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Metabolic Cages (metabolic + cage)
Selected AbstractsChronic acid ingestion promotes renal stone formation in rats treated with vitamin D3INTERNATIONAL JOURNAL OF UROLOGY, Issue 1 2007Naohiko Okamoto Objective: Although hypercalciuria, a well-established adverse effect of vitamin D3, can be a risk factor of renal stone formation, the risk of nephrolithiasis has not been well defined. The consumption of a diet high in acid precursors is often cited as a risk factor for the development of calcium-based kidney stones. In the present study, we investigated the effect of chronic acid ingestion on kidney stone formation in rats treated with calcitriol (1,25[OH]2 D3). Methods: Control rats (C-C), calcitriol-treated rats (C-V; three treatments of 0.5 µg of calcitriol per week) and acid-ingested (water containing 0.21 mol/L NH4Cl), calcitriol-treated (three treatments of 0.5 µg of calcitriol per week) rats (A-V) were fed in metabolic cages. After 1 month, urine, blood, kidney and bone samples were analyzed. Results: The A-V rats exhibited elevated serum calcium concentrations, urinary calcium and phosphate excretion, urinary type I collagen cross-linked N-peptide (NTx)/creatinine values, mRNA expression of osteopontin in the kidney, and renal calcium contents as well as decreased bone mineral densities, compared with the C-C and C-V rats. Urinary citrate excretion was lower and NaDC-1 mRNA expression in the kidney was higher in the A-V rats than in the C-C and C-V rats. Calcium phosphate kidney stones were found in the A-V rats. Conclusions: The ingestion of NH4Cl, an acid precursor, promotes calcium phosphate kidney stone formation in calcitriol-treated rats. The chronic intake of a diet rich in acid precursors may be a risk factor for the development of kidney stones in subjects who are being treated with calcitriol. [source] Genetic Hypercalciuric Stone-Forming Rats Have a Primary Decrease in BMD and Strength,,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 8 2009Marc Grynpas Abstract Kidney stone patients often have a decrease in BMD. It is unclear if reduced BMD is caused by a primary disorder of bone or dietary factors. To study the independent effects of hypercalciuria on bone, we used genetic hypercalciuric stone-forming (GHS) rats. GHS and control (Ctl) rats were fed a low Ca (0.02% Ca, LCD) or a high Ca (1.2% Ca, HCD) diet for 6 wk in metabolic cages. All comparisons are to Ctl rats. Urine Ca was greater in the GHS rats on both diets. GHS fed HCD had reduced cortical (humerus) and trabecular (L1,L5 vertebrae) BMD, whereas GHS rats fed LCD had a reduction in BMD similar to Ctl. GHS rats fed HCD had a decrease in trabecular volume and thickness, whereas LCD led to a ,20-fold increase in both osteoid surface and volume. GHS rats fed HCD had no change in vertebral strength (failure stress), ductibility (failure strain), stiffness (modulus), or toughness, whereas in the humerus, there was reduced ductibility and toughness and an increase in modulus, indicating that the defect in mechanical properties is mainly manifested in cortical, rather than trabecular, bone. GHS rat cortical bone is more mineralized than trabecular bone and LCD led to a decrease in the mineralization profile. Thus, the GHS rats, fed an ample Ca diet, have reduced BMD with reduced trabecular volume, mineralized volume, and thickness, and their bones are more brittle and fracture prone, indicating that GHS rats have an intrinsic disorder of bone that is not secondary to diet. [source] Paradoxical Sleep Deprivation and Sleep Recovery: Effects on the Hypothalamic,Pituitary,Adrenal Axis Activity, Energy Balance and Body Composition of RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2006D. C. Hipólide Abstract Numerous studies indicate that sleep deprivation alters energy expenditure. However, this conclusion is drawn from indirect measurements. In the present study, we investigated alterations of energy expenditure, body composition, blood glucose levels, plasma insulin, adrenocorticotropic hormone (ACTH) and corticosterone levels immediately after 4 days of sleep deprivation or after 4 days of sleep recovery. Rats were sleep deprived or maintained in a control environment (groups sleep-deprived/deprivation and control/deprivation). One half of these animals were sacrificed at the end of the deprivation period and the other half was transported to metabolic cages, where they were allowed to sleep freely (groups sleep-deprived/recovery and control/recovery). At the end of the sleep recovery period, these rats were sacrificed. After