scholarly journals Gastroparesis and lipid metabolism-associated dysbiosis in Wistar-Kyoto rats

2017 ◽  
Vol 313 (1) ◽  
pp. G62-G72 ◽  
Author(s):  
J. E. Dalziel ◽  
Karl Fraser ◽  
Wayne Young ◽  
Catherine M. McKenzie ◽  
Shalome A. Bassett ◽  
...  
Keyword(s):  
Small Intestine ◽  
Liquid Chromatography ◽  
Gastric Emptying ◽  
Delayed Gastric Emptying ◽  
Wky Rats ◽  
Sd Rats ◽  
Wistar Kyoto Rat ◽  
Rat Strain ◽  
Gi Transit ◽  
Wistar Kyoto

Altered gastric accommodation and intestinal morphology suggest impaired gastrointestinal (GI) transit may occur in the Wistar-Kyoto (WKY) rat strain, as common in stress-associated functional GI disorders. Because changes in GI transit can alter microbiota composition, we investigated whether these are altered in WKY rats compared with the resilient Sprague-Dawley (SD) rats under basal conditions and characterized plasma lipid and metabolite differences. Bead transit was tracked by X-ray imaging to monitor gastric emptying (4 h), small intestine (SI) transit (9 h), and large intestine transit (12 h). Plasma extracts were analyzed by lipid and hydrophilic interaction liquid chromatography (HILIC) and liquid chromatography-mass spectrometry (LC-MS). Cecal microbial composition was determined by Illumina MiSeq 16S rRNA amplicon sequencing and analysis using the QIIME pipeline. Stomach retention of beads was 77% for WKY compared with 35% for SD rats. GI transit was decreased by 34% (9 h) and 21% (12 h) in WKY compared with SD rats. Excluding stomach retention, transiting beads moved 29% further along the SI over 4–9 h for WKY compared with SD rats. Cecal Ruminococcus, Roseburia, and unclassified Lachnospiraceae genera were less abundant in WKY rats, whereas the minor taxa Dorea, Turicibacter, and Lactobacillus were higher. Diglycerides, triglycerides, phosphatidyl-ethanolamines, and phosphatidylserine were lower in WKY rats, whereas cholesterol esters and taurocholic acids were higher. The unexpected WKY rat phenotype of delayed gastric emptying, yet rapid SI transit, was associated with altered lipid and metabolite profiles. The delayed gastric emptying of the WKY phenotype suggests this rat strain may be useful as a model for gastroparesis. NEW & NOTEWORTHY This study reveals that the stress-prone Wistar-Kyoto rat strain has a baseline physiology of gastroparesis and rapid small intestine transit, together with metabolic changes consistent with lipid metabolism-associated dysbiosis, compared with nonstress-prone rats. This suggests that the Wistar-Kyoto rat strain may be an appropriate animal model for gastroparesis. View this article's corresponding video summary at https://youtu.be/BeI39Jh2BLk .

scholarly journals Exacerbated LPS/GalN-Induced Liver Injury in the Stress-Sensitive Wistar Kyoto Rat Is Associated with Changes in the Endocannabinoid System

Molecules ◽  
2020 ◽  
Vol 25 (17) ◽  
pp. 3834
Author(s):  
Marykate Killilea ◽  
Daniel M. Kerr ◽  
Beth M. Mallard ◽  
Michelle Roche ◽  
Antony M. Wheatley
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Endocannabinoid System ◽  
Hepatic Function ◽  
Receptor Expression ◽  
Sprague Dawley ◽  
Wky Rats ◽  
Sd Rats ◽  
Rat Strain ◽  
Wistar Kyoto

Acute liver injury (ALI) is a highly destructive and potentially life-threatening condition, exacerbated by physical and psychological stress. The endocannabinoid system plays a key role in modulating stress and hepatic function. The aim of this study was to examine the development of acute liver injury in the genetically susceptible stress-sensitive Wistar-Kyoto (WKY) rat compared with normo-stress-sensitive Sprague Dawley (SD) rats, and associated changes in the endocannabinoid system. Administration of the hepatotoxin lipopolysaccharide/D-Galactosamine (LPS/GalN) resulted in marked liver injury in WKY, but not SD rats, with increased alanine aminotransferase (ALT), aspartate aminotransferase (AST) and glutamate dehydrogenase (GLDH) plasma levels, significant histopathological changes, increased hepatic pro-inflammatory cytokine expression and caspase-3 activity and expression and reduced Glutathione (GSH) activity. Furthermore, compared to SD controls, WKY rats display increased anandamide and 2-Arachidonoylglycerol levels concurrent with decreased expression of their metabolic enzymes and a decrease in cannabinoid (CB)1 receptor expression following LPS/GalN. CB1 antagonism with AM6545 or CB2 agonism with JWH133 did not alter LPS/GalN-induced liver injury in SD or WKY rats. These findings demonstrate exacerbation of acute liver injury induced by LPS/GalN in a stress-sensitive rat strain, with effects associated with alterations in the hepatic endocannabinoid system. Further studies are required to determine if the endocannabinoid system mediates or modulates the exacerbation of liver injury in this stress-sensitive rat strain.

