Deficient Chow Research Articles

Effect of Vitamin D on YKL-40: Rat Hypercholesterolemia Model.

YKL-40 is considered to be associated with cardiovascular disease (CVD). In this study, the effect of serum 25(OH) vitamin D [25(OH)VitD] differences between groups on YKL-40 was evaluated on a hypercholesterolemia rat model. Thirty-two male rats (wistar albino) were equally divided into 4 groups. The first group was the control group; the second group was high-cholesterol (H-CH) adequate vitamin D (VitD) group (H-AdeVD). The third group was the H-CH deficient VitD group (H-DefVD), and the last group was designed with the H-CH supplement VitD (H-SupVD). The feeding process consisted of 2 stages. At the first stage (5 months), the H-DefVD group was fed on VitD deficient chow, while the other groups (control, H-AdeVD, H-SupVD) were fed on standard chow. At the second stage (3 months), the H-AdeVD and the H-SupVD groups were fed on the H-CH chow, whereas the H-DefVD group was fed on the H-CH-VitD deficient chow. Moreover, the H-SupVD group was given 100 IU/kg/day VitD along with the H-CH chow. Compared with the control group, interleukin-6 (IL-6), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), and YKL-40 values in the H-DefVD groups increased significantly (p<0.001, p<0.001, p=0.009, p=0.005; sequentially). It can be concluded that VitD can suppress the YKL-40, thus, it will prevent CVD development in rat. Therefore, further clinical studies related with human will reveal the effect of VitD and YKL-40 on CVD development.

Estimating in vivo potassium distribution and fluxes with stable potassium isotopes.

Extracellular potassium (K+) homeostasis is achieved by a concerted effort of multiple organs and tissues. A limitation in studies of K+ homeostasis is inadequate techniques to quantify K+ fluxes into and out of organs and tissues in vivo. The goal of the present study was to test the feasibility of a novel approach to estimate K+ distribution and fluxes in vivo using stable K+ isotopes. 41K was infused as KCl into rats consuming control or K+-deficient chow (n = 4 each), 41K-to-39K ratios in plasma and red blood cells (RBCs) were measured by inductively coupled plasma mass spectrometry, and results were subjected to compartmental modeling. The plasma 41K/39K increased during 41K infusion and decreased upon infusion cessation, without altering plasma total K+ concentration ([K+], i.e., 41K + 39K). The time course of changes was analyzed with a two-compartmental model of K+ distribution and elimination. Model parameters, representing transport into and out of the intracellular pool and renal excretion, were identified in each rat, accurately predicting decreased renal K+ excretion in rats fed K+-deficient vs. control diet (P < 0.05). To estimate rate constants of K+ transport into and out of RBCs, 41K/39K were subjected to a simple model, indicating no effects of the K+-deficient diet. The findings support the feasibility of the novel stable isotope approach to quantify K+ fluxes in vivo and sets a foundation for experimental protocols using more complex models to identify heterogeneous intracellular K+ pools and to answer questions pertaining to K+ homeostatic mechanisms in vivo.

Persistent Changes in Salt Intake by Estrogen‐Treated Rats after Repeated Episodes of Dietary Sodium Deficiency

