girls who were underweight were less likely (OR, 0.44; 95% CI, 0.22-0.91) to be enrolled in physical education. CONCLUSIONS: Weight status among high school students is correlated with selected physical activity behavior, especially among adolescent boys. Interventions to increase physical activity for high school students should target adolescents of all shapes and sizes, and may best be achieved by school policies requiring physical education or after-school sports.

Adolescent↗