Distribution of kallikrein-binding protein mRNA in kidneys and difference between SHR and WKY rats

1994 ◽  
Vol 267 (2) ◽  
pp. F325-F330 ◽  
Author(s):  
T. Yang ◽  
Y. Terada ◽  
H. Nonoguchi ◽  
M. Tsujino ◽  
K. Tomita ◽  
...  
Keyword(s):  
Blot Analysis ◽  
Binding Protein ◽  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Sd Rats ◽  
Medullary Collecting Duct ◽  
Wistar Kyoto

We investigated kallikrein-binding protein (KBP) mRNA distribution in the kidney of Sprague-Dawley (SD) rats, spontaneously hypertensive rats (SHR), and Wistar-Kyoto strain (WKY) rats. Northern blot analysis revealed that KBP mRNA was located mainly in the medulla and with lower amounts in SHR than in WKY rats. KBP mRNA in microdissected nephron segments was detected by reverse transcription and polymerase chain reaction (RT-PCR) followed by Southern blot analysis. In SD rats, the most abundant signals were consistently found in inner medullary collecting duct (IMCD), with small amounts in outer medullary collecting duct, proximal convoluted tubule, and glomerulus. No signals were found in connecting tubule and cortical collecting duct. The nephron distribution of KBP mRNA was similar in WKY and SD rats. Only a small amount of signal was found, however, in IMCD of SHR. In conclusion, 1) KBP mRNA was predominantly distributed in the medullary segments of the distal nephron, downstream from the known kallikrein activity site in the collecting duct, and 2) KBP mRNA expression was significantly decreased in the kidney of SHR.

scholarly journals Differential visceral nociceptive, behavioural and neurochemical responses to an immune challenge in the stress-sensitive Wistar Kyoto rat strain

2013 ◽  
Vol 253 ◽  
pp. 310-317 ◽  
Author(s):  
Siobhain M. O’ Mahony ◽  
Gerard Clarke ◽  
Declan P. McKernan ◽  
Javier A. Bravo ◽  
Timothy G. Dinan ◽  
...  
Keyword(s):  
Immune Challenge ◽  
Wistar Kyoto Rat ◽  
Rat Strain ◽  
Wistar Kyoto

Endorphinergic mechanism in the central cardiovascular and analgesic effects of clonidine

1987 ◽  
Vol 65 (8) ◽  
pp. 1624-1632 ◽  
Author(s):  
G. Kunos ◽  
R. Mosqueda-Garcia ◽  
J. A. Mastrianni ◽  
F. V. Abbott
Keyword(s):  
Receptor Antagonist ◽  
Arcuate Nucleus ◽  
Monosodium Glutamate ◽  
Opiate Receptors ◽  
Cardiovascular Effects ◽  
Male Rats ◽  
Sprague Dawley ◽  
Wky Rats ◽  
Sd Rats ◽  
Wistar Kyoto

In urethane-anesthetized male rats, injection of 5 nmol clonidine into the nucleus of the solitary tract (NTS) causes hypotension and bradycardia. These effects are greater in spontaneously hypertensive rats (SHR) and normotensive Sprague–Dawley (SD) rats than in normotensive Wistar–Kyoto (WKY) rats. The effects of clonidine are stereoselectively inhibited by 100 ng intra-NTS naloxone in SHR and SD but not in WKY rats. In SHR, the effects of clonidine are also inhibited by intra-NTS administration of ICI 174864 (a δ-receptor antagonist) but not by β-funaltrexamine (a μ-receptor antagonist), while in SD rats only the μ- and not the δ-antagonist was effective. Neonatal treatment of SHR with monosodium glutamate (MSG) reduced the β-endorphin content of the arcuate nucleus and the NTS, reduced the cardiovascular effects of clonidine, and abolished their naloxone sensitivity. MSG treatment of newborn WKY reduced the β-endorphin content of the arcuate nucleus but not the NTS and did not affect the responses to clonidine. Measurement of pain sensitivity by the formalin test indicated that clonidine was more potent as an analgesic in SHR and SD than in WKY rats, and its effect was inhibited by naloxone (2 mg/kg i.p.) in the former two strains but not in WKY. It is proposed that a naloxone-sensitive component of the cardiovascular effects of clonidine is due to release of a β-endorphin-like opioid from the NTS, and that this mechanism is present in SHR and SD but not in WKY rats. The opiate receptors mediating the effects of the opioid appear to be of the μ-subtype in SD rats and of the δ-subtype in SHR. The results also support a close relationship between central cardiovascular and pain regulatory mechanisms.