sleep deprivation, sleep-deprived rats exhibited loss of body weight, augmented energy expenditure and reduced metabolic efficiency compared to control rats. These alterations were normalised during the sleep recovery period. The body composition of sleep-deprived rats was altered insofar as there was a loss of fat content and gain of protein content in the carcass compared to control rats. However, these alterations were not reversed by sleep recovery. Finally, plasma levels of insulin were reduced during the sleep deprivation period in both control and sleep deprived groups compared to the recovery period. After the deprivation period, plasma ACTH and corticosterone levels were increased in sleep-deprived rats compared to control rats, and although ACTH levels were similar between the groups after the sleep recovery period, corticosterone levels remained elevated in sleep-deprived rats after this period. By means of direct measurements of metabolism, our results showed that sleep deprivation produces increased energy expenditure and loss of fat content. Most of the alterations were reversed by sleep recovery, except for corticosterone levels and body composition. [source] Lipid signaling changes in smooth muscle remodeling associated with partial urinary bladder outlet obstructionNEUROUROLOGY AND URODYNAMICS, Issue 2 2006Edward LaBelle Abstract Aims Hypertrophy of the urinary bladder smooth muscle (detrusor) is associated with partial bladder outlet obstruction (PBOO). Hypertrophied detrusor smooth muscle (DSM) reveals altered contractile characteristics. In this study, we analyzed the lipid-dependent signaling system that includes phospholipase A2 in PBOO-induced DSM remodeling and hypertrophy to determine whether the release of arachidonic acid (AA) from phospholipid is altered in the detrusor. Methods Partial bladder outlet obstruction (PBOO) was produced by partial ligation of the urethra in New Zealand white rabbits. Two weeks after the surgery, the bladder function was studied by keeping the rabbits in metabolic cages for 24 hr. Bladders were removed from rabbits that had bladder dysfunction (increased urinary frequency and decreased void volume) and the DSM separated from mucosa and serosa. The isolated smooth muscle was incubated with [3H] AA to equilibrate the cytoplasmic AA. The level of AA release was compared with the level obtained with 2-week sham-operated rabbits. Results The rate of AA release was high in DSM from bladders with PBOO-induced hypertrophy. Carbachol stimulated AA release in control DSM but DSM from obstructed rabbits revealed no further increase from the elevated basal AA release. The half-maximal concentration of carbachol that was required to stimulate AA release from control samples of detrusor was 35 µM. Conclusions The increased levels of AA release that are observed in this tissue after PBOO indicate the activation of phospholipase A2. The finding that carbachol could induce contraction, but not an increase in AA, indicates that the carbachol-induced contraction in the obstructed bladders is independent of lipid signaling pathways that involve AA. It is possible that the increased rate of arachidonic acid release from obstructed bladders correlates with the enhanced rates of prostaglandin production reported by other investigators from the same tissue. Neurourol. Urodynam. © 2006 Wiley-Liss, Inc. [source] Effects of high potassium chloride supplementation on water intake, urine volume and nitrogen balance in miceANIMAL SCIENCE JOURNAL, Issue 1 2010Iori MURAI ABSTRACT Sixteen ICR male mice were assigned to a control diet group or a KCl diet group in metabolic cages to clarify the effects of KCl supplementation on water intake, urine volume and N balance, and 5% of KCl was supplemented in KCl diets for 4 or 8 weeks. Bodyweight of KCl supplemented mice was significantly higher than that of control mice from 24 to 28 days after treatment. Feed intake, water intake and urine volume of KCl supplemented mice were significantly higher than those of control mice, and the increased water intake and urine volume in KCl supplemented mice were 4.49 and 4.15 g, respectively. Urinary N, K and Cl excretion were significantly higher in KCl supplemented mice. Although N retention was not significantly different between control and KCl supplemented mice, N retention in KCl supplemented mice tended to be lower. Serum creatinine concentration at 8 weeks after treatment was lower in KCl supplemented mice. Histological alteration using hematoxylin-eosin and Sirius red staining was not found in the kidney of each mouse at 4 and 8 weeks