Regular Diet Group Research Articles

Use of Contralateral Knee as Control in the Destabilization of Medial Meniscus Osteoarthritis Rat Model

Destabilization of the medial meniscus (DMM) is a common surgical procedure used to induce osteoarthritis (OA) in a rodent model. However, there is a lack of evidence on using the contralateral limb as a control. Contralateral rat knees have been used as the control in noninvasive OA pain models, but not DMM models; and the contralateral limb of guinea pigs has been used to study the development of OA after DMM surgery. In a previous study, we examined the effects of DMM and obesity on the development and progression of OA in a rat model. In that study, 42 female Lewis rats were randomly assigned to 4 groups: Group 1 received a sham surgery (control) and was on a regular diet, Group 2 received a DMM surgery and was on a regular diet, Group 3 received a sham surgery and was on a high‐fat diet, and Group 4 received a DMM surgery and was on a high‐fat diet. The rats were on their respective diets for 4 weeks, underwent surgery, and were sacrificed 4 weeks after surgery. The knee joints of surgical and contralateral limbs were harvested. The Osteoarthritis Research Society International (OARSI) scoring system was used to score the damage to the articular cartilage of the knee. In the surgical limbs, DMM resulted in significantly greater OARSI scores than the sham surgery in the lateral and medial compartments of the knee in both diet groups. After that study, the contralateral knee tissues were stored in 10% formalin. For the current study, we used those stored tissues to determine whether the contralateral limbs could serve as a control in future studies that involve DMM in a rat model. Knees were decalcified, embedded in paraffin, and sectioned coronally at 10 μm. Slides were stained using Safranin O and fast green for counterstain. Four articular surfaces of the knee (medial and lateral femoral condyles and medial and lateral tibial plateaus) were histologically evaluated for degenerative changes by a blinded scorer. A generalized linear mixed model was used to analyze differences between the rat knee groups. Comparison of sham and DMM rat knees across both diet groups showed no significant difference in OARSI scores (P=.61). When comparing within each of the diet groups, there was no significant difference between the DMM and sham scores in the high‐fat diet groups (P>.99) or regular diet groups (P=.49). After comparing the knee surface scores for all groups, the medial tibial plateau had significantly lower scores than the other 3 surfaces (P<.001). Based on results of the current study, we believe the contralateral limb can be used as a control in short‐term (4 weeks or less) OA studies using DMM in a rat model. This will save time and resources by achieving an adequate sample size with fewer animals. Our results also showed that the medial tibial plateau was significantly less susceptible to the development of spontaneous OA compared to the other 3 articular surfaces studied.Support or Funding InformationSupport for this project was received from Dr. Peter Kondrashov, Department of Anatomy, A.T. Still University, Kirksville College of Osteopathic Medicine.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Short‐term Western Diet Induces Cardiometabolic Syndrome in Female Rats is Associated with Increased Cardiovascular Protein Lysine Acetylation.

The western diet (WD), which is rich in fat, carbohydrates, and refined sugars, is a major contributor to the global epidemic of metabolic syndrome in our modern society. Despite the well‐documented cardioprotection exhibited by the pre‐menopausal female population, studies have indicated that certain stressors may abolish this cardiovascular protection. Studies on the impact of the WD on the cardiometabolic profile of female cohorts remains limited. Lysine acetylation, a reversible posttranslational modification of histone and non‐histone proteins, has been closely associated with metabolic disorders. Based on these factors, we hypothesized that short‐term exposure to the WD alters cardiometabolic parameters in premenopausal rats and alters levels of lysine acetylation in the cardiovascular tissues. Adult female Wistar rats were randomized in two groups: Control Group (n=8) was assigned a regular chow diet and WD Group (n=12) received WD (40% fat, 43% carbohydrates, and 17% protein) for 17 weeks. Results showed that WD group exhibited increased body weight (376 ± 49 vs 305 ± 41g, p<0.05), periabdominal fat content (30 ±11 vs 11 ±2g, p<0.01), % body fat (8.1 ±1.0 vs 3.6 ±0.4%, p<0.01), and serum triglyceride levels (56 ± 13 vs 25 ± 4 mg/dl, p<0.01) compared to controls. Although the WD group exhibited significant increases in glucose intolerance (AUC: 17068.5 ± 730 vs. 13787.67± 814 a.u, p<0.01) and insulin resistance (HOMA‐IR: 5.75 ± 0.9 vs. 3.25 ± 0.62 control, p<0.05), no differences in fasting blood glucose and hemoglobin A1C were found. Using direct arterial blood pressure measurements via carotid artery catheterization, we observed increased systolic blood pressure (146.19 ±9.4 vs 126.22 ± 9.8 mmHg controls, p<0.001), which is contradictory with previous studies. Our vascular reactivity studies revealed that short‐term WD markedly impaired endothelial‐dependent relaxation. Additionally, using DHE staining we found that aortas from the WD group exhibited augmented levels of oxidative stress (3.1‐fold increase vs. control, p<0.001). Strikingly, levels of global lysine acetylation were markedly elevated in the aortas (2.2‐fold increase vs. control, p<0.01) and heart (1.4‐fold increase vs. control, p<0.05) of WD group. Levels of acetyltransferase PCAF were significantly upregulated in the aortas (2.2‐fold increase vs. control, p<0.05). Interestingly, PCAF and deacetylase HDAC9 expression was diminished in hearts from WD group (30% reduction vs. control, p<0.05) and (85% reduction vs. control, p<0.05), respectively. Besides these cardiovascular alterations, the WD also led to the development of non‐alcoholic fatty liver disease (NAFLD) and robust increases in hepatic global lysine acetylation (3.0‐fold increase vs. control, p<0.001). Taken together, our results demonstrated that, even under short‐term exposure, the WD negatively affects the metabolic and cardiovascular parameters of female rats and it is associated with elevated levels of global lysine acetylation in cardiometabolic tissues. This study will be further conducted to identify the specific proteins acetylated in blood vessels and heart from female population under WD regimes.Support or Funding InformationIn‐house Grant NYIT to MACSThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Supplementation of Bacillus subtilis-based probiotic reduces heat stress-related behaviors and inflammatory response in broiler chickens.