AimsPrevious research from our lab and others demonstrated sex differences in sodium intake, though estrogen’s role in these differences is unclear. Further, previous studies analyzing salt intake with repeated episodes of sodium depletion using furosemide showed that stimulated salt intake was similar between males and females; however, there were clear sex differences in sodium intake after rats were no longer sodium depleted. We aimed to further elucidate the long‐term effects of estrogen on sodium intake using repeated episodes on a low salt diet, a more physiological challenge.MethodsOvariectomized rats were placed on two‐week periods of access to regular chow (NaR) or sodium deficient chow (NaD), which we alternated for a total of two exposures to each diet. Estrogen benzoate (EB) or oil injections were given twice weekly throughout the experiment. At the end of each diet period, rats were given a 2‐hour two bottle test (water and 0.5 M NaCl). At the end of the experiment, rats were sacrificed and trunk blood was collected and centrifuged to collect plasma. Plasma protein levels were measured. Uteri were collected and 1 cm segments of the uterine horns were weighed.ResultsWe confirmed the efficacy of EB treatment on body weight, uterine weight, and plasma proteins. As expected, EB‐treated rats maintained body weight throughout the experiment, with transient decreases, while oil‐treated rats gained weight. Both plasma proteins and uterine weights were greatly increased in EB‐treated compared to oil rats. During two‐bottle tests, both EB‐ and oil‐treated rats had similar baseline intakes of 0.5 M NaCl and water. When salt intake was stimulated by dietary sodium deficiency, both EB‐ and oil‐treated rats drank similarly increased amounts of 0.5 M NaCl. Interestingly, EB‐treated rats drank more 0.5 M NaCl and water than oil‐treated rats after returning to regular chow. The period of dietary sodium deficiency again elicited similar intakes of 0.5 M NaCl and water by EB‐ and oil‐treated rats.ConclusionsOur study demonstrated that estrogen did not alter induced salt intake induced by the physiological challenge, dietary sodium deficiency. However, the low salt diet led to persistent changes in behavior, as demonstrated by the continued consumption of salt and water by EB‐treated rats even after lost dietary sodium was replenished.

Maternal vitamin D deficiency programmes adult renal renin gene expression and renal function.

Renin is essential for renal development and in adult kidneys vitamin D deficiency increases renin gene expression. We aimed to determine whether maternal vitamin D deficiency upregulates fetal renal renin expression, and if this is sustained. We also examined growth and the long-term renal effects in offspring on a normal diet. Female Sprague-Dawley rats in UVB-free housing were fed either vitamin D deficient chow (DEF) or normal chow from 4 weeks and mated with vitamin D replete males at 10 weeks. Fetuses were collected at E20 or dams littered and the pups were weaned onto normal chow. Kidney mRNA levels for renin, (pro)renin receptor [(P)RR], transforming growth factor β 1 (TGF-β1), and nephrin were determined in E20 fetuses and in male offspring at 38 weeks. Renal function was assessed at 33 weeks (24 h, metabolic cage) in both sexes. Renal mRNA expression was upregulated for renin in fetuses (P < 0.05) and was almost doubled in adult male offspring from DEF dams (P < 0.05). Adult males had reduced creatinine clearance, solute excretion and a suppressed urinary sodium-to-potassium ratio (P < 0.05). Female adult DEF offspring drank more and excreted more urine (P < 0.05) but creatinine clearance was not impaired. We conclude that maternal vitamin D depletion upregulates fetal renal renin gene expression and this persists into adulthood where, in males only, there is evidence of sodium retention and compromised renal function. Importantly these effects occurred despite the animals being on a normal diet from the time of weaning onwards.

Activation of K-Ras in Arf-Null Mice Is Not Sufficient for Malignant Transformation of Post-Germinal Center B-Cells

