Increase in body mass index from normal weight to overweight in a cross-sectional sample of healthy research volunteers.

Current literature provides limited information about healthy volunteers serving as controls for biomedical research. This study describes trends in body mass index (BMI), a ratio of weight to height (kilograms per square meter), of the population of healthy volunteers at the National Institutes of Health Clinical Center (NIH CC) and compares these trends to a nationally representative sample, as reported by the National Health and Nutrition Examination Survey. We hypothesized that BMI trends at the NIH CC would follow those of the US population.

Chronic alcohol accentuates nutritional, metabolic, and immune alterations during asymptomatic simian immunodeficiency virus infection.

Background: Alcohol abuse has been reported to have a high prevalence in the human immunodeficiency virus (HIV)-infected population. However, its impact on disease progression is unknown. Studies dissecting the drug-induced or alcohol-induced metabolic derangements that are likely to alter the course of disease progression are lacking.

Consequences of alcohol-induced early dysregulation of responses to trauma/hemorrhage.

Acute alcohol intoxication is a frequent underlying condition associated with traumatic injury. Studies from our laboratory have been designed to examine the early hemodynamic, proinflammatory, and neuroendocrine alterations in responses to hemorrhagic shock in surgically catheterized, conscious, unrestrained, male Sprague-Dawley rats during acute alcohol intoxication (1.75-g/kg bolus, followed by a constant 15-h infusion at a rate of 250-300 mg/kg/h).

Hemodynamic and immune consequences of opiate analgesia after trauma/hemorrhage.

The regulation of compensatory hemodynamic, inflammatory, and metabolic counter-regulatory responses to traumatic injury (trauma/hemorrhage [tx/hem]) and subsequent inflammatory challenges during the post-tx/hem period relies on balanced activation of neuroendocrine and opioid pathways. Pharmacological interventions during the rescue period as well as during the early post-tx/hem period that target these regulatory pathways can potentially affect the activation or efficacy of compensatory mechanisms. Their impact on mechanisms involved in these responses has not been well defined.

Acetate and butyrate are the major substrates for de novo lipogenesis in rat colonic epithelial cells.

The objective of these experiments was to investigate the source of substrates used for lipid synthesis and the pathways of substrate incorporation into lipids by epithelial cells of the colon. Within replicates, cells were exposed to all treatments evaluated in that experiment. By comparing the relative incorporation rates of several 14C-labeled substrates into lipids, acetate made a significantly larger carbon contribution to lipids than propionate, butyrate, glucose or glutamine under the in vitro conditions utilized in this study.