after treatment. These results suggest that high KCl supplementation increases water intake, urine volume and urinary N excretion in mice. [source] Immunosuppression with mycophenolate mofetil attenuates the development of hypertension and albuminuria in deoxycorticosterone acetate-salt hypertensive ratsCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2010Erika I Boesen Summary 1. The interplay between the immune and renin,angiotensin systems is emerging as a crucial factor in the development and progression of hypertension. The aim of the present study was to determine the involvement of immune cells in the hypertension and renal injury produced by a non-angiotensin II-dependent form of hypertension, namely deoxycorticosterone acetate (DOCA)-salt-induced hypertension, in rats. 2. Male Sprague-Dawley rats underwent uninephrectomy and received either a sustained-release pellet of DOCA s.c. and 0.9% NaCl (saline) to drink for 21 days or a placebo pellet and water to drink for 21 days. Additional groups of DOCA-salt- and placebo-treated rats were treated concurrently with the immune suppressant mycophenolate mofetil (MMF; 30 mg/kg per day). Rats were placed in metabolic cages for 24 h urine collection prior to and at weekly intervals during the 21 day experimental period. 3. Mycophenolate mofetil significantly attenuated the development of hypertension in DOCA-salt rats compared with untreated DOCA-salt hypertensive rats (mean arterial pressure by telemetry on Day 18 146 ± 7 vs 180 ± 3 mmHg, respectively; P < 0.001), as well as proteinuria (87 ± 27 vs 305 ± 63 mg/day, respectively, on Day 21) and albuminuria (51 ± 15 vs 247 ± 73 mg/day, respectively, on Day 21). Creatinine clearance was better preserved in MMF-treated DOCA-salt rats compared with untreated DOCA-salt rats (0.74 ± 0.07 vs 0.49 ± 0.09 mL/min, respectively; P < 0.05), but was still significantly reduced compared with that in the placebo group (1.15 ± 0.12 mL/min; P < 0.05). Finally, MMF treatment significantly attenuated the DOCA-salt-induced rise in renal cortical T-lymphocyte and macrophage infiltration (P < 0.05). 4. These data indicate that immune cells play a deleterious role in both the hypertension and renal injury associated with DOCA-salt hypertension. [source] Folic acid supplementation on red kidney bean-induced diarrhoea and enteric bacterial translocation into mesenteric lymph nodes in rats: a pilot studyACTA PAEDIATRICA, Issue 1 2002R Shoda Deaths following childhood diarrhoea, a major health problem in developing countries, are often associated with malnutrition and septicaemic complications. Folic acid has been used in the treatment of acute and chronic diarrhoea in the tropics. Using a rat model, we evaluated the protective effect of large doses of folic acid on diarrhoea, small intestinal bacterial overgrowth and translocation of enteric bacteria into mesenteric lymph nodes induced by a raw red kidney bean-based diet containing lectin (phytohemagglutinin). Long-Evans rats in 2 groups of 5 each (60 g to 70 g in weight, 28 d old) were used. All 10 rats, individually kept in metabolic cages, received a raw red kidney bean-based diet for 10 d, and 5 of them also received a daily folic acid supplement (160 ,g/g feed) both during and for 10 d before the experiment. The faecal weight was measured and a quantitative aerobic bacterial culture of the small intestinal mucosal scrapings and of the mesenteric lymph nodes was made. Folic acid supplementation did not reduce faecal output nor did it prevent loss of body weight associated with lectin-induced diarrhoea. However, the mean total count of enteric bacteria translocated to the mesenteric lymph nodes was significantly reduced in the supplemented rats (1.27 ± 0.61 vs 2.66 ± 0.84, p= 0.028) and a trend towards reduced bacterial count in the small intestinal mucosal scrapings (0.40 ± 0.89 vs 1.42 ± 1.31, p= 0.16) was documented. A significant positive correlation was also seen between the bacterial count in the jejunal mucosal scrapings and in the mesenteric lymph nodes. Conclusion: Although large-dose folic acid supplementation did not prevent diarrhoea and malnutrition induced by a lectin-based diet, it substantially reduced the count of enteric bacteria translocated into the mesenteric lymph nodes and showed a trend towards a reduction in indigenous bacteria adhering to jejunal mucosa. These findings could be of relevance in the prevention of septicaemic complications following many clinical conditions, including diarrhoea with malnutrition in children known to have bacteraemic and septicaemic complications. [source] | ||||||||||