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Separate assessment of intestinal and hepatic first-pass effects using a rat model with double cannulation of the portal and jugular veins.

To separately assess intestinal and hepatic first-pass effects with absorption ratio data, we have established an experimental model of rats double-cannulated into the portal and jugular veins. The model allows us to take blood samples simultaneously from conscious rats that have recovered from surgical damage. Double cannulation did not alter the physiological and hematological conditions. Moreover, the plasma concentration profiles of unchanged drug following oral and intravenous administration in the double-cannulated rats were not different from those of rats single-cannulated into the jugular vein. These results suggest that the model can be useful for separately assessing intestinal and hepatic first-pass effects. We evaluated the first-pass effects in the intestine and the liver separately using this model. S-1452, as a model drug with 94% absorption ratio, was administered intravenously and orally to the double-cannulated rats, and the drug concentrations in the portal and systemic plasma were determined, and the rates of elimination from the intestine and liver were estimated. In the first pass, approximately 26% and 56% of the dose were extracted by the intestine and liver, respectively. This method, in which the animal is not restricted nor under anesthesia, allows us to obtain reliable values of individual first pass effects in the intestine and liver. This method can also be an effective tool for assessing the site and extent of drug-drug interaction on the first-pass effects.

Journal Article↗

[Effect of GETO on expression of protein in postsynaptic dense zone of Alzheimer's disease model rats].

OBJECTIVE: To observe the effect of GETO on expression of PSD-95 and Shank-1 protein in postsynaptic dense zone in Alzheimer disease (AD) model rats. METHODS: The AD model rats were established by beta-amyloid protein (Abeta(1-42)) injection into hippocampus CA1 zone. They were assigned into the model group, the donepezil treated group and the GETO treated group, besides, a normal group was set for control. Four weeks after modeling, Morris water maze test was applied to determine the learning and memory function of the AD rats, the number of PSD-95 and Shank-1 protein positive neuron as well as the optical density (OD) in post-synaptic dense zone of hippocampus CA1 area were determined by using immuno-histochemical stain and computerized graphic analysis techniques. RESULTS: Morris water maze test showed that the mean escape latent period (MELP) of the model rats obviously prolonged than that of the normal rats, and the times of traversing flat roof obviously decreased (P < 0.01), while in the model rats after being treated by GETO, the two parameters were significantly shortened and increased respectively (P < 0.01), reaching the level insignificantly different to those in the donepezil group and the normal group. Immunohistochemical test showed that the number of positive stained neuron of PSD-95 and Shank-1 in hippocampus CA1 zone in the model group was significantly different to those in the normal group (P < 0.01), while in the GETO group those indexes were insignificantly different to those in the donepezil group and the normal group (P > 0.05), but showed a significant difference when compared with those in the model group (P < 0.05). CONCLUSION: GETO can obviously improve the function of learning and memory of AD rats induced by Abeta(1-42), and the mechanism may be associated with its actions in improving expressions of PSD-95 and Shank-1 protein in hippocampus CA1 zone, and recovering the structure and function of synapse and enhancing its plasticity.

Adaptor Proteins, Signal Transducing↗

High-fat emulsion-induced rat model of nonalcoholic steatohepatitis.

Non-alcoholic fatty liver disease (NAFLD) is emerging as a common medical problem. Nonalcoholic steatohepatitis (NASH) is the critical turning point at which NAFLD progresses to more advanced stages such as hepatic fibrosis, cirrhosis and even hepatocellular carcinoma. However, the study of the pathogenic or therapeutic factors involved in NASH has been hampered by the absence of a suitable experimental model. The aim of the present work was to establish a high-fat emulsion-induced rat model of NASH. Male Sprague-Dawley rats were fed a high-fat emulsion via gavage for 6 weeks. Animals were examined for weight gain, serum and hepatic biochemistry, insulin sensitivity, hepatic malondialdehyde (MDA), superoxide dismutase (SOD) and tissue morphology, as well as cytochrome P-450 2E1 (CYP2E1) and peroxisome proliferator-activated receptor alpha (PPARalpha) expression in the liver. The results showed that rats treated with high-fat emulsion became obese, demonstrated abnormal aminotransferase activity, hyperlipoidemia, hyperinsulinemia, hyperglycemia and insulin resistance. The model rats exhibited an increased concentration of serum TNF-alpha, total cholesterol (TC), triglyceride (TG), MDA and reduced SOD levels in the liver. Immunoblot analysis showed that the expression of CYP2E1 was increased, whereas PPARalpha was reduced in the NASH model rat liver. Moreover, morphological evaluation revealed that hepatic steatosis, inflammation and mitochondrial lesions were also reproduced in this model. In conclusion, a practical and repeatable new rat model of steatohepatitis was established by feeding with high-fat emulsion via gavage. This model provides a valuable research tool and reproduces many of the clinical indices of human NASH.

