Maria Paz Nava

Hematology and plasma chemistry of house sparrows (Passer domesticus) along the summer months and after testosterone treatment

Abstract Young and adult male house sparrows were captured once reproduction had finished (early summer) and before molting had taken place. They remained in outdoor aviaries until molting was completed (late summer). Half of them received a chronic treatment of testosterone. A blood sample was collected both at the beginning and at the end of the captivity period. Both young and adult birds showed a hemoconcentration from the beginning to the end of the summer, which is suggested to be related to the natural cycle of water shortage. White blood cell number was higher in young than in adults but no change was observed during the study period. Plasma proteins and their nitrogenous wastes decreased over the summer months which raised the hypothesis of plasma proteins as a store for amino acid needs during molting. Testosterone increased erythrocyte number and blood hemoglobin content. It also altered leucocyte number, but in an age dependent manner. It also increased plasma proteins, but only in adult birds. Plasma triglycerides were unaltered by age, month of sampling or testosterone treatment.

Inactivation of brown adipose tissue thermogenesis by oestradiol treatment in cold-acclimated rats

Both cold-acclimated female rats and rats at thermoneutrality received 0.15–0.20 mg daily of 17β-oestradiol over 15 days via a Silastic capsule implanted subcutaneously. Controls received empty implants. Comparison between the oestradiol-treated animals and the untreated controls revealed that at thermoneutrality, oestradiol treatment decreased food intage and body weight gain, but did not affect brown adipose tissue (BAT) thermogenesis and composition. By contrast, in cold-acclimated rats, oestradiol treatment did not modify food intake or body weight gain, but it decreased BAT thermogenesis. It is concluded that the effects of oestradiol treatment on BAT depend on the activity of the tissue, i.e. it has no effect on BAT when the tissue is thermogenically inactive, but it decreases cold-induced BAT thermogenesis. It is suggested that oestradiol could be the hormonal factor responsible for the previously observed inactivation of BAT thermogenesis during pregnancy in cold-acclimated rats.

Proinflammatory Liver and Antiinflammatory Intestinal Mediators Involved in Portal Hypertensive Rats

Proinflammatory (TNF-α, IL-1β, and NO) and antiinflammatory (IL-10, CO) levels were assayed in serum, liver, and small bowel in order to verify a hypothetic inflammatory etiopathogeny of portal hypertension that could be the cause of its evolutive heterogeneity. Male Wistar rats were divided into one control group (n = 11) and one group with a triple stenosing ligation of the portal vein (n = 23) after 28 days of evolution. In one subgroup of portal hypertensive rats, portal pressure, collateral venous circulation, mesenteric vasculopathy, and liver and spleen weights were determined. In the remaining rats with portal hypertension TNF-α, IL-1β, and IL-10 were quantified in liver and ileum by enzyme-linked immunosorbent assay. NO synthase activity was studied in liver and ileum. CO and NO were measured in portal and systemic blood by spectrophotometry and Griess reaction, respectively. Portal hypertensive rats with mayor spleen weight show hepatomegaly and mayor development of collateral circulation. Ileum release of IL-10 (0.30 ± 0.12 versus 0.14 ± 0.02 pmol/mg protein; P < .01) is associated with a liver production of both proinflammatory mediators (TNF-α: 2 ± 0.21 versus 1.32 ± 0.60 pmol/mg protein; P < .05, IL-1β: 19.17 ± 2.87 versus 5.96 ± 1.84 pmol/mg protein; P = .005, and NO: 132.10 ± 34.72 versus 61.05 ± 8.30 nmol/mL; P = .005) and an antiinflammatory mediator (CO: 6.49 ± 2.99 versus 3.03 ± 1.59 pmol/mL; P = .005). In short-term prehepatic portal hypertension a gut-liver inflammatory loop, which could be fundamental in the regulation both of the portal pressure and of its complications, could be proposed.

