Consumption of sweeteners at different stages of life: effects on body mass, food and drink intake in male and female Wistar rats.

The consumption of non-nutritive sweeteners has increased in the last decades. However, there are doubts about its consumption and its impact on body mass and metabolic alterations. For this reason, this study investigates the effects of the consumption of nutritive and non-nutritive sweeteners on body mass in different life stages of male and female Wistar rats: Childhood, adolescence, young adult, adulthood, and aged. For this purpose, 8 groups of male and female rats were used (10 per group/gender): sucrose 10%, glucose 14%, fructose 7%, acesulfame K 0.05%, aspartame:acesulfame mixture 1.55%, sucralose 0.017%, saccharin 0.033%, and a control group. Only in aged male rats (504 days) there were significant differences in body mass. In both genders, there were differences in food, drink, and energy intake along all life stage. It is concluded that non-nutritive sweeteners when consumed together with a balanced diet did not cause a greater body mass gain.

Subchronic stress effects on vascular reactivity in C57BL/6 strain mice.

BACKGROUND AND AIMS: There is a close relationship between psychosocial stress and the development of cardiovascular diseases. It has been reported that there are different alterations in endothelial function in this relationship. However, results obtained in different experimental stress models are controversial. Herein, we studied the effects of subchronic stress induced by movement restraint on several cardiovascular responses and plasma corticosterone concentration in male adult mice. METHODS: Experiments were performed in adult male mice of C57BL/6 strain. Animals were allocated into three groups: Control group A, without manipulation; Control group B, with manipulation (quantitation of blood pressure); and Experimental group, with quantitation of blood pressure and exposure to movement restraint. In vivo, heart rate and blood pressure were registered. In vitro, in aortic rings, vascular reactivity was analyzed. Additionally, plasma corticosterone concentration was quantified. RESULTS: In vivo, subchronic stress did not produce changes on heart rate either on blood pressure. In vitro, aortic rings with and without endothelium from control group B and experimental group showed: 1) a significant decrease in the maximal tension developed in response to phenylephrine; 2) this decrease was reverted by L-NAME. However, aortic rings from all groups, developed the same tension in response to high K+ solution. In aortic rings from animals of the experimental group, an increase in the maximal relaxation induced by carbachol was observed. This relaxation was prevented and/or reversed by L-NAME. Plasma corticosterone concentration was higher in the experimental group than that in the control group A. CONCLUSIONS: Exposition to subchronic movement restraint did not produce alterations in neurovegetative responses in this strain mice. But according to vasomotor responses observed, the results suggest that this subchronic stress model induces an increase in the synthesis/release of nitric oxide, both from endothelial cells and vascular smooth muscle. In accordance with the aforementioned results, we propose that C57BL/6 mice strain is sensitive to subchronic movement restraint stress model.

Enhanced Ca(2+)-induced Ca(2+) release from intracellular stores contributes to catecholamine hypersecretion in adrenal chromaffin cells from spontaneously hypertensive rats.

Adrenal chromaffin cells (CCs) from spontaneously hypertensive rats (SHRs) secrete more catecholamine (CA) upon stimulation than CCs from normotensive Wistar Kyoto rats (WKY). Unitary CA exocytosis events, both spontaneous and stimulated, were amperometrically recorded from cultured WKY and SHR CCs. Both strains display spontaneous amperometric spikes but SHR CCs produce more spikes and of higher mean amplitude. After a brief stimulation with high K(+) or caffeine which produces voltage-gated Ca(2+) influx or intracellular Ca(2+) release, respectively, more spikes and of greater mean amplitude and unitary charge were recorded in SHR CCs. Consequently, peak cumulative charge was ~2-fold higher in SHR CCs. Ryanodine (10 µM), a specific blocker of the ryanodine receptors reduced depolarization-induced peak cumulative charge by ~10 % in WKY and ~77 % in SHR CCs, suggesting, a larger contribution of Ca(2+)-induced Ca(2+) release to CA exocytosis in SHR CCs. Accordingly, Ca(2+) imaging showed larger [Ca(2+)]i signals induced both by depolarization and caffeine in SHR CCs. Distribution amplitude histograms showed that small amperometric spikes (0-50 pA) are more frequent in WKY than in SHR CCs. Conversely, medium (50-190 pA) and large (190-290 pA) spikes are more numerous in SHR than in WKY CCs. This study reveals that the enhanced CA secretion in SHR CCs results from a combination of (1) larger depolarization-induced Ca(2+) transients, due to a greater Ca(2+)-induced intracellular Ca(2+) release, (2) more exocytosis events per time unit, and (3) a greater proportion of medium and large amperometric spikes probably due to a higher mean CA content per granule. Enhanced CA release by excessive amplification by Ca(2+) induced Ca(2+) release and larger granule catecholamine content contributes to the increased CA plasma levels and vasomotor tone in SHRs.

Connexin 36 is expressed in beta and connexins 26 and 32 in acinar cells at the end of the secondary transition of mouse pancreatic development and increase during fetal and perinatal life.

To identify when during fetal development connexins (Cxs) 26 (Cx26) 32 (Cx32), and 36 (Cx36) begin to be expressed, as well as to characterize their spatial distribution, real time polymerase chain reaction and immunolabeling studies were performed. Total RNA from mouse pancreases at 13 and 18 days postcoitum (dpc) and 3 days postpartum (dpp) was analyzed. In addition, pancreatic sections of mouse at 13, 14, 15, 16, 18 dpc and 3 dpp and of rat at term were double labeled with either anti-insulin or anti-α-amylase and anti-Cx26 or -Cx32 or -Cx36 antibodies and studied with confocal microscopy. From day 13 dpc, Cxs 26, 32, and 36 transcripts were identified and their levels increased with age. At 13-14 dpc, Cxs 26 and 32 were localized in few acinar cells, whereas Cx36 was distributed in small beta cell clumps. From day 14 dpc onwards, the number of labeled cells and relative immunofluorescent reactivity of all three Cxs at junctional membranes of the respective cell types increased. Cxs 26 and 32 colocalized in fetal acinar cells. In rat pancreas at term, a similar connexin distribution was found. Relative Cxs levels evaluated by immunoblotting also increased (two-fold) in pancreas homogenates from day 18 dpc to 3 dpp. The early cell specific, wide distribution, and age dependent expression of Cxs 26, 32, and 36 during fetal pancreas ontogeny suggests their possible involvement in pancreas differentiation and prenatal maturation.