We investigated the involvement of opioid receptors such as the mu and delta receptors in the predominant elevation of corn oil appetite just after 5-day repeated treatment of corn oil ingestion. Rats were given 5% corn oil emulsified with 0.3% xanthan gum for 20 min at the same hour for 5 consecutive days. A strong appetite for fat was formed after the 5 days presentation, and it was inhibited by naloxonazine, a selective antagonist of the mu-1 receptor, at doses of 3 mg/kg, but not by antagonists of the opioid delta receptor. In days 6, after the formation of a strong appetite for corn oil, an additional injection of naloxonazine suppressed fat intake 0-30, 30-60, 60-90 and 90-150 min after the presentation of the corn oil, but antagonists of the opioid delta receptor did not. These data suggested that the opioid mu receptor is involved in the sharp elevation of corn oil appetite during repeated presentation of corn oil to rats.
At least three kinds of Cl-/HCO3- exchangers, SLC26A3, SLC26A6 and AE2, have been demonstrated to be expressed in the intestinal epithelial cell. To examine the functional expression of these exchangers in the native enterocyte, we studied the Cl-/HCO3-- exchange activity in isolated villi from the mouse ileum by microfluorometric intracellular pH (pHi) measurement. The pHi value increased upon Cl- removal when the villus was superfused with an HCO3-/CO2-buffered solution, while the response was blunted when superfused with an HCO3-/CO2-free, Hepes-buffered solution. The recovery of pHi value induced by Cl- re-addition (after initial Cl- removal) was totally or partially mimicked by the addition of Br-, I-, F-, NO3-, or SO42- (in the absence of Cl-). The increase in pHi value induced by Cl- removal was partially inhibited in the presence of DIDS (30 μM), tenidap (10 μM), niflumic acid (30 μM) or NPPB (30 μM). Increasing the K+ concentration from 5 mM to 60 mM in the superfusion solution induced a reversible increase in pHi value under the HCO3-/CO2-buffered condition, while it had hardly any effect on pHi under the Hepesbuffered condition. The K+-induced pHi changes were partially suppressed by removing Cl- from the superfusion solution. These results, together with the reported findings of mouse slc26a3, slc26a6 and AE2 in heterologously expressed systems, suggest the possibility that these three exchangers may all be functionally expressed in mouse ileal villous cells.
We immunohistochemically evaluated the involvement of five cancer cachexia-related factors, including leukemia-inhibitory factor (LIF), zinc-α2-glycoprotein (ZAG), interleukin 6 (IL-6), proteolysis-inducing factor (PIF) and tumor necrosis factor α (TNF α) in causing cancer cachexia. Twenty-six xenografts implanted into mice were examined for the expression of the cancer cachexia-related factors, in relation to the body weight loss of the hosts. Five xenografts were categorized in the cachectic group, and the remaining 21 xenografts belonged to the non-cachectic group. LIF was extensively expressed in both the cachectic and non-cachectic groups. ZAG and IL-6 were expressed in one of the cachectic and some non-cachectic xenografts. PIF and TNF α were detected in one and two non-cachectic xenografts, respectively, but in none of the cachectic ones. Any of five factors examined were not conclusive for causing cancer cachexia in the murine xenograft model. Further analysis is needed in order to elucidate the mechanisms responsible for cancer cachexia.
The aim of the present study was to compare the hypoxic and inflammatory effects of transfusing hemoglobin-vesicles (HbV) or lactated Ringer's (LR) solution on several organs in a hemorrhagic shock model. Hemorrhagic shock was induced in 48 anesthetized rats by withdrawing 28 mL/kg blood. The animals were resuscitated by replacing the blood with an equal volume of HbV solution or three times the volume of LR solution. The heart, lung, liver, kidney and spleen were extracted at different time points following resuscitation, and mRNA expression levels of hypoxia-induced factor 1-alpha (HIF-1α) and tumor necrosis factor-alpha (TNF-α) were determined. Blood lactate concentrations in the HbV group rapidly returned to baseline levels, whereas elevated lactate concentrations in the LR group were prolonged. There were no significant differences between the two resuscitation groups in terms of HIF-1α and TNF-α expression in the organs examined. HIF-1α and TNF-α expression in the lungs was significantly greater than in other organs. Our results suggest that resuscitation from hemorrhagic shock with HbV did not increase hypoxic or inflammatory effects in major organs, compared with resuscitation using LR solution, despite prolonged elevation of blood lactate.
Connexin (Cx) 43-mediated gap-junctional intercellular communication (GJC) mainly regulates the osteoblastic differentiation, but much of the function of Cx43 on the differentiation of bone marrow cells is unclear. This study is aimed to clarify relationship between the differentiation of rat bone marrow cells and the function of Cx43. Bone marrow cells derived from four-week-old Wistar strain rats were grown in the presence and absence of 18-α-glycyrrhetinic acid (AGA, 100 μM) to inhibit Cx43-mediated GJC. Expression of Cx43 gene and protein, and the level of intracellular cyclic adenosine monophosphate (cAMP) were determined as the assessment of the function in Cx43-mediated GJC, and alkaline phosphatase (ALP) activity and mineralization were measured as the assessment of osteoblastic differentiation. The Cx43 gene expression was first observed at 2 days, but under the condition in which rat bone marrow cells were treated with AGA, there was no significant effect on the Cx43 gene expression. By administrating AGA to rat bone marrow cells, all parameters of maturation but the Cx43 gene expression significantly decreased. The results of this experiment suggest that Cx43-mediated GJC plays a critical role in rat bone marrow cells, progress toward maturation.
We studied the physiological and behavioral effects of subchronic intracisternal administration of transforming growth factor-β (TGF-β) for 7 days. Subchronic intracisternal administration of TGF-β significantly inhibited the increase in body weight of rats but did not affect food intake. In the measurement of locomotor activity after the final intracisternal administration on day 7, the total count for 1.5 h increased significantly in the TGF-β group compared with the vehicle group. However, that for 10 h was not different between both groups. Furthermore, significant elevations in oxygen consumption were observed in the TGF-β group during both light and dark phase. Subchronic TGF-β treatment induced a significant decrease in the number of total leukocytes and lymphocytes and the relative weight of the thymus, and a significant increase in brown adipose tissue weight. Corticotropin-releasing factor (CRF) is the primary neuroendocrine factor released in response to stress. Subchronic treatment with CRF, as a positive control, significantly affected body weight, food intake, oxygen consumption, total leukocyte and lymphocyte counts, and thymus and adrenal weight. Subchronic TGF-β administration partially mimicked the stress responses, implicating a role for TGF-β in the brain in stress.