Probiotics reduce stress-related inflammation and abnormal behaviors in humans and rodents via regulation of the microbiota-gut-brain axis. The objective of this study was to determine if probiotic, Bacillus subtilis, has similar functions in broiler chickens under heat stress (HS). Two hundred forty 1-d-old broiler chicks were assigned to 48 pens with 4 treatments: Thermoneutral (TN)-RD (regular diet), TN-PD (the regular diet mixed with 1 × 106 CFU/g feed probiotic), HS-RD and HS-PD. Probiotic (Sporulin) was fed from day 1; and HS at 32°C for 10 h daily was initiated at day 15. The data showed that final BW, average daily gain , and feed conversion efficiency were improved in PD groups as compared to RD groups regardless of the ambient temperature (P < 0.01). Heterophil to lymphocyte ratio was affected by treatment and its value was in the order of HS-RD > HS-PD > TN-RD > TN-PD birds (P < 0.01). Compared to TN birds, HS birds spent more time in wing spreading, panting, squatting close to the ground, drinking, sleeping, dozing, and sitting but spent less time in eating, standing, and walking (P < 0.05 or 0.01). In addition, HS birds had greater levels of hepatic IL-6, IL-10, heat shock protein (HSP)70, and HSP70 mRNA expression (P < 0.01) and greater levels of cecal IgA and IgY (P < 0.01) compared to TN birds. Within TN groups, TN-PD birds had greater concentrations of hepatic IL-10 (P < 0.05) and cecal IgA (P < 0.01) than TN-RD birds. Within HS groups, HS-PD birds spent less time in wing spreading, panting, squatting close to the ground, drinking, sleeping, dozing, and sitting but spent more time in eating, foraging, standing, and walking than HS-RD birds (P < 0.05 or 0.01). The HS-PD birds also had lower concentrations of hepatic IL-6 and HSP70 (P < 0.01), whereas greater levels of IL-10 (P < 0.05) and lower concentrations of cecal IgA and IgY (P < 0.01). These results indicate that broilers fed the probiotic, B. subtilis, are able to cope with HS more effectively by ameliorating heat-induced behavioral and inflammatory reactions through regulation of microbiota-modulated immunity.

Antidiabetic effects of SGLT2 inhibitor ipragliflozin in type 2 diabetic mice fed diets containing different carbohydrate contents

AimsDaily intake of carbohydrates differs among individual patients with type 2 diabetes. Here, we investigated whether or not dietary carbohydrate content affects the efficacy of the sodium-glucose cotransporter 2 (SGLT2) inhibitor ipragliflozin in type 2 diabetic mice. Main methodsDiabetic mice were fed a regular (50% kcal), high (75% kcal)-, or low (25% kcal)-carbohydrate diet. Ipragliflozin was orally administered once a day for 4 weeks. Key findingsIn all groups, mice exhibited characteristics of type 2 diabetes, including hyperglycemia, hyperinsulinemia, and obesity. Hyperglycemia was more severe in the high-carbohydrate diet group and milder in the low-carbohydrate diet group than in the regular diet group. In all diabetic mice, ipragliflozin significantly increased urinary glucose excretion and improved hyperglycemia, hyperinsulinemia, glucose tolerance, insulin resistance, obesity, and nephropathy. Although these antidiabetic effects of ipragliflozin were more marked in the high-carbohydrate diet group (which showed more severe hyperglycemia) than in the other two groups, no significant differences in effective dose or degree of response were observed among the three groups. SignificanceThe antidiabetic effects of ipragliflozin were not greatly affected by dietary carbohydrate content, suggesting that ipragliflozin may have similar efficacy for patients with type 2 diabetes regardless of carbohydrate intake.