Abstract 5016Activating mutations in Ras (N- and K-) are the most common mutations in multiple myeloma (MM), and are associated with advanced clinical stage and poor outcomes. As previously reported, we re-sequenced coding regions of highly expressed cytokine signaling candidate genes from MM patient samples and found the most common mutations to affect Ras oncogenes (N and K-). To test the role of Ras activation in MM pathogenesis directly, we generated mice harboring a mutant K-ras allele, Lox-stop-lox(LSL)- K-ras G12D (K-ras+/G12D) with Cγ1-Cre knock-in mice (Cγ1+/Cre), activated specifically in germinal center (GC) cells. K-ras+/+/Cγ1+/Cre mice served as negative controls. We found 58% of unstimulated K-ras+/G12D/Cγ1+/Cre mice developed fatal double-positive CD4/8 T-cell lymphomas (n=12) and 42% developed lung adenocarcinomas (n=12), phenotypes that have previously been reported for K-ras+/G12D mice. Tumor cells demonstrated successful recombination of the K-Ras locus. We showed recombination in splenic germinal center cells (B220+, GL7+ and IgG1+), as well as in post-germinal center cells (B220-, CD138+). No evidence of plasma cell proliferation was seen by serum ELISA, SPEP, flow cytometry or histological examination. We confirmed these results by crossing the K-ras+/G12D mice to a second strain, AID-Cre, which expresses the recombinase earlier and more specifically in the GC. We found 100% (n=20) of K-ras+/G12D/AID-Cre-YFP mice possessed visible, small benign papillomas on the ventral neck, as early as 3 weeks of age. To stimulate malignant transformation, vitamin D deficient chow and/or sub-lethal radiation was given to K-ras+/G12D/AID-Cre-YFP and negative control, K-ras+/G12D mice. Dual treatment increased the size and number of papillomas, giving a median survival of 26 weeks, compared to 52 weeks with control. However, no evidence of MM was detected by serum ELISA, SPEP, flow cytometry or histological examination. Finally, we generated AID-Cre-K-ras+/G12D triple transgenic mice in a tumor prone Arf-null background. After 13 wks, we found sarcomas in 66% (n=3) of K-ras+/G12D/AID-Cre-YFP/Arf−/− mice. Additionally, 100% (n=3) of these mice had rapid growing benign papillomas and only a minimal increase in the plasma cell compartment, compared to K-ras+/G12D/AID-Cre/Arf +/− control. Together, these data demonstrate that Ras activation is not sufficient to transform primary germinal center or plasma cells, even in an Arf-null context, and suggests that specific myeloma events, yet to be identified, are required for malignant transformation. Disclosures:No relevant conflicts of interest to declare.

Effects of K‐deficient diets ± Na supplementation on Na, K, and H2O transporters’ abundance along the nephron

Previous studies of K deficiency compared chow with 2% KCl, 0.74% NaCl (2K1Na ) to K deficient chow: 0.03% KCl, 0.74% NaCl (0K1Na ). We tested whether previously reported responses to 0K diet are due to low electrolytes, rather than hypokalemia. SD rats were fed 6 d with gelled diet prepared from powdered base adjusted to 2K1Na, 0K1Na, and with added NaCl: 2% KCl, 2% NaCl (2K2Na) and 0.03% KCl, 2% NaCl (0K2Na). Abundance was assessed by immunoblot of homogenates, densities normalized to mean of 2K groups.Results1) In both 0K groups, plasma K fell to 2.5 mM, urine K fell to &lt; 10 μmol/hr and outer medulla hypertrophied. 2) The only differences seen in both 0K groups are: ↓cortex ENaC and ↑medulla Na,K‐ATPase (NKA). 3) The following changed in 0K1Na but not 0K2Na: ↑cortex gastric H,K‐ATPase (HKA), ↑medulla NHE3, NHE3‐P and ↓AQP2. 4) In 0K2Na but not 0K1Na: cortex SPAK and OSR1 ↑ despite lowest plasma aldo in 0K2Na (172 pg/ml) vs. 0K1Na (413 pg/ml) and 2K2Na (417 pg/ml) and with no changes in NCC‐P or NKCC‐P.ConclusionsDespite profound hypokalemia and low urinary K, previously reported changes with 0K diets (↑NHE3, ↓NKCC, ↓NCC, ↓ROMK, ↑c‐Src, ↑HKA, ↓AQP2) were not observed; some may be secondary to low electrolytes. ↓ENaC can decrease driving force for K secretion, and ↑NKA is secondary to hypertrophy. Changes in transporter distribution and activity appear more important for conserving K than changes in abundance. DK0837854

Delayed alternation performance in rats following recovery from early iron deficiency

Early iron deficiency (ID) is one of the most common nutrient deficiencies in both developed and developing countries. This condition has been linked to perturbations in myelin formation, alterations of monoamine neurotransmitter systems particularly in the striatum, and deficits in energy metabolism particularly in the hippocampus (HP) and prefrontal cortex (PFC) in rats. Early ID has also been traced to long-term behavioral consequences in children in domains linked to these neuropathologies. The current experiment assesses formerly iron deficient (FID) adult rats on a delayed alternation (DA) task — a procedure thought to be sensitive to PFC dysfunction. Rat dams were started on an iron deficient chow at gestational day (G) 2 and maintained on this diet until postnatal day (P) 7; behavioral training began at P 65 when animals were iron replete. FID animals exhibited accelerated acquisition (p = 0.002) and fewer errors (p = 0.003) on the DA task compared to controls. These findings may reflect an imbalance between hippocampal and prefrontal modulation of this behavior most likely emanating from long-term hippocampal disinhibition by early ID that persists in spite of early iron treatment from P 7.