Dissociation between brown adipose tissue thermogenesis and sympathetic activity in rats with high plasma levels of oestradiol

It has been shown previously that high plasma levels of oestradiol inhibit brown adipose tissue thermogenesis. Since rats and mice show a close association between thermogenic activity in and sympathetic discharge to brown fat, we measured the noradrenaline turnover in rats with high plasma levels of oestradiol to establish whether the observed inhibition of thermogenic activity is brought about by a reduction in the sympathetic drive to brown adipocytes. Oestradiol-filled Silastic capsules were implanted subcutaneously in female rats previously acclimated either to thermoneutrality or to cold. Control rats received empty implants. After 15 days treatment, noradrenaline turnover was measured by blocking its synthesis with α-methyl-p-tyrosine. As expected, noradrenaline turnover was higher in cold-acclimated rats than in rats kept at thermoneutrality. The presence of high plasma oestradiol levels did not alter sympathetic activity in any of the treated groups despite reducing thermogenic activity. This result reveals that oestradiol dissociates the thermogenic activity of brown adipose tissue from its sympathetic activation. Such dissociation has never been previously reported in rats, although it seems to be common in Syrian hamsters. However the causative factor in this species is unknown.

Cold-induced and diet-induced thermogenesis in progesterone-treated rats

Both cold-acclimated rats and rats at thermoneutrality received 1.5 mg/day of progesterone over a period of 15 days by means of two subcutaneously implanted Silastic capsules. Progesterone treatment increased total food intake and body mass gain in both groups of treated animals when compared with their controls at the same ambient temperature. However, the interscapular brown adipose tissue (BAT) of the treated rats showed the same thermogenic activity (assessed by GDP-binding), mass and gross composition as that of their respective controls. If it is assumed that enhanced food intake is the physiological drive for diet-induced thermogenesis, it could be concluded that progesterone inhibits diet-induced thermogenesis at thermoneutrality, but has no effect in cold-induced thermogenesis. However, if the physiological drive for diet-induced thermogenesis is not enhanced food intake, but an imbalance in the diet, then given that the same diet was offered to all animals thoroughout the experimental period, it could be that progesterone does not affect BAT, either at thermoneutrality or in the cold.

Oxygen consumption of oestradiol-treated rats

Rectal temperature and oxygen consumption (üüO2) were monitored in female rats acclimated either to cold or to thermoneutrality and with and without chronic administration of oestradiol. The hormone is known to inactivate brown adipose tissue (BAT) and to reduce its response to noradrenaline (NA). The role of sympathetic control was studied by administering NA or the adrenergic blocker propranolol. Oestradiol treatment did not affect rectal temperature in the states of acclimation to thermoneutrality and to cold, nor did it change the hypothermic response of cold-exposed rats to temporary food deprivation. In the cold-acclimated rats, both controls and oestradiol-treated animals exhibited similar degrees of metabolic reduction after propranolol administration in the cold and similar degrees of metabolic activation by NA at thermoneutrality. Rats acclimated to thermoneutrality showed a larger metabolic response to NA when treated with oestradiol. The results suggest that oestradiol, while inactivating the BAT response to NA, activates the NA responsiveness of other metabolically active tissues in cold-induced thermogenesis. The observation of a greater oxidative capacity in the kidney and the rectus abdominis muscle of oestradiol-treated, cold-acclimated rats would be in line with this proposal.

Effects of Female Sex Steroids in Thermogenic Tissues

The great heat generating power of brown adipose tissue (BAT) has a profound influence in energy balance. Cold-acclimated animals become hyperphagic to sustain the high substrate combustion in brown fat depots without reducing body energy stores. On the other hand, the low activity of brown fat in obese animals contributes to the low energy expenditure and the development of obesity. Reproduction is one of the major energy challenges in the mammalian life cycle. On viewing the profound influence of BAT in energy balance, it seems not surprising that brown adipose tissue is suppressed during late pregnancy and lactation as a way to save substrates for growth of mother and litter (1,13). Female sex steroids, 17s-oestradiol and progesterone seem to be involved in such disactivation. Brown adipocytes isolated from female rats with high plasma levels of sex steroids show a lower responsiveness to noradrenaline (NA) -as revealed by the lower increase in respiration rate after NA addition to the incubation medium-than that displayed by adipocytes isolated from untreated controls (10). The decreased responsiveness of brown adipocytes when plasma levels of oestradiol are high leads to a reduction of BAT thermogenic activity in cold-acclimated rats (11). This poses two additional questions, i.e., are oestradiol-treated females rats hypothermic? or are there alternative adjustments that compensate for the low BAT thermogenesis? On the contrary, progesterone impairment of responsiveness to NA does not decrease BAT thermogenesis (9). This raises another question, how progesterone treated animals maintain BAT thermogenesis despite the low responsiveness of brown adipocytes to NA? As in the case of oestradiol a compensatory adjustment was hypothesized.