Eugenosedin-A improves glucose metabolism and inhibits MAPKs expression in streptozotocin/nicotinamide-induced diabetic rats

This study examined the effects of eugenosedin-A (Eu-A) in a streptozotocin (STZ)/nicotinamide-induced rat model of type II diabetes mellitus (T2DM). Six-week-old Sprague–Dawley rats were randomly divided into three groups: (1) RD group, normal rats fed a regular diet (RD), (2) DM group, T2DM rats fed a high-fat diet, and (3) Eu-A group, T2DM rats fed a high fat diet plus oral Eu-A (5 mg/kg/day). After 30 days, the DM group had higher body weight, higher blood glucose and lower insulin levels than the RD group. The DM group also had increased protein expression of glycogen synthase kinase (GSK) in liver and skeletal muscle and decreased protein expression of insulin receptor (IR), insulin receptor substrate-1 (IRS-1), IRS-2, AMP-activated protein kinase (AMPK), glucose transporter-4 (GLUT-4), glucokinase (GCK), and peroxisome proliferator-activated receptor γ (PPAR-γ). STZ/nicotinamide-induced T2DM increased the expression of mitogen-activated protein kinases (MAPKs: p38, ERK, JNK) and inflammatory p65 protein. In the Eu-A treated T2DM rats, however, blood glucose was attenuated and the insulin concentration stimulated. Changes in IR, IRS-1 and IRS-2 proteins as well as AMPK, GLUT-4, GCK, GSK, PPAR-γ, MAPKs, and inflammatory p65 proteins were ameliorated. These results suggested that Eu-A alleviates STZ/nicotinamide-induced hyperglycemia by improving insulin levels and glucose metabolism, and inhibiting the MAPKs- and p65-mediated inflammatory pathway.

Exposure assessment to bisphenol A (BPA) in Portuguese children by human biomonitoring.

Exposure to bisphenol A (BPA) is known to be widespread and available data suggests that BPA can act as an endocrine disruptor. Diet is generally regarded as the dominant BPA exposure source, namely through leaching to food from packaging materials. The aim of this study was to evaluate the exposure of 110 Portuguese children (4-18years old), divided in two groups: the regular diet group (n=43) comprised healthy normal weight/underweight children with no dietary control; the healthy diet group (n=67) comprised children diagnosed for obesity/overweight (without other known associated diseases) that were set on a healthy diet for weight control. First morning urine samples were collected and total urinary BPA was analyzed after enzymatic hydrolysis via on-line HPLC-MS/MS with isotope dilution quantification. Virtually, all the children were exposed to BPA, with 91% of the samples above the LOQ (limit of quantification) of 0.1μg/L. The median (95th percentile) urinary BPA levels for non-normalized and creatinine-corrected values were 1.89μg/L (16.0) and 1.92μg/g creatinine (14.4), respectively. BPA levels in the regular diet group were higher than in the healthy diet group, but differences were not significant. Calculated daily BPA intakes, however, were significantly higher in children of the regular diet group than in children of healthy diet group. Median (95th percentile) daily intakes amounted to 41.6 (467) ng/kg body weight/day in the regular diet group, and 23.2 (197) ng/kg body weight/day in the healthy diet group. Multiple logistic regression analysis revealed that children in the healthy diet group had 33% lower intakes than children in the regular diet group (OR 0.67; 95% CI 0.51-0.89). For both groups, however, urinary BPA levels and daily BPA intakes were within the range reported for other children's populations and were well below health guidance values such as the European Food Safety Authority (EFSA) temporary tolerable daily intake (t-TDI) of 4μg/kg body weight/day. In addition, lower daily BPA intakes were more likely linked with the inherent dietary approach rather than with high BMI or obesity.

Short-Term High-Fat Diet Increases Leptin Activation of CART Neurons and Advances Puberty in Female Mice.