Post-ingestive signals and satiation of water and sodium intake of male rats

This study investigated the role of post-ingestive signals in the satiation of thirst or salt appetite. Post-ingestive signals, defined as those arising from the passage of fluid into the duodenum and proximal jejunum, were manipulated by implanting rats with gastric fistulas. After recovery, rats were water deprived and the following day gastric fistulas were opened (sham-drinking) or closed (control). Deprivation-induced thirst significantly increased water intake with sham-drinking rats consuming four-fold more than controls after 120 min access. Subsequently, rats were given sodium deficient chow for 48 h and the next day were administered furosemide and urine was collected. Twenty-four hours later, gastric fistulas were manipulated and rats were given water and 0.5 M NaCl and intakes were measured. After 120 min of access, rats were sacrificed and plasma sodium (pNa) and plasma-renin-activity (PRA) were measured. Furosemide resulted in a loss of 2.2 mEq of sodium in urine and sham-drinking rats consumed significantly more water and 0.5 M NaCl when compared to controls. At 120 min sham-drinking rats consumed 7.5 mEq of sodium nearly twice that of controls but had significantly lower pNa and significantly increased PRA. Interestingly, the ratio of water to 0.5 M NaCl intake was similar in both groups, with each making a mixture of ≈ 0.25 M NaCl. The results suggest that post-ingestive signals are necessary for the satiation of thirst and salt appetite.

Long-term impact of an antioxidant-deficient neonatal diet on lipid and glucose metabolism

Newborn infants are at risk for oxidative stress leading to metabolic syndrome features. Oxidative stress can be induced by oxidant load such as oxygen supplementation, peroxides from intravenous nutrition, or low antioxidant defenses. We hypothesize that a modulation of antioxidant defenses during the neonatal period, without external oxidant challenge, will have a long-term influence on energy metabolism. Guinea pigs were fed between their third and their seventh day of life a regular chow leading to “mature” antioxidant defenses or a deficient chow leading to lower antioxidant defenses. Between weeks 1 and 14, the animals were fed regular chow. The hepatic oxidized redox status of glutathione associated with the deficient diet (− 221 ± 2 vs − 228 ± 1 mV, p < 0.01) was maintained until 14 weeks. At 13–14 weeks, animals fed the deficient diet presented lower plasma TG (479 ± 57 vs 853 ± 32 μM, p < 0.01), lower blood glucose (5.8 ± 0.3 vs 6.9 ± 0.3 mM, p < 0.05), and better tolerance to glucose ( p < 0.05). Blood glucose correlated negatively with the redox status ( r 2 = 0.47, p < 0.01). Low antioxidant defenses during the neonatal period induce a better energy substrate profile associated with an oxidized redox status later in life. These findings suggest being aware of negative consequences when adopting “aggressive” antioxidant therapies in newborn infants.

Role of Defective High-Affinity Thiamine Transporter slc19a2 in Marrow from a Mouse Model of Thiamine-Responsive Anemia Syndrome: Evidence for Defective Deoxyribose and Heme Synthesis.

