East-West Flap After Mohs Micrographic Surgery. / Colgajo este-oeste después de la cirugía micrográfica de Mohs.

Repair of distal nasal defects resulting from Mohs micrographic surgery is a challenge, but surgeons can choose from a number of techniques. We present 3 cases in which an east-west flap was used to close the defect. The east-west flap is an easily conceived advancement flap that consists of a superior triangle used to cover the defect and an inferior triangle whose base is located along the advancement line. The flap results in an optimal cosmetic outcome and involves minimum movement of tissue (preserving the nasal architecture) and well-camouflaged suture lines.

Dual control of cytochrome-c oxidase activity by female sex steroids.

Female sex steroids modify cytochrome-c oxidase (COX) activity in brown adipose tissue. To check the possibility of extending this modulating effect upon oxidative capacity to other tissues, COX activity was measured in different tissues from cold-acclimated female rats that were (1) intact in proestrus and diestrus I, (2) ovariectomized or (3) ovariectomized and treated with oestradiol and/or progesterone. In intact rats, COX activity varied within the oestrous cycle in brown adipose tissue and soleus muscle. Ovariectomy induced an increase in COX activity in most of the tissues studied, an increase reversed only after 10 days of treatment with oestradiol and/or progesterone. These results indicate both a short-term (oestrous cycle) and a long-term (ovariectomy) control of COX activity by female sex steroids, probably mediated by allosteric modulation and control of the enzyme synthesis respectively. In thermogenic tissues, that is brown adipose tissue and skeletal muscles, the short-term control is interpreted as a cooperation between tissues to fulfil the requirements of temperature maintenance.

Progesterone does not alter sympathetic activity in tissues involved in energy balance.

Female rats acclimated to thermoneutrality to avoid cold influences received progesterone by means of subcutaneous implants. They increased their food intake and body weight above the values recorded in control animals. None the less, despite the enhanced food intake, no sign of activation of the sympathetic nervous system was observed, as judged by the unaltered noradrenaline content, half-life and turnover rate in brown adipose tissue, pancreas and heart. This indicates that progesterone increases food intake but prevents non-energy-conservation processes regulated by the sympathetic nervous system from taking place. Thus, it facilitates in two different ways the building up of energy stores. Because overfeeding induced by palatable diets increases the sympathetic tone to the organs studied, it is suggested that the central mechanisms regulating energy balance are probably influenced in a different manner by progesterone than by the sensory properties of palatable diets.

Food intake and body weight in rats with daily food-availability restrictions.

Male Wistar rats were offered food for either 24, 6, or 1 h a day at two different ambient temperatures -21 or 6 degrees C. At room temperature, rats offered food for 6 h a day matched their food intake to that of rats with 24 h of food-availability in 2-3 days, so that no main changes in total food intake, gross food efficiency, and body weight were recorded. No impairment of thermoregulatory capacity was recorded as judged by the unaltered oxidative capacity of brown adipose tissue and skeletal muscle. Nonetheless, a transient hypothermia was recorded at the beginning of the experiment in the food-restricted group. Rats that were only offered food 1 h a day were unable to sustain the food intake of the control animals, so that a continuous decline in body weight and a negative gross food efficiency ensured. In the cold, the food intake of rats offered food for only 6 or 1 h a day was similar to that showed by the corresponding groups at 21 degrees C. These results suggest a maximum rate for digestive processes, irrespective of ambient temperature. However, such levels of food intake were clearly insufficient to cope with the thermoregulatory enhanced energy demand at 6 degrees C, ad judged by the decrease in body weight.

Adiponectin values are unchanged during pregnancy in rats.

Adiponectin is believed to be a key factor in determining insulin sensitivity. In turn, insulin sensitivity is known to change from an enhanced state in early pregnancy to a reduced one in late pregnancy. A role for adiponectin in these changes has been proposed for mice but questioned for humans. We addressed this issue in rats by measuring adiponectin expression in both visceral and subcutaneous white adipose tissue, together with tissue content and release of the hormone in non-pregnant and in pregnant rats by days 8, 15 and 19 of pregnancy. Plasma concentration was also determined. No differences were found in any of the parameters measured between non-pregnant and pregnant rats at any time of pregnancy despite changes in white adipose tissue mass and insulin sensitivity. Adiponectin was also detected in cerebrospinal fluid at a concentration 1,000 times lower than in plasma, but again no differences were found between non-pregnant and pregnant animals. It is concluded that adiponectin does not play any role in regulating changes in insulin sensitivity during pregnancy in rats.

Inhibition of diet-induced thermogenesis during pregnancy in the rat.

Both virgin and pregnant rats were maintained at two different ambient temperatures (28 degrees C and 10 degrees C) for 19 days. Virgin rats maintained their daily food intake and body weight at both temperatures. At 28 degrees C pregnant rats showed a greater daily food intake and body weight than virgin ones and their brown adipose tissue suffered regressive changes in composition when compared with brown fat of virgin rats. At 10 degrees C the increases in daily food intake and body weight of pregnant rats took place from day 15-16 of pregnancy onward and foetuses taken from these pregnant rats were smaller than those taken from pregnant rats at 28 degrees C. It is concluded that pregnant rats at thermoneutrality, although hyperphagic, do not show diet-induced thermogenesis. However, it is proposed that pregnant rats in the cold may show BAT cold-induced thermogenesis.