Leptin is a permissive factor for puberty initiation, participating as a metabolic cue in the activation of the kisspeptin (Kiss1)-gonadotropin-releasing hormone neuronal circuitry; however, it has no direct effect on Kiss1 neurons. Leptin acts on hypothalamic cocaine- and amphetamine-regulated transcript (CART) neurons, participating in the regulation of energy homeostasis. We investigated the influence of a short-term high-fat diet (HFD) on the effect of leptin on puberty timing. Kiss1-hrGFP female mice received a HFD or regular diet (RD) after weaning at postnatal day (PN)21 and were studied at PN28 and PN32. The HFD increased body weight and plasma leptin concentrations and decreased the age at vaginal opening (HFD, 32 ± 0.53 days; RD, 38 ± 0.67 days). Similar colocalization of neurokinin B and dynorphin in Kiss1-hrGFP neurons of the arcuate nucleus (ARC) was observed between the HFD and RD groups. The HFD increased CART expression in the ARC and Kiss1 messenger RNA expression in the anteroventral periventricular (AVPV)/anterior periventricular (Pe). The HFD also increased the number of ARC CART neurons expressing leptin-induced phosphorylated STAT3 (signal transducer and activator of transcription 3) at PN32. Close apposition of CART fibers to Kiss1-hrGFP neurons was observed in the ARC of both RD- and HFD-fed mice. In conclusion, these data reinforce the notion that a HFD increases kisspeptin expression in the AVPV/Pe and advances puberty initiation. Furthermore, we have demonstrated that the HFD-induced earlier puberty is associated with an increase in CART expression in the ARC. Therefore, these data indicate that CART neurons in the ARC can mediate the effect of leptin on Kiss1 neurons in early puberty induced by a HFD.

Effect of high-fat diet and growth stage on the diversity and composition of intestinal microbiota in healthy bovine livestock.

This study aimed to investigate the composition of bacteria in the bovine rectum and their functions during growth, in relation to different diets. Fecal samples were collected from 6-, 12-, 18- and 24-month cattle fed high-fat diet, and healthy female parents fed regular diet. Total DNA was amplified (V3-V4 of 16S rRNA) and submitted to barcode-DNA pyrosequencing. Intestinal microbiota profiles and functions were then analyzed. A total of 114 512 operational taxonomic units were detected from the 1 802 243 sequences obtained. In 6-month-old and female parent groups, the top three abundant phyla were Bacteroidetes (37.6%, 32.2%), Firmicutes (34.4%, 48.2%) and Proteobacteria (9.1%, 6.3%); in the 12-, 18- and 24-month groups, they were Proteobacteria (45.5%, 47.1%, 38.8%), Firmicutes (27.4%, 22.2%, 20.1%) and Bacteroidetes (14.9%, 19.4%, 17.7%), respectively. Paludibacter and Desulfopila in abundance showed negative (P < 0.001) and positive (P < 0.05) correlation, respectively, to cattle weight gain through metagenomic functional prediction of methane, cysteine and methionine metabolism. Meanwhile, cofactor/vitamin and amino acid metabolic processes were significantly higher in bacteria from the regular diet group than high-fat diet groups, with markedly lower cellular processes and signaling, and reduced glycan biosynthesis and metabolism (P < 0.01). The 6-month cattle and female parents shared similar intestinal bacteria; the community structure of fecal microbiota was significantly affected by high-fat diet in older cattle. © 2017 Society of Chemical Industry.

Rimonabant improves metabolic parameters partially attributed to restoration of high voltage-activated Ca2+ channels in skeletal muscle in HFD-fed mice.

Cannabinoid type 1 receptor (CB1R) inhibition tends to be one of the promising strategies for the treatment of obesity and other related metabolic disorders. Although CB1R inhibition may cause adverse psychiatric effects including depression and anxiety, the investigation of the role of peripheral CB1R on weight loss and related metabolic parameters are urgently needed. We first explored the effect of rimonabant, a selective CB1R antagonist/inverse agonist, on some metabolic parameters in high fat-diet (HFD)-induced obesity in mice. Then, real-time PCR and electrophysiology were used to explore the contribution of high voltage-activated Ca2+ channels (HVACCs), especially Cav1.1, on rimonabant's effect in skeletal muscle (SM) in HFD-induced obesity. Five-week HFD feeding caused body weight gain, and decreased glucose/insulin tolerance in mice compared to those in the regular diet group (P<0.05), which was restored by rimonabant treatment compared to the HFD group (P<0.05). Interestingly, HVACCs and Cav1.1 were decreased in soleus muscle cells in the HFD group compared to the control group. Daily treatment with rimonabant for 5 weeks was shown to counter such decrease (P<0.05). Collectively, our findings provided a novel understanding for peripheral CB1R's role in the modulation of body weight and glucose homeostasis and highlight peripheral CB1R as well as Cav1.1 in the SM as potential targets for obesity treatment.

High Dietary Fructose Intake on Cardiovascular Disease Related Parameters in Growing Rats.