The rare autosomal recessive human disorder, TRMA syndrome (thiamine-responsive anemia with diabetes and deafness, OMIM 249270 ), is caused by mutations in the high affinity vitamin B1 transporter, SLC19A2. In human TRMA, ringed sideroblasts and megaloblastic changes are found in the marrow, suggesting potential defects in heme synthesis or mitochondrial function, and DNA synthesis, respectively. The mechanism whereby defective marrow thiamine transport causes these findings in the marrow was examined in a mouse model for TRMA. We previously demonstrated in fibroblasts from humans with TRMA a defect in the rate and pathway used for de novo ribose synthesis using Stable Isotope Dynamic Metabolic Profiling (SIDMaP analysis - Boros et al, Blood 102: 3556, 2003).To examine whether this fibroblast defect accurately defined the marrow pathophysiology, we have now examined this pathway in detail in mice defective for the orthologous slc19a2 gene by targeted gene disruption (Fleming et al, Mol Genet Metab 80:234, 2003). Slc19a2 mutant (−/−) or wildtype (+/+) mice were subjected to normal mouse chow (22 mg/kg thiamine), or thiamine deficient chow diet. Diets were confirmed thiamine deficient by chemical analysis. To examine heme biosynthesis, we used 55Fe-transferrin, ex vivo, to label marrow from +/+ or −/− mice maintained for 10 days in thiamine replete or deficient chow. Mutant mice had cell surface labeling indistinguishable from +/+ at 0°C (P>0.3), reflecting available transferrin receptors. Total cellular 55Fe uptake at 37 C was equal to or slightly greater than that of +/+ marrow in thiamine depleted state. However, incorporation of 55Fe into heme lagged in −/− cells (7.3 +/− 0.4 pmol/106cells/7 min) compared to +/+ (8.6 +/− 0.5 pmol/106 cells, P =0.018 in triplicate experiments). To examine deoxyribose (dRibose) synthesis, mice were maintained on thiamine replete or depleted chow for 10 days, then [1,2 13C] glucose was administered intraperitoneally overnight and 3 hours before sacrifice and marrow harvest. DNA from whole marrow and from sorted basophilic erythroblasts (CD71+/Ter119+) was isolated, hydrolized, derivatized, and dRibose analyzed by GC-MS. The initial rate of incorporation of 13C into DNA dRibose, reflecting de novo synthetic rate, was reduced 34% in basophilic erythroblasts of −/− mice after thiamine depletion (n=3 in duplicate experiments, P<0.001). dRibose enrichment at position C1 and C2 (m2) compared to C1 onl1 (m1) reflects synthesis via transketolase (thiamine dependent, non-oxidative, m2), vs G6PD (oxidative, non-thiamine dependent, m1). The m2/m1 ratio was 0.73 in +/+ cells, but only 0.36 in −/− erythroblasts, demonstrating defective non-oxidative branch of the pentose phosphate pathway. Thus, defective slc9a2 leads to two distinct erythropoietic defects. De novo DNA dRibose synthesis via transketolase is markedly impaired. Further, while iron uptake by marrow cells is maintained at normal levels, the heme biosynthetic rate is decreased in −/− mice in thiamine-depleted status. This is the first direct demonstration of a role for thiamine in normal erythrocyte heme and DNA metabolism. Together, these defects can account directly for the meglaoblastosis and sideroblasts of human SLC19A2 defects in TRMA.

Dopamine D2 receptor plays a role in memory function: implications of dopamine–acetylcholine interaction in the ventral hippocampus

The role of the hippocampal dopaminergic system in mnemonic function has not been clarified yet. We previously reported that the dopamine D2 receptor (D2R) is involved in the regulation of acethylcholin (ACh) release in the hippocampus. In this study, we further investigated ACh-dopamine (DA) interaction in the hippocampus and its involvement in mnemonic function. For experiment 1, rats fed with Cholin (Ch)-deficient chow were used. We examined the effects of D2R antagonist, raclopride, on cognitive performance using a passive avoidance task. We further carried out in vivo microdialysis to assess the effect of infusion of D2R agonist, quinpirole, into the ventral hippocampus on its capacity to release ACh. For experiment 2, rats fed with normal chow were used. The performance of a radial arm maze task was assessed to examine the effects of hippocampal injection of D2R agonist, quinpirole, on memory impairment induced by scopolamine, a muscarinic ACh antagonist. In experiment 1, rats fed with Ch-deficient chow showed impaired performances indicated by prolonged latency on retention trials of a passive avoidance task following the hippocampal injection of D2R antagonist, and showed reduced capacity to release ACh following the injection of D2R agonist compared with rats fed with normal chow. In experiment 2, memory impairment induced by the intraperitoneal injection of scopolamine was ameliorated by the injection of D2R agonist into the ventral hippocampus. These results indicate the possible involvement of hippocampal ACh-DA interaction in mnemonic processing.