Animals↗

Effect of cirrhosis on antibiotic efficacy in a rat model of pneumococcal pneumonia.

A rat model was used to study the effects of cirrhosis on antibiotic therapy of pneumococcal pneumonia. Cirrhotic and control male Sprague-Dawley rats were infected transtracheally with type 3 Streptococcus pneumoniae. Treatment began 18 h later with phosphate-buffered saline (PBS), azithromycin (50 mg/kg), trovafloxacin (50 mg/kg), or ceftriaxone (100 mg/kg) injected subcutaneously twice daily for 5 days. Antibiotic concentrations were measured by high-performance liquid chromatography. Azithromycin, trovafloxacin, and ceftriaxone were all equally effective at preventing mortality in both cirrhotic and normal rats. Free fraction area under the curve to minimum inhibitory concentration ratio (AUC/MIC) and maximum calculated serum concentration to MIC ratio (C(max)/MIC) and percent time that the serum concentration exceeded the MIC (%T > MIC) were greater for ceftriaxone compared with azithromycin or trovafloxacin. Azithromycin achieved higher concentrations in bronchoalveolar lavage fluid (BALF), epithelial lining fluid (ELF), and BAL white blood cells than ceftriaxone or trovafloxacin in cirrhotic rats. Macrolide, beta-lactam, or fluoroquinolone antibiotic efficacy in a pneumococcal pneumonia model does not appear to be affected by hepatic cirrhosis.

Animals↗

Rat model of congenital toxoplasmosis.

A rat model of congenital toxoplasmosis is described for the study of protective immunity and chemotherapy during pregnancy. Six Sprague-Dawley 7- to 15-day gestational rats were inoculated orally (three rats, trial A) or subcutaneously (three rats, trial B) with 10,000 infective oocysts of the CT-1 strain of Toxoplasma gondii. The tissues of rat pups born from these rats were bioassayed for T. gondii infection. T. gondii was recovered from 30 of 33 (90.9%, trial B) and 23 of 28 (82.17%, trial A) rat pups bioassayed at 1 to 134 days of age. Two 10- to 14-day gestational pregnant rats were inoculated subcutaneously (trial C) with 10,000 infective bradyzoites from tissue cysts; 10 of 23 (43.8%) of the newborn pups were infected with T. gondii. Congenital infection occurred only when rats were infected during pregnancy. None of three rats in trial A that had given birth to congenitally infected rat pups produced congenitally infected rat pups during the second pregnancy.

Animals↗

Immune responsiveness in a rat model for type II diabetes (Zucker rat, fa/fa): susceptibility to Candida albicans infection and leucocyte function.

There is a causal relationship between obesity-associated diabetes and an increased risk of infection. The ability of obese (fa/fa) Zucker rats, a model for non-insulin-dependent diabetes mellitus (NIDDM), to clear Candida albicans from the circulation and tissues was compared to that of lean (Fa/fa, Fa/Fa) Zucker rat controls as a measure of immune function. The ID50 necessary to establish tissue colonisation in lean Zucker rats was 1.18 log10 times greater than that determined for the obese Zucker rats. Nine days after intravenous (i.v.) injection of a yeast suspension, the organs of obese rats had a 10-fold greater yeast/g organ burden than did lean rats. The kidney was determined to be the primary target organ for colonisation. Germ-tube formation by C. albicans occurred at a rate 1.5 times faster in serum from obese rats than in serum from lean rats. Peritoneal polymorphonuclear leucocytes, resident macrophages and thioglycollate-elicited macrophages from lean Zucker rats displayed a significantly higher ability to kill ingested yeast cells than analogous cell populations from obese Zucker rats.

Animals↗

Osteoinduction by a collagen mineral composite combined with isologous bone marrow in a subcutaneous rat model.