The objective of this study was to determine the effects of a high-fructose diet on cardiovascular disease (CVD)-related parameters in growing rats. Three-week-old female Sprague Dawley rats were randomly assigned to four experimental groups; a regular diet group (RD: fed regular diet based on AIN-93G, n = 8), a high-fructose diet group (30Frc: fed regular diet with 30% fructose, n = 8), a high-fat diet group (45Fat: fed regular diet with 45 kcal% fat, n = 8) or a high fructose with high-fat diet group (30Frc + 45Fat, fed diet 30% fructose with 45 kcal% fat, n = 8). After an eight-week treatment period, the body weight, total-fat weight, serum glucose, insulin, lipid profiles and pro-inflammatory cytokines, abdominal aortic wall thickness, and expressions of eNOS and ET-1 mRNA were analyzed. The result showed that total-fat weight was higher in the 30Frc, 45Fat, and 30Frc + 45Fat groups compared to the RD group (p < 0.05). Serum triglyceride (TG) levels were highest in the 30Frc group than the other groups (p < 0.05). The abdominal aorta of 30Frc, 45Fat, and 30Frc + 45Fat groups had higher wall thickness than the RD group (p < 0.05). Abdominal aortic eNOS mRNA level was decreased in 30Frc, 45Fat, and 30Frc + 45Fat groups compared to the RD group (p < 0.05), and also 45Fat and 30Frc + 45Fat groups had decreased mRNA expression of eNOS compared to the 30Frc group (p < 0.05). ET-1 mRNA level was higher in 30Frc, 45Fat, and 30Frc + 45Fat groups than the RD group (p < 0.05). Both high fructose consumption and high fat consumption in growing rats had similar negative effects on CVD-related parameters.

Effect of gluten free diet on gastrointestinal and behavioral indices for children with autism spectrum disorders: a randomized clinical trial

Genetic and environmental factors are both responsible for the etiology of autism spectrum disorders (ASD). Although epidemiological studies have been conducted to clarify the association between restriction diets and ASD, the conclusion remains unclear. This study was undertaken to investigate the effect of gluten free diet (GFD) on gastrointestinal symptoms and behavioral indices in children with ASD. In this randomized clinical trial, 80 children diagnosed with ASD by the Autism Diagnostic Interview-Revised (ADI-R) were assigned into GFD (n=40) and regular diet (RD) (n=40) groups for 6 weeks. At the beginning and end of the intervention, the ROME Ш questionnaire for evaluating gastrointestinal symptoms and Gilliam Autism Rating Scale 2 questionnaire (GARS-2) for assessing psychometric properties were completed. Of the 80 children, 53.9% had gastrointestinal abnormalities. In the GFD group, the prevalence of gastrointestinal symptoms decreased significantly (P<0.05) after intake of GFD (40.57% vs. 17.10%) but increased insignificantly in the RD group (42.45% vs. 44.05%). GFD intervention resulted in a significant decrease in behavioral disorders (80.03±14.07 vs. 75.82±15.37, P<0.05) but an insignificant increase in the RD group (79.92±15.49 vs. 80.92±16.24). This study suggested that GFD may be effective in controlling gastrointestinal symptoms and ASD behaviors.

High fat diet induced alterations of atrial electrical activities in mice.

Obesity is a well-known risk factor for various cardiovascular diseases. Recent clinical data showed that overweight and obese patients have higher incidence of atrial fibrillation (AF) compared with individuals with normal body weights, but the underlying mechanisms remain to be elucidated. In this study, we investigated the effects of a high fat diet on atrial activities in mice. ICR male mice were fed a regular diet (RD) or a high fat diet (HFD) for 8 weeks. Mice fed HFD showed significantly greater body weight gains and visceral fat accumulation compared with RD mice. Under anesthetic condition, baseline arterial blood pressure and heart rate were not significantly different between RD and HFD groups. Although no spontaneous or atrial stimulation-induced atrial fibrillation was observed, this study revealed several alterations in the activities and protein levels in the atria in HFD mice. Surface electrocardiogram (ECG) revealed significantly shortened PR interval in HFD mice. In the atrial stimulation experiments, the sinoatrial (SA) node recovery time was significantly prolonged whereas the atrial effective refractory period was significantly reduced in HFD mice as compared with RD mice. Western blot showed protein levels of two major potassium channels, Kv1.5 and Kv4.2/3, were significantly increased in atria of HFD mice. These data indicate that HFD induces atrial electrophysiological remodeling in mice, which may be a potential mechanism underlying the increased risk for atrial arrhythmias in obesity and metabolic disorders.