Cold acclimation in food-restricted rats.

Food intake, body weight and brown adipose tissue (BAT) mass and composition of rats exposed at 6 degrees C either with food ad libitum or food-restricted were compared with those of rats in the thermoneutral zone, with food ad libitum. Cold acclimation with food ad libitum increases food intake and prevents body weight gains. IBAT (interscapular BAT) increases its mass and changes its composition after 3 weeks of cold exposure. Cold acclimation with food restriction produces a progressive decrease in body weight. IBAT mass increases after 3 weeks but changes in composition occur sooner. It is concluded that the overfeeding that accompanies cold acclimation is not necessary for non-shivering thermogenesis in BAT.

Brown adipose tissue thermogenesis in T3-treated rats.

T4 treatment results in an inactivation of brown adipose tissue (BAT) which has been attributed to a reduced need of thermoregulatory heat production. Since T3 formation in brown adipocytes is governed by a type II T4 5'-deiodinase which is inhibited by T4, we analyzed the possibility that results obtained by T4 treatment were due to a lack of T3 in the tissue. Hyperthyroidism was induced in adult rats by administration of T3 (50 micrograms/kg body weight daily s.c.). Euthyroid and hyperthyroid rats were maintained at 23 degrees C or exposed at 6 degrees C for 3 weeks. Hyperthyroid rats at 23 degrees C showed an increase in BAT mass and in DNA and total lipids contents; however, BAT thermogenic activity was depressed. BAT from cold-exposed hyperthyroid rats showed the same mass and DNA content than at 23 degrees C, but it showed an increase in thermogenic activity, this increase being lower than in cold-exposed euthyroid rats. We conclude that high levels of T3 in BAT do not stimulate the thermogenic activity of the tissue. On the contrary, they inhibit it in response to lower requirements of facultative thermogenesis, both at 23 degrees C and at 6 degrees C.

Cold-induced thermogenesis in hypothyroid rats.

Hypothyroidism was induced in adult rats by oral administration of methimazole. Euthyroid and hypothyroid rats were maintained at 23 degrees C or exposed at 6 degrees C for 3 weeks. Both euthyroid and hypothyroid rats maintained at 23 degrees C had similar interscapular brown adipose tissue (BAT) composition and thermogenic activity. Cold-exposed hypothyroid rats showed the same interscapular BAT mass and gross tissue composition as cold-exposed euthyroid animals, but the interscapular BAT of cold-exposed hypothyroid rats did not show the characteristic increase in GDP binding, and the increase in mitochondrial mass was lower than in euthyroid rats. From these results we conclude that thyroid hormones do not influence BAT significantly when thermogenic requirements are moderate, but they participate in the trophic response of the tissue when thermogenic requirements are intense. This thyroid hormone participation in the BAT trophic response occurs at the mitochondrial level, both in quantitative (mitochondrial mass) and qualitative (GDP-binding) aspects.

Reduced noradrenaline responsiveness of brown adipocytes isolated from estradiol-treated rats.

High plasma levels of estradiol are known to reduce the GDP binding of brown adipose tissue. Since GDP binding depends on the level of sympathetic discharge to brown adipose tissue, we measured the responsiveness to noradrenaline of brown adipocytes isolated from female rats with high plasma levels of estradiol. Noradrenaline responsiveness was assessed by measuring the respiration rate of isolated brown adipocytes in the presence of different concentrations of noradrenaline. Both control and treated adipocytes showed the same basal respiratory rate (27 +/- 6 and 24 +/- 4 nmol O2.min-1.10(-6) cells, respectively). The presence of noradrenaline (0.1, 1, and 10 microM) in the medium increased the respiration rate of both kinds of adipocytes in a dose-dependent manner. However, the response was markedly reduced in adipocytes isolated from estradiol-treated rats. These results suggest that estradiol impairs the responsiveness of brown adipose tissue to the sympathetic nervous system. Three possible mechanisms are suggested as accounting for the observed decreased responsiveness to noradrenaline, i.e., a direct action of estradiol in brown adipocytes, a modulatory role of estradiol in the central control of the sympathetic discharge to brown adipose tissue, and the interference of catecholestrogens with noradrenaline synthesis at the sympathetic terminals.

Oxygen consumption of oestradiol-treated rats.

Rectal temperature and oxygen consumption (Vo2) 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.

Brown adipose tissue thermogenesis above the lower critical temperature.

Heat-acclimated rats show lighter IBAT deposit with different gross composition and lower GDP-binding than controls at thermoneutrality. A thermal disactivation of the tissue is then inferred. Cafeteria regime increased IBAT mass and GDP-binding when offered to rats at a thermoneutral ambient temperature. These results indicate that BAT thermogenesis at thermoneutrality is not the lowest one of the tissue and that diet-induced thermogenesis can take place even at thermoneutrality.