In a subcutaneous implant rat model, Collagraft alone (n=8), Collagraft plus isologous bone marrow (n=8), and marrow alone (n=8) were evaluated. Twelve rats were euthanized at 11 days and 12 at 21 days. Explants were evaluated histologically for evidence of bone formation, and osteogenic activity was determined by an assay for alkaline phosphatase. Histological bone formation was absent in all groups at 11 days. At 21 days, in the Collagraft alone and bone marrow alone groups, no bone induction was noted. In contrast, 21-day specimens from the Collagraft plus bone marrow group showed newly formed bone. Alkaline phosphatase activity was negligible (<0.05 units/mg) in all 11-day specimens. Activity in Collagraft plus bone marrow specimens at 21 days (0.38 units/mg) was significantly higher than any other group (P<.001 for all comparisons). This study demonstrates that Collagraft plus bone marrow is an osteoinductive matrix.

Animals↗

A germ-line insertion in the Birt-Hogg-Dubé (BHD) gene gives rise to the Nihon rat model of inherited renal cancer.

A rat model of hereditary renal carcinoma (RC) was found in a rat colony of the Sprague-Dawley strain in Japan and named the "Nihon" rat. In heterozygotes, RCs, predominantly the clear cell type, develop from early preneoplastic lesions, which began to appear as early as 3 weeks of age, to adenocarcinomas by the age of 6 months. The Nihon rat is an example of a Mendelian dominantly inherited predisposition for development of RCs like the Eker (Tsc2 gene mutant) rat. We have previously shown that the Nihon mutation was tightly linked to genes that are located on the distal part of rat chromosome 10. The order of the genes is the Eker (Tsc2 gene (human 16p13.3)-Il3 gene-Nihon gene-Llgl1 locus- Myhse gene. We now describe a germ-line mutation in the Birt-Hogg-Dubé gene (Bhd) (human 17p11.2) caused by the insertion of a single nucleotide in the Nihon rat, resulting in a frameshift and producing a stop codon 26 aa downstream. We found that the homozygous mutant condition was lethal at an early stage of fetal life in the rat. We detected a high frequency of loss of heterozygosity (LOH) in primary RCs (10/11) at the Bhd locus and found a point mutation (nonsense) in one LOH-negative case, fitting Knudson's "two-hit" model. The Nihon rat may therefore provide insights into a tumor-suppressor gene that is related to renal carcinogenesis and an animal model of human BHD syndrome.

Animals↗

Aqueous extract of black tea (Camellia sinensis) prevents ethanol+cholecystokinin-induced pancreatitis in a rat model.

Black Tea Extract (BTE), a phytocompound has been attributed with a plethora of health-promoting actions. We have previously demonstrated that BTE inhibits chronic hepatitis in a rat model induced with high-fat and ethanol (EtOH). This study reports that BTE prevents altered pancreatic acinar cell functions, oxidative stress, inflammatory changes and DNA damage in the EtOH+cholecystokinin (CCK)-induced model of pancreatitis. The EtOH+CCK model rats were administered with BTE, and were examined the activity of pancreatic digestive enzymes (amylase and lipase), proinflammatory cytokines (IL-6 and TNF-alpha), oxidative and antioxidative enzymes (nitric oxide, NO; malondialdehyde, MDA; superoxide dismutase, SOD; catalase, CAT), antioxidant level (glutathione, GSH), histopathological changes and the integrity of genomic DNA. Results show that because of chronic EtOH treatment, serum level of amylase and lipase (two biomarkers for pancreatitis) and pancreatic levels of MDA and NO (two biomarkers of oxidative stress) increased significantly, which could be effectively blunted by BTE. BTE could normalize EtOH+CCK-induced suppressed activities of SOD and CAT, and GSH content of pancreatic tissue. Also, histopathological and inflammatory changes during EtOH+CCK-induced pancreatitis could be blunted by BTE. Furthermore, BTE could effectively reduce EtOH+CCK-induced increase in DNA fragmentation and damage. These findings suggest that BTE prevents pancreatitis caused by chronic EtOH+CCK toxicity presumably by enhancing antioxidant, anti-inflammatory and antiapoptotic activity in rats.

Amylases↗

[Determination of protein allergenicity--BN rat model].

OBJECTIVE: Protein allergenicity was investigated in BN rat model. METHODS: OVA or BSA was administered i.p. (1 mg/ml) or orally (10 mg/ml) to male BN rats for 6 weeks. In different intervals, blood samples were obtained from the orbital plexus for PCA and histamine determination. In addition, blood pressure of rats in OVA-treated group and control group was measured. RESULTS: Relatively high titres (1/32-1/128) IgE responses were provoked by administration of OVA, while BSA stimulated only low titres (1/2-1/4) IgE. Compared with the controls, the plasma histamine concentrations of OVA groups were higher. An oral challenge with OVA did not induce a clear effect on blood pressure in the majority of rats. However, two rats demonstrated a temporary drop in blood pressure. CONCLUSION: BN rat model may be a suitable animal model to determine protein allergenicity.