Effect of Hypercholesterolemia on Fatty Infiltration and Quality of Tendon-to-Bone Healing in a Rabbit Model of a Chronic Rotator Cuff Tear

Background: The incidence of healing failure after rotator cuff repair is high, and fatty infiltration is a crucial factor in healing failure. Purpose: To verify the effect of hypercholesterolemia on fatty infiltration and the quality of tendon-to-bone healing and its reversibility by lowering the cholesterol level in a chronic tear model using the rabbit supraspinatus. Study Design: Controlled laboratory study. Methods: Forty-eight rabbits were randomly allocated into 4 groups (n = 12 each). After 4 weeks of a high-cholesterol diet (groups A and B) and a regular diet (groups C and D), the supraspinatus tendon was detached and left alone for 6 weeks and then was repaired in a transosseous manner (groups A, B, and C). Group D served as a control. Group A continued to receive the high-cholesterol diet until the final evaluation (6 weeks after repair); however, at the time of repair, group B was changed to a general diet with administration of a cholesterol-lowering agent (simvastatin). Histological evaluation of the fat-to-muscle proportion was performed twice, at the time of repair and the final evaluation, and an electromyographic (EMG) test, mechanical test, and histological test of tendon-to-bone healing were performed at the final evaluation. Results: For the EMG test, group A showed a significantly smaller area of compound muscle action potential compared with groups C and D (all P <.01), and group B showed a larger area than group A, almost up to the level of group C (P = .312). Similarly, group A showed significantly lower mechanical properties both in load-to-failure and stiffness compared with groups C and D (all P <.05). In addition, although not significantly different, the mechanical properties of group B were higher than those of group A (mean load-to-failure: group A = 42.01 N, group B = 58.23 N [P = .103]; mean stiffness: group A = 36.32 N/mm, group B = 47.22 N/mm [P = .153]). For the histological test, groups A and B showed a significantly higher fat-to-muscle proportion than did groups C and D at 6 weeks after detachment (all P <.05), but at the final evaluation, group B showed a decreased fat-to-muscle proportion (mean ± SD: from 64.02% ± 11.87% to 54.68% ± 10.47%; P = .146) compared with group A, which showed increased fat-to-muscle proportion (from 59.26% ± 17.80% to 78.23% ± 10.87%; P = .015). Groups B and C showed better tendon-to-bone interface structures than did group A, which showed coarse and poorly organized collagen fibers with fat interposition. Conclusion: Hypercholesterolemia had a deleterious effect on fatty infiltration and the quality of tendon-to-bone repair site, and lowering hypercholesterolemia seemed to halt or reverse these harmful effects in this experimental model. Clinical Relevance: Systemic diseases such as hypercholesterolemia should be tightly controlled during the perioperative period of rotator cuff repair.

Early cardiac changes induced by a hypercaloric Western-type diet in "subclinical" obesity.

"Obesity cardiomyopathy" effects have been widely described; however, the specific contribution of metabolic changes and altered adipokine secretion are still uncharacterized. Moreover, a diagnosis based on body mass index might not be the most accurate to identify increased adiposity and its outcomes. In this study, we aimed to determine the impact of a Western-type diet [hypercaloric diet (HCD)] ingestion on biventricular structure and function, as well as the metabolic and endocrine changes that occur before the establishment of overt obesity. Wistar rats were fed for 6 wk with a regular diet or HCD. At the end of the protocol, metabolic tests, cardiac structure, and functional evaluation were performed, and blood and tissue samples collected to perform histological, molecular biology, and functional studies. The animals that ingested the HCD presented increased adiposity and larger adipocyte cross-sectional area, but similar body weight compared with the regular diet group. At the cardiac level, HCD induced biventricular cardiomyocyte hypertrophy, fibrosis, increased stiffness, and impaired relaxation. Galectin-3 plasma expression was likewise elevated in the same animals. The nutritional modulation also altered the secretory pattern of the adipose tissue, originating a proinflammatory systemic environment. In this study, we observed that before "clinical" overweight or frank obesity is established, the ingestion of a HCD-induced cardiac remodeling manifests by increased biventricular stiffness and diastolic dysfunction. The mechanism triggering the cardiac alterations appears to be the proinflammatory environment promoted by the adipose tissue dysfunction. Furthermore, galectin-3, a profibrotic molecule, might be a potential biomarker for the myocardial alterations promoted by the HCD before overweight or obesity.

Comparison of Serum Adiponectin in Smoke-induced Pulmonary Emphysema Rats Fed Different Diets.