Effects of thyroxine and 3,5,3'-triiodothyronine in brown adipose tissue of rats.

Rats of both sexes were either cold acclimated (6 +/- 1 degree C) or treated with thyroxine (T4) or 3,5,3'-triiodothyronine (T3) (500 micrograms/kg body wt daily s.c. for 3 weeks). Wet weight, total proteins, lipids and nucleic acids in the interscapular brown adipose tissue (IBAT) were measured. Values obtained with T4 treatment were similar to those obtained with T3 treatment. T3 is the main thyroidal hormone in the rat and it is formed from T4 deiodination in liver and kidney. As T4-treated rats have not received T3 directly and its IBAT has a similar composition to that of T3-treated rats, it is concluded that peripheral T4 deiodination is governed by the plasma T4 levels. Total proteins and DNA content were similar in cold-acclimated and T3- or T4-treated rats, which is interpreted as thyroidal hormones having an action at these levels.

Reduced oxygen consumption of brown adipocytes isolated from progesterone-treated rats.

It has been previously shown that responsiveness to noradrenaline is reduced in brown adipocytes isolated from estradiol-treated rats. The possibility that high plasma levels of progesterone could also alter adrenergic response was checked. The oxygen consumption of brown adipocytes isolated from control and progesterone-treated rats was monitored in basal conditions and in the presence of increasing concentrations of noradrenaline. In both situations, cells isolated from treated animals showed a lower respiratory rate than those from control animals. These results suggest that not only estradiol but also progesterone could modulate the adrenergic response of brown adipocytes. The study of alpha 1- and beta-adrenergic responses indicates that the beta-response parallels the general reduction in oxygen consumption, although the alpha 1-response seems to be more deeply depressed. Estimation of cell number in brown fat depots indicates some hyperplasia induced by progesterone; this increase in cell number could counterbalance partially but not totally the decreased cellular oxygen consumption at the organ level.

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 throughout the experimental period, it could be that progesterone does not affect BAT, either at thermoneutrality or in the cold.

Effect of acute cold exposure on the expression of the adiponectin, resistin and leptin genes in rat white and brown adipose tissues.

Leptin, adiponectin, and resistin are key hormones produced by adipose tissue. In the present study, we have examined the effects of acute cold exposure (18 h at 6 degrees C) on the expression of the genes encoding these hormones in both brown and white fat of rats. Acute cold exposure resulted in a significant (p < 0.001) increase in the level of UCP1 and metallothionein-1 mRNAs in brown adipose tissue, indicative of an activation of thermogenesis. Leptin mRNA was decreased (p < 0.001) in brown fat in the cold, and there was also a small but statistically significant (p < 0.05) decrease in adiponectin mRNA; resistin mRNA did not change significantly (p > 0.05). In white fat, the level of leptin mRNA also fell in the cold (p < 0.05), but there was no significant change (p > 0.05) in either adiponectin or resistin mRNA. The serum concentration of adiponectin was unchanged following acute cold exposure. We conclude that while leptin gene expression is inhibited by exposure to cold, there is no major effect on the expression of either the adiponectin or resistin genes in white or brown fat despite the cold-induced stimulation of sympathetic activity and fatty acid flux. Thus, adiponectin and resistin are unlikely to play a key role in the extensive metabolic adaptations to cold.

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 alpha-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.

Hematology and blood chemistry of chicks of white and black storks (Ciconia ciconia and Ciconia nigra).

1. The hematology and blood chemistry of 15-68-day-old chicks have been studied. 2. Red cell numbers (1,900,000/mm3), hemoglobin content (11.5 g/dl) and hematocrit (37.5) were similar in both species of storks. 3. Total numbers of leucocytes (63,000/mm3) were similar in both species, whilst differential leucocyte counts were not. 4. Higher levels of plasma protein, GOT and cholesterol in HDL were found in white storks when compared with black storks but not differences were detected in plasma levels of triglycerides, total cholesterol, urea, uric acid, GPT and alkaline phosphatase.

Brown adipose tissue thermogenesis in testosterone-treated rats.

The participation of sexual hormones in body weight regulation is partly accomplished by altering food intake. Nonetheless, female sexual hormones also alter brown adipose tissue thermogenesis in females. This study was aimed to find out if male hormones could alter brown adipose tissue thermogenesis in male rats. Testosterone was administered by means of Silastic capsules in adult male rats acclimated either at 28 degrees C (thermoneutrality) or at 6 degrees C (cold), treatment lasting 15 days. Food intake and body weight gain were reduced by hormonal treatment. However, brown adipose tissue mass, protein content, mitochondrial mass and GDP-binding were unchanged at both environmental temperatures. Accordingly, testosterone participation in body weight regulation is thought to be carried out without altering brown adipose tissue thermogenesis. A reduction in the weight of the sex accessory glands was also observed after cold acclimation.

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 17 beta-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 intake 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.