Ontogeny of homeothermy in the immature rat: metabolic and thermal responses

Steady-state thermoregulatory responses were measured in the immature rat at 5, 7, 9, 11, 13, 15, 17, and 19 days of age. Tests were conducted at controlled ambient temperatures (Ta) ranging from 22.5 to 37.0 degrees C. Colonic (Tco) and skin (tail, interscapular, abdominal) temperatures were measured, as was O2 consumption from which metabolic rate (M) was calculated. Significant improvements in homeothermic ability occurred from 5 to 19 days of age. Although the resting level of M (RMR) increased by 6.9 W/m2 and the lower Ta limit for RMR (LCT) decreased by 2.5 degrees C as age advanced from 5 to 19 days, Tco at LCT was 36.8-37.1 degrees C at all ages studied. Below LCT the elevation of M to a given decrease in Tco was greater the older the animal. A comparable response to a change in skin temperature was not age dependent. Improvement in thermal insulation was the primary factor responsible for increases in homeothermic ability between 5 and 19 days of age.     

Post-traumatic metabolic shifts and epileptogenic plasticity in the CNS

Metabolic and ultrastructural disturbances in the brain tissues, which developed within a remote period after light craniocerebral trauma, and their dependence on the dynamics of formation of a post-traumatic epileptic nidus (EN), were studied in the experiments on rabbits. Manifestations of disturbances in energy metabolism (tissue respiration, oxidative phosphorylation, and ATP synthesis), activation of the antioxidant glutathione system, modification of the membrane phospholipid composition, and marked activation of epileptogenic-type plastic processes were revealed in the EN tissues.     

Dissociation by colchicine of the wet weight and the cGMP responses to estradiol in immature rat uterus

We previously reported on a positive correlation between two effects of estrogen on rat uterus, namely the early increases in cGMP and in water content of the organ suggesting that they were under the control of the same hormone sensitive regulatory process or linked by a cause to effect relationship. Up to now we were unable to find experimental conditions that would dissociate the two responses. In this work, immature Wistar rats were treated with colchicine (50 micrograms/animal) given at the same time as estradiol-17 beta (1 microgram/animal) or with estradiol alone. The experiments showed: (1) that the estradiol induced increase in uterine wet weight that occurs during the first 8 h after hormone injection was completely suppressed in the presence of colchicine indicating that it might depend on an intact microtubular system and (2) that, by contrast, the estrogen-induced increase in uterine cGMP remained unaffected by the colchicine presence. These data allow to conclude that the cGMP response to estradiol can be dissociated from the wet weight response and, therefore, that it is not controlled by the latter. From this and from data in the literature the hypothesis is proposed that the increase in uterine cGMP content might trigger the wet weight response, this possibly through a positive action on some microtubular function.     

Beyond glucose: metabolic shifts in responses to the effects of the oral glucose tolerance test and the high-fructose diet in rats

High-fructose diet-fed rats as one of the insulin resistant models was used widely for understanding the mechanisms of type 2 diabetes mellitus. Systems-level metabolic profiling of the rat model, however, has not been deciphered clearly. To address this issue, mass spectrometry-based metabolomics was employed to unlock the metabolic snapshots of the oral glucose tolerance test (oGTT) effect in either healthy or diabetic rats, as well as to delineate the metabolic signatures in tissues of rats fed with high-fructose diet. Several differentiating metabolites were highlighted to reveal the metabolic perturbation of the oGTT effects in healthy and diabetic rats, which involved amino acid biosynthesis, polyunsaturated fatty acids, phospholipids and purine metabolism. Surprisingly, the patterns of relationships for the metabolic phenotypes by using data mining revealed that glucose ingestion might induce the healthy group to display its trajectory towards diabetic status, while only a very slight influence was observed on the high-fructose diet-fed rats 120 min after glucose ingestion. The data treatment for liver, skeletal muscle and brain tissues suggested that oxidative stress, such as lipid peroxidation and the declined antioxidant, the elevated amino acids and the perturbation of fatty acids, were caused by the high-fructose diet in liver and skeletal muscle tissues. On the other hand, the up-regulation in purine biosynthesis and the decreased concentrations for amino acids were observed in the cerebral cortex and hippocampus tissues. Collectively, the obtained results might provide a new insight not only for the impairment of glucose tolerance but also for the dietary style in rats.     