Background:Smoking and body mass index (BMI) are the key risk factors for chronic obstructive pulmonary disease (COPD). Adiponectin with both anti-inflammatory and pro-inflammatory properties is a vital modulator of inflammatory processes, which is expressed in epithelial cells in the airway in COPD-emphysema. The aim of this study was to examine the effects of adiponectin on tobacco smoke-induced emphysema in rats, which were fed different diets.Methods:Seventy-six adult (6–8 weeks old) male Sprague-Dawley rats (average weight 220 ± 20 g) were exposed to smoke or smoke-free room atmosphere and fed different diets (regular, high-fat, or low-fat diets) for 6 months. The rats were randomly divided into six groups. They are nonsmoke-exposed regular diet (n = 10), nonsmoke-exposed high-fat diet (n = 14), nonsmoke-exposed low-fat diet (n = 14), smoke-exposed regular diet (n = 10), smoke-exposed high-fat diet (n = 14), and smoke-exposed low-fat diet groups (n = 14). A full 23 factorial design was used to evaluate the effect of independent variables on smoke exposure and different rearing methods. Serum adiponectin and inflammatory cytokines were measured by the enzyme-linked immunosorbent assay (ELISA).Results:Serum adiponectin levels in rats fed low-fat and regular diets exposed to smoke exposure were remarkably higher than that of rats exposed to room air while serum adiponectin levels of fat-rich diet rats exposed to tobacco smoke were lower than that of rats exposed to room air. Compared with regular diet or low-fat diet group, serum adiponectin levels in high-fat diet rats exposed to tobacco smoke were lower (t = 6.932, 11.026; all P < 0.001). BMI was inversely correlated with serum adiponectin levels (r = −0.751, P = 0.012). Serum interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), and 4-hydroxy 2-nonenal (HNE) levels in rats exposed to low-fat or fat-rich diets were remarkably higher than that of rats exposed to normal diets (IL-6, t = 4.196, 3.480; P < 0.01, P = 0.001; TNF-α, t = 4.286, 3.521; P < 0.01, P = 0.001; 4-HNE, t = 4.298, 4.316; all P < 0.001). In nonhigh-fat diet rats exposed to tobacco smoke, serum adiponectin levels correlated positively with serum IL-6, TNF-α, and 4-HNE, bronchoalveolar lavage cell count, and mean linear intercept. In contrast, in high-fat diet rats, serum adiponectin levels correlated inversely with these parameters.Conclusions:In smoke-induced emphysema and fat-rich diet rat model, serum adiponectin level was decreased, and the anti-inflammatory effect was attenuated. By contrast, nonhigh-fat diet elevated serum adiponectin and enhanced the role of pro-inflammatory.

Gynura procumbens extract improves insulin sensitivity and suppresses hepatic gluconeogenesis in C57BL/KsJ-db/db mice.

BACKGROUND/OBJECTIVESThis study was designed to investigate whether Gynura procumbens extract (GPE) can improve insulin sensitivity and suppress hepatic glucose production in an animal model of type 2 diabetes.MATERIALS/METHODSC57BL/Ksj-db/db mice were divided into 3 groups, a regular diet (control), GPE, and rosiglitazone groups (0.005 g/100 g diet) and fed for 6 weeks.RESULTSMice supplemented with GPE showed significantly lower blood levels of glucose and glycosylated hemoglobin than diabetic control mice. Glucose and insulin tolerance test also showed the positive effect of GPE on increasing insulin sensitivity. The homeostatic index of insulin resistance was significantly lower in mice supplemented with GPE than in the diabetic control mice. In the skeletal muscle, the expression of phosphorylated AMP-activated protein kinase, pAkt substrate of 160 kDa, and PM-glucose transporter type 4 increased in mice supplemented with GPE when compared to that of the diabetic control mice. GPE also decreased the expression of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase in the liver.CONCLUSIONSThese findings demonstrate that GPE might improve insulin sensitivity and inhibit gluconeogenesis in the liver.

Low iodine diet does not improve the efficacy of radioiodine for the treatment of Graves’ disease

Consuming a low-iodine diet (LID) is a widely accepted practice before administering radioiodine (131I) to evaluate and to treat thyroid disease. Although this procedure is well established for the management of patients with differentiated thyroid cancer, its use in patients with benign disease is unclear. So, we aimed to evaluate the influence of a LID on the outcome in patients with Graves' disease (GD) treated with 131I. We evaluated 67 patients with GD who were divided into 2 groups: one group (n = 31) consumed a LID for 1-2 weeks, and the second group (n = 36) was instructed to maintain a regular diet (RD). The LID group experienced a 23% decrease in urinary iodine after 1 week on the diet and a significant 42% decrease after 2 weeks on the diet. The majority (53%) of the patients in the LID group had urinary iodine levels that were consistent with deficient iodine intake. However, there was no difference in the rate of hyperthyroidism's cure between the LID and the RD groups 6 months after 131I therapy. Furthermore, the therapeutic efficacy did not differ in patients with varying degrees of sufficient iodine intake (corresponding urinary iodine levels: < 10 μg/dL is deficient; 10-29.9 μg/dL is sufficient; and > 30 μg/dL is excessive). In the present study, we demonstrated that although a LID decreased urinary iodine levels, those levels corresponding with sufficient or a mild excess in iodine intake did not compromise the therapeutic efficacy of 131I for the treatment of GD.