Altered NaCl taste responses precede increased NaCl ingestion during Na + deprivation

It has been suggested that Na + deficiency alters the sensitivity of taste receptors, thereby rendering NaCl solutions more palatable or preferred and more likely to be ingested. Increased ingestion of concentrated NaCl solutions by rats during dietary Na + deprivation occurs only after approximately 8–10 days. To determine whether changes in gustatory responses mediate the deprivation-induced NaCl ingestion (salt appetite), we evaluated taste responses to a range of NaCl concentrations before, during, and after dietary Na + deprivation. Rats were trained to lick rapidly in short-duration (10 s) tests by mixing NaCl solutions in a dilute sucrose solution. This method elicited consistent, interpretable rates of licking, even of normally avoided NaCl concentrations, without the necessity of depriving the rats of water. The licking rate increased after dietary Na + deprivation of only 2 days, increased further after 5 days of Na + deprivation and, after 10 days, was not different from that after 2 days. These results suggest that a change in the response to NaCl taste, as evidenced by increased rates of licking during short-access tests, occurred after 2 days of dietary Na + deprivation. In contrast, a significant increase in the 24-h ingestion of a concentrated NaCl solution occurred only after approximately 1 week of maintenance on Na +-deficient chow. Thus, it is unlikely that a delayed change in the response to NaCl taste to more palatable or preferred underlies the delayed increase in 24-h NaCl intake during dietary Na + deprivation.

Temporal responses of oxidative vs. glycolytic skeletal muscles to K+ deprivation: Na+ pumps and cell cations.

When K+ output exceeds input, skeletal muscle releases intracellular fluid K+ to buffer the fall in extracellular fluid (ECF) K+. To investigate the mechanisms and muscle specificity of the K+ shift, rats were fed K+-deficient chow for 2-10 days, and two muscles at phenotypic extremes were studied: slow-twitch oxidative soleus and fast-twitch glycolytic white gastrocnemius (WG). After 2 days of low-K+ chow, plasma K+ concentration ([K+]) fell from 4.6 to 3.7 mM, and Na+-K+-ATPase alpha2 (not alpha1) protein levels in both muscles, measured by immunoblotting, decreased 36%. Cell [K+] decreased from 116 to 106 mM in soleus and insignificantly in WG, indicating that alpha2 can decrease before cell [K+]. After 5 days, there were further decreases in alpha2 (70%) and beta2 (22%) in WG, not in soleus, whereas cell [K+] decreased and cell [Na+] increased by 10 mM in both muscles. By 10 days, plasma [K+] fell to 2.9 mM, with further decreases in WG alpha2 (94%) and beta2 (70%); cell [K+] fell 19 mM in soleus and 24 mM in WG compared with the control, and cell [Na+] increased 9 mM in soleus and 15 mM in WG; total homogenate Na+-K+-ATPase activity decreased 19% in WG and insignificantly in soleus. Levels of alpha2, beta1, and beta2 mRNA were unchanged over 10 days. The ratios of alpha2 to alpha1 protein levels in both control muscles were found to be nearly 1 by using the relative changes in alpha-isoforms vs. beta1- (soleus) or beta2-isoforms (WG). We conclude that the patterns of regulation of Na+ pump isoforms in oxidative and glycolytic muscles during K+ deprivation mediated by posttranscriptional regulation of alpha2beta1 and alpha2beta2 are distinct and that decreases in alpha2-isoform pools can occur early enough in both muscles to account for the shift of K+ to the ECF.

Excitotoxic lesions of the parabrachial nuclei prevent conditioned taste aversions and sodium appetite in rats.