Thermoregulatory responses of the immature rat following repeated postnatal exposures to 2,450-MHz microwaves

This study was designed to determine the changes that occur in the thermoregulatory ability of the immature rat repeatedly exposed to low-level microwave radiation. Beginning at 6-7 days of age, previously untreated rats were exposed to 2,450-MHz continuous-wave microwaves at a power density of 5 mW/cm2 for 10 days (4 h/day). Microwave and sham (control) exposures were conducted at ambient temperatures (Ta) which represent different levels of cold stress for the immature rat (ie, "exposure" Ta = 20 and 30 degrees C). Physiological tests were conducted at 5-6 and 16-17 days of age, in the absence of microwaves, to determine pre- and postexposure responses, respectively. Measurements of metabolic rate, colonic temperature, and tail skin temperature were made at "test" Ta = 25.0, 30.0, 32.5, and 35.0 degrees C. Mean growth rates were lower for rats exposed to Ta = 20 degrees C than for those exposed to Ta = 30 degrees C, but microwave exposure exerted no effect at either exposure Ta. Metabolic rates and body temperatures of all exposure groups were similar to values for untreated animals at test Ta of 32.5 degrees C and 35.0 degrees C. Colonic temperatures of rats repeatedly exposed to sham or microwave conditions at exposure Ta = 20 degrees C or to sham conditions at exposure Ta = 30 degrees C were approximately 1 degrees C below the level for untreated animals at test Ta of 25.0 degrees C and 30.0 degrees C. However, when the exposure Ta was warmer, rats exhibited a higher colonic temperature at these cold test Ta, indicating that the effectiveness of low-level microwave treatment to alter thermoregulatory responses depends on the magnitude of the cold stress.     

Erythrocytic reactions and metabolic shifts in long-term experimental hypercatecholaminemia

The experiments on intact dogs have revealed that daily two-hour infusions of stressor norepinephrine doses are accompanied by the elevation in erythrocyte, hematocrit and hemoglobin levels, changes in circulating blood volume and signs of compensated metabolic acidosis. These adaptive responses become excessive in persistent hypercatecholaminemia and promote the development of stress-induced organic lesions.     

Progesterone binding in the immature mouse and rat uterus

The use of a highly active progestin, 17, 21-dimethyl-19-nor-4, 9-pregnadiene-3, 20-dione (R 5020), as a tag has established that progesterone binds to a specific “7–8S” uterus cytosol component in both the immature mouse and rat.     

Oestrogen-induced expression of oncogenes in the immature rat uterus

4 h after a single precocious administration of oestrogen there was a considerable but short-lived surge in the uterine levels of myc-encoded polyadenylated mRNA. This was followed by a further peak 28 h after hormone administration. The expression of rasHa showed a totally different time course with a build up of hybridizable message that peaked 8 h after oestrogen administration.     

Effects of metabolic rate on thermal responses at different air velocities in -10 degrees C

The effects of exercise intensity on thermoregulatory responses in cold (-10 degrees C) in a 0.2 (still air, NoWi), 1.0 (Wi1), and 5.0 (Wi5) m x s(-1) wind were studied. Eight young and healthy men, preconditioned in thermoneutral (+20 degrees C) environment for 60 min, walked for 60 min on the treadmill at 2.8 km/h with different combinations of wind and exercise intensity. Exercise level was adjusted by changing the inclination of the treadmill between 0 degrees (lower exercise intensity, metabolic rate 124 W x m(-2), LE) and 6 degrees (higher exercise intensity, metabolic rate 195 W x m(-2), HE). Due to exercise increased heat production and circulatory adjustments, the rectal temperature (T(re)), mean skin temperature (Tsk) and mean body temperature (Tb) were significantly higher at the end of HE in comparison to LE in NoWi and Wi1, and T(re) and Tb also in Wi5. Tsk and Tb were significantly decreased by 5.0 m x s(-1) wind in comparison to NoWi and Wi1. The higher exercise intensity was intense enough to diminish peripheral vasoconstriction and consequently the finger skin temperature was significantly higher at the end of HE in comparison to LE in NoWi and Wi1. Mean heat flux from the skin was unaffected by the exercise intensity. At LE oxygen consumption (VO2) was significantly higher in Wi5 than NoWi and Wi1. Heart rate was unaffected by the wind speed. The results suggest that, with studied exercise intensities, produced without changes in walking speed, the metabolic rate is not so important that it should be taken into consideration in the calculation of wind chill index.     

Weaning and metabolic regulation in the rat

Premature weaning of rats to high carbohydrate diets causes a variety of short- and long-term changes in lipid metabolism, but the mechanisms involved are unclear. It is likely that interaction of diet with certain emerging hormonal control patterns during weaning might condition metabolic control and (or) subsequent adaptations in the adult organism. This implies that the adaptive responses of infant animals to diet may differ from those of the mature organism. For example, premature weaning leads to early appearance of rat liver malic enzyme (ME), even when fat supplies as much as 65% of the dietary energy; the same diet suppresses ME activity in 45-day-old rats. The levels of plasma glucagon and thyroid hormones are elevated during the weaning period. Several studies have shown that triiodothyronine evokes hepatic ME in suckling rats. Conversely, glucagon infusion into prematurely weaned rats suppresses the early appearance of the enzyme. Premature weaning, regardless of fat intake, leads to a rapid decline in plasma glucagon levels. Since glucagon is known to antagonize the actions of triiodothyronine on liver ME, the interaction of diet with glucagon and thyroid hormones is conceivably part of the mechanism responsible for the early appearance of hepatic malic enzyme, whereby the decline of plasma glucagon permits triiodothyronine to act on liver ME. Insulin probably exerts a permissive action subsequently. The manner in which these events relate to the long-term consequences of premature weaning is unknown.