Preparation and characterization of cellulose fibers from Meghatyrsus maximus: Applications in its chemical derivatives.

Non-wood lignocellulosic fibers have emerged and are becoming increasingly important as an alternative source of cellulose for derivatives, functional materials, and biofuels. This work aimed, to obtain cellulose from Meghatyrsus maximus grass with adequate properties through an alkaline delignification and alkaline hydrogen peroxide bleaching. Meghatyrsus maximus was chemically characterized as lignocellulosic biomass, which consisted of 45.0 %, cellulose, 35.0 % hemicellulose, and 20.0 % lignin. The obtained cellulose was characterized by Fourier transform infrared spectroscopy, X-ray diffraction analysis, thermogravimetric analysis, and scanning electron microscopy. The alpha-cellulose content was 98.50 % with a crystallinity of 61.0 %. The morphological study by scanning electron microscopy images indicates a clean surface and removal of non-cellulosic components present in the initial raw fibers. These results showed that high-quality cellulose was obtained and is comparable to a commercial alpha-cellulose, highlighting Meghatyrsus maximus as an alternative source of lignocellulosic fibers.

Moderate exercise prevents the cell atrophy caused by hypothyroidism in rats.

Adult­onset hypothyroidism is associated with an increase in cell atrophy of the hippocampal pyramidal neurons. Physical exercise implies diverse actions on the neural tissue that promote neuron proliferation and survival. The beneficial effects of exercise seem to be inversely linked to its intensity, so that strenuous exercise has reduced protective effects. In this study we evaluated the capacity of a moderate forced­exercise routine to counteract the neurodegenerative effects of a hypothyroid condition induced during adulthood. Simultaneously with a chronic anti­thyroid chemical treatment, a group of rats was forced to walk in a motorized wheel for 30 min daily five times a week. In four weeks of treatment the rats developed a plain hypothyroid condition that in non­exercised rats was accompanied by a marked increase in the number of atrophic cells in all CA regions of the hippocampus. The forced­exercise treatment did not counter the development of hypothyroidism and its signs, but it did prevent almost completely the associated neuronal damage in all CA regions. The forced exercise also improved the cognitive function in a spatial­learning test. These results indicate that moderate exercise has the potential to prevent the structural and functional deficits associated with a hypothyroid condition.

The homeostatic feeding response to fasting is under chronostatic control.

Eating behavior is controlled by the energy needs of the organism. The need to provide a constant supply of energy to tissues is a homeostatic drive that adjusts feeding behavior to the energetic condition of the organism. On the other hand, food intake also shows a circadian variation synchronized to the light-dark cycle and food availability. Thus, feeding is subjected to both homeostatic and circadian regulation mechanisms that determine the amount and timing of spontaneous food intake in normal conditions. In the present study we contrasted the influence of the homeostatic versus the chronostatic mechanisms on food intake in normal conditions and in response to fasting. A group of rats was subjected to food deprivation under two different temporal schemes. A constant-length 24-h food deprivation started at different times of day resulted in an increased compensatory intake. This compensatory response showed a circadian variation that resembled the rhythm of intake in non-deprived animals. When subjected to fasting periods of increasing length (24-66 h), the amount of compensatory feeding varied according to the time of day in which food was made available, being significantly less when the fast ended in the middle of the light phase or beginning of the dark phase. These oscillatory changes did not have a correlation with variations in the level of glucose or ß-hydroxybutyrate in the blood. The results suggest that the mechanism of homeostatic compensation is modulated chronostatically, presumably as part of the alternation of catabolic and anabolic states matching the daily cycles of activity.

The long-term regulation of food intake and body weight depends on the availability of thyroid hormones in the brain.

OBJECTIVES: We evaluated the contribution of the thyroid hormones to the long-term maintenance of feeding behavior and body weight, while distinguishing their direct central effects from those resulting from the metabolic rate in the peripheral tissues. METHODS: We assessed the effect of hypothyroidism on the long-term (6 months) regulation of food intake, body weight, and energy expenditure in rats. We then generated the recovery of a euthyroid condition in the brain while maintaining a low T3 availability for the peripheral organs, i.e. a combined condition of central euthyroidism with peripheral hypothyroidism, with the aid of a pharmacological combination. RESULTS: Hypothyroidism caused a decrease in the daily food intake, body weight, and body temperature. The food intake and body temperature stabilized at a lower value, whereas body weight kept decreasing at a constant rate. The administration of exogenous T4 increased food intake and body-weight gain, but had no effect on body temperature. CONCLUSIONS: The thyroid hormones are necessary for the long-term regulation of energy intake, storage, and expenditure by different mechanisms. The feeding behavior seems to be partially dependent on a direct action of the thyroid hormones on the brain and this effect is independent of the energy expenditure in the peripheral organs. The body weight is closely dependent on the thyroid status and its maintenance seems to involve thyroid action on mechanisms other than feeding and metabolic rate.

