Aging is a complex process in which responsiveness of various tissues to several hormonal and pharmacological stimuli decreases progressively. We propose that nutritional status in general and the deficiency of riboflavin in particular may modulate these age- related changes. We have recently observed that the binding of receptors to beta-adrenergic ligands and adenosine in rat adipose tissue declines with age. Our preliminary data indicate that early in riboflavin deficiency (less than 14 weeks) the binding of beta- adrenergic ligand is reduced and that in prolonged deficiency the age-related decline in the beta-adrenergic receptor binding is abolished. Adenosine receptor binding is not affected by either early or prolonged riboflavin deficiency. The altered ratio of beta-adrenergic to adenosine receptor binding during prolonged riboflavin deficiency might explain some of the adaptive changes which occur during long term deprivation of this vitamin. In the proposed study, we will evaluate in adipose tissue whether the duration and/or the onset of riboflavin deficiency is critical in modifying the age-related changes in beta-adrenergic receptor binding. Furthermore, we will determine whether the affinity or the number of binding sites is altered during aging and riboflavin deficiency. Since both beta-adrenergic agonists and adenosine have profound effects on cardiac muscle and coronary arteries, we will extend these studies to heart. The age-related changes in the binding of these ligands in heart and the influence of riboflavin deficiency will be evaluated. In addition to conducting receptor binding assays, the functional response to beta- adrenergic and adenosine stimulation will also be investigated by measuring cyclic AMP production, lipolysis, heart rate, and serum T3 and T4 levels. These studies should provide useful guidelines for effective pharmacological and nutritional management of elderly patients and for delaying and diminishing the age-related changes in body composition.
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