scholarly journals Epigastric Fullness

2000 ◽  
Vol 14 (suppl d) ◽  
pp. 141D-144D
Author(s):  
Georg Stacher
Keyword(s):  
Small Intestine ◽  
Targeted Therapy ◽  
Gastric Emptying ◽  
Motor Function ◽  
Delayed Gastric Emptying ◽  
Benign Disease ◽  
Clinical Impression ◽  
Proximal Small Intestine ◽  
Gastric Motor Function ◽  
Underlying Disorder

Epigastric fullness may be caused by a disordered gastric motor function, resulting in delayed gastric emptying, but may also be caused by rapid emptying, leading to a distention of the proximal small intestine. A rational diagnostic approach to a patient complaining of epigastric fullness is needed to reveal the underlying disorder or disease and to enable an adequate, targeted therapy. The clinical impression based on symptoms is unreliable and cannot distinguish function disorders and benign disease from severe conditions.

Temperature regulation in biotelemetered spontaneously hypertensive rats

1990 ◽  
Vol 258 (4) ◽  
pp. R1064-R1069 ◽  
Author(s):  
R. M. Morley ◽  
C. A. Conn ◽  
M. J. Kluger ◽  
A. J. Vander
Keyword(s):  
Open Field ◽  
Core Temperature ◽  
Acute Stress ◽  
Spontaneously Hypertensive Rat ◽  
Temperature Response ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto Rat ◽  
Wistar Kyoto ◽  
Stressful Environments

Core temperature of the spontaneously hypertensive rat (SHR) was not found to be different from the core temperature of the control rat, the Wistar-Kyoto rat (WKY), when the rats were left undisturbed in their home cages. When the rats were exposed to a variety of stressful environments, including cage switching, exposure to an open field, and handling, both SHR and WKY rats showed an increase in temperature. For the set of rats supplied by Charles River, the SHR temperature response to the stress was identical to the WKY rats' temperature response. For the set of rats supplied by Taconic Farms, the SHR was found to have a greater temperature response to the acute stress and the open-field stress. The Taconic Farms rats were also exposed to restraint stress, which resulted in a rise in temperature that was greater for the SHR when compared with the WKY. Because we have observed the increased lability in body temperature of the SHR compared with the WKY rats during restraint, we believe that it is important that studies with these strains of rat be done using minimal or no restraint.

Inbreeding of Wistar–Kyoto rat strain with hyperactivity but without hypertension

1986 ◽  
Vol 45 (1) ◽  
pp. 1-16 ◽  
Author(s):  
Edith D. Hendley ◽  
Diane J. Wessel ◽  
Judith Van Houten
Keyword(s):  
Wistar Kyoto Rat ◽  
Rat Strain ◽  
Wistar Kyoto

Transport of calcium by duodenum of spontaneously hypertensive rat

1981 ◽  
Vol 241 (4) ◽  
pp. G344-G347 ◽  
Author(s):  
M. A. Toraason ◽  
G. L. Wright
Keyword(s):  
Calcium Transport ◽  
Spontaneously Hypertensive Rat ◽  
Detectable Effect ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Before And After ◽  
Rat Strain ◽  
Wistar Kyoto

The absorption of calcium by segments of duodenum obtained from spontaneously hypertensive (SH) rats and normotensive Wistar-Kyoto (WKy) rats was measured before and after the development of hypertension. The systolic blood pressure (SBP) of 5-wk-old SH rats (116 +/- 4 Torr) was significantly elevated above that of age-matched WKy rats (103 +/- 3 Torr) but was not at a level generally considered to be hypertensive. Values obtained for calcium transport [ratio of serosal-to-mucosal fluid 45Ca2+ concn (S/M ratio)] from everted duodenal sacs were similar between the two groups at this age. At 12 wk of age, SH rats exhibited a SBP (153 +/- 4 Torr) well above that of WKy controls (127 +/- 3 Torr), and calcium S/M ratios for duodenal sacs were significantly greater than the WKy control values. Similarly, the in vivo uptake of calcium in duodenal segments was significantly elevated in 12-wk-old SH rats compared with WKy controls. The administration of vitamin D3 or its metabolite, 25-hydroxycholecalciferol, had no detectable effect on duodenal transport of calcium in 12-wk-old SH or WKy rats. By comparison, 1,25-dihydroxycholecalciferol produced a significant increase in duodenal calcium transport both in vitro and in vivo in WKy but not in SH rats. The results indicate a distinct abnormality in the transport of calcium in the duodenum of SH rats, suggesting that the decrease in duodenal uptake of calcium that normally occurs with maturation is slow to develop in this rat strain.

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