Electrolytic lesions of the parabrachial nuclei (PBN) disrupt conditioned taste aversion (CTA) in the rat, but it is not known whether this effect is due to damaging axons of passage or to destruction of intrinsic neurons. We tested 10 rats with electrophysiologically guided, ibotenic acid lesions of the PBN (PBNx) to determine whether they could acquire a LiCl-induced CTA to l-alanine (0.3 M) or demonstrate a sodium appetite following furosemide treatment and overnight access to sodium deficient chow. Vehicle-treated and nonsurgical controls were included in the design. PBNx rats failed to develop a CTA, even after 3 conditioning trials. Moreover, more than 8 months later, a subset of the PBNx rats were again unable to learn a CTA using NaCl as the conditional stimulus (CS). After the furosemide treatment, the control rats drank an average of 20.3 ml of strong salt in 24 hr. The PBNx rats drank virtually no NaCl during the first 2 hr and averaged only 4.0 ml in 24 hr. In the PBN, damage to neuronal somata is more critical than interrupting fibers of passage for producing deficits in taste-guided behaviors.

Survey of parasites of rhesus monkeys housed in small social groups.

AbstractA survey of specific parasites in fecal samples randomly collected from socially housed rhesus monkeys was done over a 1‐year period. Differences in frequency of samples with parasites, and number of different species per sample, were assessed by social group composition, social group size, female reproductive status, and season of the year. Common parasites were Entamoeba coli, Iodamoeba bütschlii, Balantidium coli, Strongyloides fülleborni, and Trichuris trichiura. Samples from juvenile/subadult groups had more species of potentially pathogenic parasites per sample but fewer species of nonpathogenic parasites per sample than samples from adult groups. When group size reached 12 to 16 animals, the number of samples with helminths doubled. Samples collected from groups with gestating/ lactating females had more species of nonpathogenic parasites than samples collected from groups with cycling or noncycling females. Fewer samples collected in the spring had helminths than samples collected during the fall, winter, and summer. The number of potentially pathogenic species present per sample was highest during the summer. Following anthelminthic treatment, the number of helminthic species present per sample and the number of samples with helminths remained low, then began increasing after 2 to 3 months. The number of potentially pathogenic species per sample decreased while animals were fed an inadvertently vitamin C deficient chow. © 1992 Wiley‐Liss, Inc.

Cosegregation analysis of salt appetite and blood pressure in genetically hypertensive and normotensive rats.

Enhanced sodium appetite is a robust behavioral characteristic of spontaneously hypertensive rats (SHR) which neither causes nor depends upon elevated blood pressure. However, the possibility remains that salt appetite and blood pressure are related by some unidentified common factor. The present study investigated the possible genetic co-determination of blood pressure and salt appetite in this animal model of hypertension. Blood pressure of SHR, Wistar/Kyoto (WKY), and their F1 and F2 populations was measured prior to salt appetite testing by the tail cuff method. Sodium intake in these groups was measured daily for 5 days as the ad lib consumption of a 1.5% NaCl solution by subjects maintained on sodium deficient chow and demineralized water. Dynamic and stable components of salt appetite were identified in the parent strains and analyzed in the hybrid offspring. The expected differences in blood pressure between SHR and WKY were observed, and the average blood pressure of the F1 and F2 groups fell roughly midway between SHR and WKY values. The SHR consumed substantially greater quantities of saline than WKY, but the F1 population consumed saline at a rate that was not different from WKY, rather than intermediate between SHR and WKY. There was no relationship in the F2 population between blood pressure and any measure of salt appetite. Thus, the high salt appetite and high blood pressure traits of SHR do not appear to share a common genetic basis. These results, considered with previously published work, suggest that approach and avoidance aspects of salt appetite may be separately inherited and also strongly suggest that neither is linked to hypertension.

Sodium consumption following lesions surrounding the anteroventral third ventricle

Consumption of sodium solution was measured in rats with lesions of the anteroventral third ventricle (AV3V) and maintained on sodium deficient chow. Rats with AV3V lesions consumed less sodium than control animals, and increased their sodium consumption following a subcutaneous injection of Formalin. These data indicate that the AV3V ablation alters the nature of the regulatory control of sodium but does not render animals insensitive to plasma sodium levels.