The effects of sympathectomy and dexamethasone in rats ingesting sucrose.

Both high-sucrose diet and dexamethasone (D) treatment increase plasma insulin and glucose levels and induce insulin resistance. We showed in a previous work (Franco-Colin, et al. Metabolism 2000; 49:1289-1294) that combining both protocols for 7 weeks induced less body weight gain in treated rats without affecting mean daily food intake. Since such an effect may be explained by an increase in caloric expenditure, possibly due to activation of the sympathetic nervous system by sucrose ingestion, in this work, and using 10% sucrose in the drinking water, male Wistar rats were divided into 4 groups. Two groups were sympathectomized using guanethidine (Gu) treatment for 3 weeks. One of these groups of rats received D in the drinking water. Of the 2 groups not receiving Gu, one was the control (C) and the other received D. After 8 weeks a glucose tolerance test was done. The rats were sacrificed and liver triglyceride (TG), perifemoral muscle lipid, and norepinephrine (NE) levels in the liver spleen, pancreas, and heart were determined. Gu-treated rats (Gu and Gu+D groups) showed less than 10% NE concentration compared to C and D rats, less daily caloric intake and body-weight gain, more sucrose intake, and better glucose tolerance. The area under the curve after glucose administration correlated significantly with the mean body weight gain of the rats, except for D group. Groups D (D and Gu+D) also showed less caloric intake and body-weight gain but higher liver weight and TG concentration and lower peripheral muscle mass. The combination of Gu+D treatments showed some peculiar results: negative body weight gain, a fatty liver, and low muscle mass. Though the glucose tolerance test had the worst results for the D group, it showed the best results in the Gu+D group. There were significant interactions for Guan X Dex by two-way ANOVA test for the area under the curve in the glucose tolerance test, muscle mass, and muscle lipids. The results suggest that dexamethasone catabolic effect is not caused by sympathetic activation.

Influence of high-calorie (cafeteria) diets on the population of Paneth cells in the small intestine of the rat.

A high-calorie (cafeteria) diet is known to cause changes in the intestinal morphology and functioning that seem to be related to calorie overfeeding. Among the cell lineages found in the small intestine epithelium, the Paneth cell (PC) population is known to be influenced by factors related mainly to the intestinal microbiota. The role of PCs in the intestinal cell concert remains unclear, because experimental evidence suggests PC involvement in local processes other than protection against pathogens. Participation of PC in digestive mechanisms has been proposed on this basis. We have analyzed the effect of high-carbohydrate (HC) and high-fat (HF) cafeteria diets on the PC population in the small intestine of the adult rat. For 8 weeks, both HC and HF diets caused a gain in body weight, but whereas the HC-fed rats showed reduced counts of intestinal crypts per 5-mum section, the HF-fed group showed the opposite. In control rats, the number of crypts per section showed a slight tendency to decrease along the duodenum - ileum axis, whereas the number of PCs per crypt was increased towards the ileum. As a result, the number of PCs per section (calculated from these data) remained constant along the three segments of the intestine. The hypercaloric diets did not modify the general tendencies seen in the crypt and PC counts, but reduced the number of PCs per section in the duodenum by 50%. HC-fed, but not HF-fed, rats showed a similar reduction in jejunum also. These changes do not correlate particularly with any of the predictable effects of diet composition, so that a multifactorial control of PC density is proposed.

Chemical sympathectomy alters food intake and thermogenic responses to catecholamines in rats.

It has been suggested that the sympathetic nervous system contributes to the short-term control of feeding. The adrenergic innervation of some splanchnic organs seems to be especially involved in such processes, since catecholamines reduce feeding only when injected intraperitoneally or intraportally. In this work, the effects of neonatal sympathetic denervation with guanethidine (Gnt) upon food intake were assessed in adult rats. Gnt-treated male rats had lower body weight gain. The hypophagic response to intraperitoneal (ip) norepinephrine was 70% higher in Gnt-treated animals as compared to controls (P < 0.05); that of epinephrine (E) by 33% (P < 0.05) and that of isoproterenol was not significantly modified. As in normal rats, the hypophagic effect was much stronger after ip than after intramuscular (im) administration (P < 0.05). On the other hand, resting oxygen consumption (VO2) was consistently lower in denervated animals. Ip E administration did not modify VO2, while im E caused increased motor activity and VO2 (P < 0.05). In contrast to control rats, the respiratory exchange ratio in ad libitum fed Gnt rats did not decrease after Ip E administration, suggesting a lack of effect upon lipid mobilization. The lower rate of body weight gain induced by neonatal Gnt sympathectomy might be due to lower daily food intake possibly related, in part, to the sensitization of the alpha-adrenergic porto-hepatic response to endogenous catecholamines. Compared with controls, Gnt-treated rats also showed a limited thermogenic capacity not related to feeding, and a greater degree of carbohydrate oxidation, possibly due to a defect in E-induced lipolysis, which is beta-adrenergic.