Animals↗

Comparison of galactomannan detection, PCR-enzyme-linked immunosorbent assay, and real-time PCR for diagnosis of invasive aspergillosis in a neutropenic rat model and effect of caspofungin acetate.

The performance of different in vitro diagnostic tests for the diagnosis of invasive aspergillosis (IA) was investigated in a transiently neutropenic rat model. Rats were immunosuppressed with cyclophosphamide and then inoculated intravenously with 1.5 x 10(4) CFU Aspergillus fumigatus spores. Animals were then either treated with caspofungin acetate, 1 mg/kg/day for 7 days, or not treated. PCR-enzyme-linked immunosorbent assay (ELISA), real-time PCR, and galactomannan (GM) detection were performed on postmortem blood samples, along with culture of liver, lung, and kidney homogenate. Caspofungin-treated animals showed a decrease in residual tissue burden of A. fumigatus from organ homogenate compared to untreated animals (P < 0.002). PCR-ELISA returned positive results for 11/17 animals treated with antifungal agents and for 10/17 untreated animals. Galactomannan was positive in 8/17 caspofungin-treated animals and 4/17 untreated animals. Real-time PCR was positive in 2/17 treated and 3/17 untreated animals. This study demonstrates that PCR-ELISA is a more sensitive test than either GM detection (P = 0.052) or real-time PCR (P < 0.01) for diagnosis of IA but that any of the three tests may return false-negative results in cases of histologically proven disease. Galactomannan indices from animals treated with antifungal agents showed a trend (P = 0.1) towards higher levels than those of untreated animals, but no effect was observed with PCR-ELISA indices (P = 0.29). GM detection, as previously described, may be enhanced by the administration of caspofungin, but PCR-ELISA appears not to be affected in the same way. We conclude that PCR-ELISA is a more sensitive and reliable method for laboratory diagnosis of IA.

Animals↗

Ethanol feeding does not affect the efficacy or pharmacokinetics of azithromycin, trovafloxacin, or ceftriaxone in a rat model of pneumococcal pneumonia.

A rat model of ethanol feeding was used to study the effects of ethanol on antibiotic therapy of pneumococcal pneumonia. Male Sprague-Dawley rats (150 g) received a liquid diet containing 36% of total calories as ethanol. Controls were pair-fed a liquid diet without ethanol or received rat chow. Diets began 7 days pre- and continued postinfection. Rats were infected transtracheally with type 3 Streptococcus pneumoniae and then treated with azithromycin (50 mg/kg), trovafloxacin (50 mg/kg), or ceftriaxone (100 mg/kg) injected subcutaneously twice daily for 5 days. Antibiotic levels in serum, lung cells, and lavage fluid were measured by HPLC. Ethanol- and pair-fed rats had depressed baseline peripheral neutrophil counts but were able to generate adequate numbers of peripheral and pulmonary polymorphonuclear leukocytes early in the course of their infection. Ethanol feeding did not alter the pharmacokinetics of azithromycin, trovafloxacin, or ceftriaxone. All three antibiotics were equally effective in curing experimental pneumococcal pneumonia, and survival rates were similar in treated ethanol-fed and control rats.

Animals↗

[Protective effects of Panax notoginseng saponins against pathological lesion of cholinergic neuron in rat model with Alzheimer' s disease].

OBJECTIVE: To observe the protective effect of Panax notoginseng saponins (PNS) against pathological lesion of cholinergic neuron in rat model with Alzheimer' s disease (AD). METHODS: The AD rat model was established by intra-peritoneal injection of D-galactose combined with excitatory neurotoxin ibotenic acid (IBA) injection into bilateral nbM. The activity and content of choline acetyltransferase (ChAT), the cell morphology and number of cholinergic neuron in brain were determined by immunohistochemistry analysis. RESULTS: PNS could reduce the pathological lesion of cholinergic neuron, including the level of ChAT and number of cholinergic neuron, as compared with those of model group's rats. CONCLUSION: PNS plays a protective role in pathological lesion of cholinergic neuron in AD rat model.

Alzheimer Disease↗

[Effect of bushen yanggan recipe on nigrostriatal function in parkinsonian model rats after long-term levodopa treatment].

