Food cravings in relation to body mass index, restraint and estradiol levels: a repeated measures study in healthy women.

The study considered the nature and extent of cravings in 108 healthy women between the ages of 20 and 37 who were tested at four time points over a 2-year period. There was substantial consistency over the four widely separated time points (3 months-1 year) in the types of foods craved, with chocolate and ice cream highest on the list, followed by fatty and spicy foods, and sweets. Women with a higher body mass index reported more consistent cravings for salty foods, especially those with high flavor intensity. There were no significant relationships between dietary restraint and the number, frequency or types of cravings. There were also no strong relationships between estradiol levels and the number, frequency or types of cravings women reported in the whole sample. The data suggest that women have a stable core of foods for which they experience cravings, relatively independent of estradiol levels, BMI or degree of dietary restraint.     

Recombinant human alpha lymphotoxin (tumor necrosis factor-beta) induces peripheral neutrophilia and lymphopenia in the rat.

Recombinant human alpha lymphotoxin (rLT) administered intravenously to Lewis rats induces peripheral neutrophilia and lymphopenia in a dose-response dependent fashion. A dose of 30,000 units of rLT induced a neutrophilia (1589 +/- 326 to 5554 +/- 1050 neutrophils/cu mm) and lymphopenia (10,368 +/- 992 to 4636 +/- 878 lymphocytes/cu mm) at 2 hours after injection that was highly significant (P less than 0.001 and P less than 0.001, respectively) in comparison with vehicle controls. The kinetics of the neutrophilia that peaked at 2 hours as well as of the lymphopenia were highly reminiscent of the neutrophilia and lymphopenia following intravenous administration of either recombinant human interleukin-1 (IL-1) alpha or beta to rats. The peripheral neutrophilia was accompanied by a significant depletion of bone marrow neutrophils (P less than 0.001), as is also known to occur after administration of IL-1. Systemic blood pressure was not affected by rLT, which suggested that the changes in circulating leukocyte subsets were not attributable to hemodynamic changes nor to the hemodynamic-change-related release of adrenal hormones. Adrenalectomy did not alter the rLT-induced neutrophilia or lymphopenia, which suggested that rLT does not mediate its hematologic effects on peripheral blood leukocytes via the release of adrenal hormones. Pretreatment of rats with dexamethasone, indomethacin, or aspirin also did not alter rLT-induced neutrophilia or lymphopenia, which suggested that rLT-induced hematologic effects were not mediated via arachidonic acid metabolites, in stark contrast to IL-1 induced neutrophilia, which is inhibited by both dexamethasone and indomethacin.     

Manipulation of intracellular calcium affects in vitro juvenile hormone synthesis by larval corpora allata of Manduca sexta.

The effect of altering intracellular free Ca2+ on juvenile hormone (JH) and acid synthesis by larval and pupally-committed corpora allata (CA) of fifth stadium Manduca sexta was investigated. Larval CA required extracellular Ca2+ greater than or equal to 0.1 mM for maximal JH synthesis, while JH acid synthesis by glands after pupal commitment was independent of extracellular Ca2+. Free Ca2+ in the hemolymph ranged from 1.4 to 2.1 mM during the fifth stadium. Both calcium ionophores and caffeine, which releases Ca2+ from intracellular stores, inhibited JH synthesis by larval CA but stimulated JH acid synthesis by post-commitment CA. These results suggest that intracellular stores may be the principal source of Ca2+ for the biosynthetic activity of the post-commitment gland. Calcium channel blockers (La3+, Cd2+) and antagonists (verapamil, isradipine and nitrendipine) decreased both JH and JH acid synthesis, indicating the existence of Ca2+ channels in the CA cell membrane. Calmodulin (CaM) antagonists inhibited the activity of both larval and post-commitment CA, suggesting an integral relationship of CaM to the effects of Ca2+ on gland activity. One of these effects is the demonstrated requirement of 0.1 mM extracellular Ca2+ for allatostatin inhibition of JH I synthesis by larval CA.     

The renal action of atrial natriuretic peptide during control of glomerular filtration

Studies were performed in anesthetized dogs (N = 7) to determine the effects of synthetic atrial natriuretic peptide (ANP) on sodium excretion in the presence and absence of control of glomerular filtration rate produced by suprarenal aortic clamping. Intrarenal infusion of synthetic atrial natriuretic peptide (0.3 micrograms/kg/min) significantly increased glomerular filtration rate from 29.3 +/- 3.0 to 43.2 +/- 4.4 ml/min, urinary sodium excretion from 20.1 +/- 10.3 to 223.3 +/- 52.3 microEq/min, fractional sodium excretion from 0.47 +/- 0.19 to 3.75 +/- 0.59%. In contrast, aortic clamping blocked the increase in glomerular filtration rate in association with an attenuated natriuresis. Urinary sodium excretion increased from 6.3 +/- 2.3 to 68.3 +/- 23.4 microEq/min and fractional sodium excretion increased from 0.15 +/- 0.04 to 0.90 +/- 0.30%. Despite this differential response in glomerular filtration rate and sodium excretion, whole kidney fractional delivery of sodium from the proximal tubule as estimated by the fractional excretion of lithium increased during both unclamped (17.7 +/- 1.8 to 30.4 +/- 0.8%) and clamped (12.9 +/- 2.1 to 23.9 +/- 2.7%) periods. These studies demonstrate that atrial natriuretic peptide-induced natriuresis is importantly mediated by an increase in glomerular filtration rate and decrease in tubular reabsorption.     

Hemorrhagic shock-induced bacterial translocation is reduced by xanthine oxidase inhibition or inactivation

Experiments were performed to determine whether bacterial translocation (BT) after hemorrhagic shock is due to a reperfusion injury mediated by xanthine oxidase-derived oxidants. Rats were subjected to 30 minutes of shock (30 mm Hg) followed by reinfusion of shed blood. Twenty-four hours after hemorrhage and reinfusion, the mesenteric lymph node, liver, and spleen were harvested from each animal for bacterial culture, and the ileum and cecum were examined histologically. Sham-shocked (control) rats were instrumented, but blood was not withdrawn. The incidence of BT was higher in the shocked rats (61%) than in the sham-shocked animals (7%) (p less than 0.01). Allopurinol (50 mg/kg, administered orally), a competitive inhibitor of xanthine oxidase, reduced the incidence of shock-induced BT to 14% (p = 0.02). Similarly, rats fed a tungsten-supplemented molybdenum-free diet, which inactivates xanthine oxidase, reduced shock-induced BT to 10% (p = 0.02). The histologic damage cause by hemorrhagic shock was prevented by blocking xanthine oxidase activity. Thus hemorrhagic shock-induced bacterial translocation from the gut appears to be mediated by oxidants generated by activation of the xanthine oxidase system.