Anne M. Ronan

Elevated atopy in healthy obese women

BACKGROUND Allergic disorders, including asthma, have increased dramatically in the United States in the past 20 y. Epidemiologic studies have found body mass index (body weight in kg/height squared in m) to be a positive independent correlate of atopy in women but not in men. OBJECTIVE We investigated the prevalence of atopy among healthy obese and nonobese women and its relation to fat mass (FM), insulin resistance, and plasma concentrations of 17beta-estradiol, interleukin 4 (IL-4), and leptin. DESIGN A cross-sectional study of 21 obese (> or = 30% body fat) and 22 nonobese (< 30% body fat) women (18-41 y of age) was performed. The following measurements were taken: FM by plethysmography, total and specific immunoglobulin E (IgE) by automated immunosorbent analysis, and blood glucose, insulin, C-peptide, 17beta-estradiol, sex hormone-binding globulin, and IL-4. Insulin sensitivity was determined on the basis of the fasting insulin resistance index and with an oral-glucose-tolerance test. RESULTS The frequency of specific IgE in the obese group was almost 3 times that in the nonobese group (P = 0.008). The total IgE concentration was not significantly different between groups. Plasma concentrations of 17beta-estradiol, the ratio of 17beta-estradiol to sex hormone-binding globulin, the fasting insulin resistance index, and C-peptide and leptin concentrations were higher in the obese than in the nonobese group (P < 0.05) after adjustment for oral contraceptive use. All factors correlated positively with FM. Logistic regression showed FM to be the only positive predictor of specific IgE (P = 0.01). CONCLUSION The findings confirm a direct relation between obesity and a T helper 2 cell immune response in women.

Differences in selenium concentrations in target tissues and their relevance to its anticarcinogenicity

Abstract At concentrations of dietary selenium (Se) that inhibit tumorigenesis in mammary gland or liver, a 12–15-fold difference exists between the Se concentrations in these tissues. This obervation is difficult to reconcile with growing evidence of a common mechanism of anticarcinogenicity for various tissues protected by Se. To examine this situation in detail, 48 female Sprague-Dawley rats were randomized and assigned to one of three treatment groups at 50 days of age. They were fed a diet containing either 0.1 ug Se/g or the same diet supplemented with an additional 2.5 or 5.0 ug Se/g. Se was provided as sodium selenite. Diets were fed for a 28-day period. At the end of this time, the experiment was terminated. Liver, lung, kidney and mammary gland were analyzed for Se by a fluorometric method. Liver and mammary gland DNA content also was determined. Se increased linearly with increased dietary Se in all tissues evaluated. Liver and mammary gland Se (ug/g wet tissue) were significantly different from each other at every concentration of diet Se. However, the pattern of Se accumulation in these two tissues in response to different diet Se concentrations was essentially identical. Diet Se had no effect on tissue DNA content. Expression of liver and mammary gland Se per unit DNA eliminated between tissue differences in Se concentration indicating a similar Se/DNA ratio at a given level of dietary Se. These data point to the potential importance of intracellular Se content for expression of an anticancer effect. It is not known, however, if absolute Se concentration, generation of a particular specie (s) of Se or metabolism of Se per se, is the critical determinant for chemoprevention.

Enhancement of Pancreatic Carcinogenesis by Dehydroepiandrosterone

Caloric intake and body weight have been established as positive risk factors in the development of several human cancers.1 Conversely, caloric restriction has been found to significantly inhibit spontaneous2,3 as well as chemically induced mammary carcinogenesis4,5 and pancreatic pre-neoplastic foci6 in laboratory rodents.