OBJECTIVE: To investigate the effect of Bushen Yanggan Recipe (BSYGR) on the function and morphology of nigrostriatal system in Parkinsonian model rats with long-term levodopa treatment. METHODS: Unilateral Parkinsonian rat models were established by injecting 6-hydroxydopamine (6-OHDA) into the substantia nigra pars compacta (SNpc) and ventral segmental area (VTA). Animals were randomly divided into four groups, the sham control group, model control group, levodopa group and levodopa plus BSYGR group. The content of striatal dopa (DA), digydroxy-phenyl acetic acid (DOPAC) and homovanilic acid (HVA) or the THmRNA expression level in the midbrain were measured. RESULTS: (1) Levels of striatal DA, DOPAC, HVA, DOPAC/DA, HVA/DA decreased in the model control group by about 90% as compared with those in sham control group (P < 0.05). These parameters in the levodopa group were higher than those in the sham control group, while in the levodopa plus BSYGR group, they were lower than those in the levodopa group (P < 0.01), approaching the levels in the sham control group (P > 0.05). (2) Striatal TH activity in the model group was lower than that in the sham control group significantly, but higher than that in the levodopa group, while in the levodopa plus BSYGR group, it showed a level obviously higher than that in the levodopa group (P < 0.05). (3) Levodopa plus BSYGR group had a higher midbrain THmRNA expression level than that in the levodopa group. CONCLUSION: BSYGR could effectively reduce the side effects resulting from the long-term treatment of levodopa.

Animals↗

[Effect of total glycoside from Clinopodium polycephalum on uterine bleeding quantity in drug abortion model rats].

OBJECTIVE: To study the effect of total glycoside from Clinopodium polycephalum (Vaniot) C. Y. Wu et Hsuan on uterine bleeding quantity in drug abortion model rats. METHOD: Mifepristone and misoprostol were given to early-pregnancy rats orally. The change of uterine bleeding quantity was observed in uncompletive abortion model rats. RESULT: TGCP (20 mg/kg) could markedly reduce uterine bleeding quantity in drug abortion model rats. CONCLUSION: TGCP has the hemostatic effect on uterine bleeding in drug abortion model rats.

Abortion, Induced↗

Biochemical validation of a rat model for polycystic kidney disease: comparison of guanidino compound profile with the human condition.

Polycystic kidney disease (PKD) accounts for 7-10% of all dialyzed renal insufficient patients. Accumulation of specific guanidino compounds (GCs) has been related to neurological, cardiovascular, hematological, and immunological complications of renal failure. In this study, we investigate whether the PKD/Mhm rat model can be used as a biochemical model for human PKD. For the validation of the rat model, we performed the first detailed evaluation of the concentrations of GCs in serum and urine of patients with PKD in addition to the GC patterns in the plasma, urine, and tissues of the PKD/Mhm rat model. The GCs were determined after separation on a cation exchange resin and fluorescence detection. The GC levels and changes observed in blood and urine of patients with PKD are comparable with those found in patients with renal insufficiency due to different etiologies. The PKD/Mhm rat model can be used as a biochemical model for human PKD as the obvious increases of urea, guanidinosuccinic acid, creatinine, guanidine, methylguanidine, and N(G)N(G)-dimethylarginine (symmetrical dimethylarginine) seen in blood of oldest heterozygous and younger homozygous PKD rats were largely within the same range as those found in the studied human PKD population, especially in patients with a glomerular filtration rate below 60 ml/min/1.73 m(2). The decreased levels of plasma guanidinoacetic acid seen at end-stage renal disease in homozygous and oldest heterozygous rats were also observed in serum of patients with a glomerular filtration rate below 20 ml/min/1.73 m(2). The PKD/Mhm rat model has, besides similar disease characteristics with human PKD, comparable GC alterations.

Animals↗

Intracranial venous hypertension and the effects of venous outflow obstruction in a rat model of arteriovenous fistula.

A model of rat arteriovenous fistula (AVF) was created using a proximal common carotid artery to distal external jugular vein anastomosis. Anatomical dissections revealed that the external jugular vein is the primary vessel draining intracranial venous blood. Physiological measurements were made with the AVF open and closed, and during venous outflow occlusion of the contralateral external jugular vein. Opening the AVF increased torcular pressure from 6.5 +/- 0.6 to 13.5 +/- 1.1 mm Hg and decreased mean arterial pressure from 82.7 +/- 1.8 to 62.8 +/- 1.8 mm Hg (both P less than .05), decreasing cerebral perfusion pressure from 76.2 +/- 1.7 to 49.3 +/- 2.2 mm Hg (P less than .05). Middle cerebral artery blood flow velocity (MCA BFV) decreased from 6.8 +/- 1.1 to 4.2 +/- 0.7 cm/s (P less than 0.05). In rats with an AVF, occlusion of venous outflow increased torcular pressure to 34.8 +/- 3.1 mm Hg (P less than 0.05), MCA BFV decreased to 1.8 +/- 0.5 cm/s (P less than 0.05), and severe ischemic changes were seen on the electroencephalogram. Under this condition, torcular pressure and systemic arterial pressure had a positive linear relationship (P less than 0.05), whereas in control rats torcular pressure and arterial pressure had no relationship. Restoration of cerebral perfusion pressure by release of venous outflow occlusion and AVF closure transiently increased MCA BFV to 69% above baseline (P less than 0.05). Histological examination 1 week after permanent venous outflow occlusion revealed venous infarction, subarachnoid hemorrhage, and severe brain edema in rats with an AVF but not in control rats without an AVF. This model of cerebrovascular steal with venous hypertension reproduces both hemodynamic and hemorrhagic complications of human AVF and emphasizes the importance of venous outflow obstruction and venous hypertension in the pathophysiology of these lesions.

Animals↗

Intimal hyperplasia following carotid endarterectomy in an insulin-resistant rat model.

Hyperhomocysteinemia, a known risk factor for cardiovascular disease, results in an elevation of intimal hyperplasia (IH) following a carotid endarterectomy (CEA) in a rat model. An exaggerated IH response following CEA has been observed in rats with dietary induced hyperhomocysteinemia. Type 2 diabetics often present with hyperhomocysteinemia and are at higher risk for developing vascular blockage following surgical procedures. To determine if insulin resistance increases IH risks following endarterectomy, the 3 goals of this study were: (1) to establish plasma homocysteine concentrations in dietary induced insulin-resistant rats and their controls, (2) to investigate whether a positive correlation of IH and plasma homocysteine response occurs following CEA in the insulin-resistant rat model, and (3) if so, to attempt to decrease IH by supplementation with folic acid, a known enzymatic cofactor in the homocysteine metabolic pathway. To achieve these aims, male rats (275 to 300 g) were fed 1 of 4 diets for a 4-month period: (1) high-fat sucrose (HFS), (2) low-fat complex carbohydrate (LFCC), (3) HFS + 25 mg/kg folic acid (HFS+F), or (4) LFCC + 25 mg/kg folic acid (LFCC+F). At the end of the 4-month period the rats underwent an open (non-balloon) unilateral CEA. Two weeks post-endarterectomy, blood, liver and carotid tissue were removed to measure plasma insulin, folic acid, and homocysteine, 2 key enzymes of homocysteine metabolism-methylenetetrahydrofolate reductase (MTHFR) and cystathionine beta-synthase (CBS)-and percent lumenal stenosis (IH%). Computer-assisted morphometric analysis was used to measure the percentage of IH in the carotid artery. Plasma homocysteine was significantly higher in the HFS group when compared with the LFCC group (11.3+/-1.3 micromol/L v 7.4+/-0.6 mircomol/L, P=.008) as was post-endarterectomy IH producing lumenal stenosis (30.7%+/-4.2% v 14.0%+/-4.3%, P=.008). Plasma insulin in the HFS group was higher than the LFCC (control) group and was significant (36.3+/-3.0 microU/mL v 21.1+/-0.8 microU/mL, P=.0004). Folic acid supplementation in the HFS group resulted in reductions of plasma homocysteine (HFS v HFS+F, 11.3+/-1.3 micromol/L v 7.95+/-1.0 micromol/L, P=.02) and post-endarterectomy IH (HFS v HFS+F, 30.7%+/-4.2 % v 10.4%+/-1.6%, P=.0001). The control or LFCC group was not statistically different from the HFS+F group in homocysteine or IH. Folate supplementation did not decrease insulin concentrations in the HFS+F group compared to the LFCC group. We conclude that the HFS diet produced an insulin-resistant state with an elevated plasma homocysteine and an exaggerated IH response following carotid endarterectomy in this rat model. Dietary folate supplementation reduced plasma homocysteine concentrations in the HFS diet, which implicates hyperhomocysteinemia as an etiologic factor in the development of post-CEA IH in this insulin-resistant rat model.

Animals↗