The Celiac Disease and Diabetes-Dietary Intervention and Evaluation Trial (CD-DIET) protocol: a randomised controlled study to evaluate treatment of asymptomatic coeliac disease in type 1 diabetes

IntroductionCoeliac disease (CD) is an autoimmune condition characterised by gluten-induced intestinal inflammation, and observed at a 5–10 fold greater prevalence in type 1 diabetes. While universal screening for CD in...

Esophageal and gastric variceal bleeding in the prevention of early rebleeding given enteral nutrition value after endoscopic variceal ligation and treatment

To observe liver cirrhosis with esophageal and gastric variceal bleeding (GEVB) after endoscopic variceal ligation and treatment of early oral nutrition liquid in patients administered to reduce the risk of early rebleeding. Seventy-eight patients with cirrhosis who received therapeutic endoscopy after GEVB and who suffered from malnutrition were randomly divided into a treatment group (oral solution group, n=40) and a control group (regular diet group, n=38).Both of the two groups received food at 12 hours after therapeutic endoscopy.After 14 days, the rates of early rebleeding rate and liver function recovery were compared for the two groups. T-test, rank test, chi-square test and Fisher's exact test were used for statistical analyses. Compared with the control group, less patients in the treatment group experienced rebleeding (0/40 vs. 5/38; x2=5.624, P=0.018); the treatment group also showed significantly improved indexes of liver function (all P less than 0.05). s GEVB after endoscopic treatment with early oral nutrition liquid administration can reduce in the early rebleeding risk and improve function and malnutrition status.

Abstract 1583: Western diet enhances benzo(a)pyrene [B(a)P]-induced colon tumorigenesis in the PIRC rat model via proinflammatory mechanisms

Abstract Colorectal cancer ranks third in terms of mortalities in the United States. Consumption of Western Diet (rich in red meat and fats), contaminated with environmental toxicants such as benzo(a)pyrene [B(a)P] has also been implicated as one of the causative factors for sporadic colon cancer. Therefore, the objective of this study was to investigate the effect of dietary fat type on B(a)P -induced colon cancer in an adult male rat model, the Polyposis In the Rat Colon (PIRC) kindred type. Groups of PIRC rats (n = 5) were fed with AIN-76A regular diet (RD) or Western diet (WD) and these rats also received 25, 50 and 100 µg B(a)P/kg body wt., daily via oral gavage for a period of 60 days. Rats that were fed with the diets alone, but no B(a)P served as controls. Food consumption and body weights of the rats were periodically monitored. Subsequent to exposure, rats were sacrificed; colons, liver and other tissues were retrieved and preserved in 10% formalin for observation of gross pathological changes. Blood samples were collected and concentrations of cholesterol, triglycerides, and adiponectin were measured. Colon tissues were scored for tumors, and preserved in 10% formalin for observation of pathological changes. Colon and liver samples were analyzed for activation of drug metabolizing enzymes (DMEs) CYP1A1, CYP1B1 and GST. The lack of change in food consumption notwithstanding, body weight loss of WD group compared to RD group and controls (p &amp;lt; 0.05) was noticed. An increased incidence of adenomas and high grade dysplasia were encountered in rats that were fed with WD compared to RD and controls (p &amp;lt; 0.05). The colon tumor counts were more in B(a)P + WD rats compared to their B(a)P + RD counterparts, and also exhibited a B(a)P dose-response relationship, with 100 µg B(a)P/kg registering greater counts. Adenomas with high grade dysplasia were prominent in B(a)P + WD rats compared to B(a)P + RD rats. Immunohistochemical analyses of colon tissue samples for PCNA, cyclin D1, TGF-β, and β-catenin revealed increased levels of cell proliferation and nuclear positivity among all treatment groups. Rats that received B(a)P + WD showed increased levels of cholesterol and triglycerides in comparison to rats that received B(a)P + RD and also controls. Levels of adiponectin did not vary much between B(a)P + WD, and B(a)P + RD groups. Western diet consumption increased DME activation among rats that were given B(a)P + WD with marked increase in rats that were administered 100 µg/kg B(a)P + WD (p &amp;lt; 0.05) compared to other treatment groups. Our results demonstrate that WD accelerates the development of colon tumors induced by B(a)P through proinflammatory action, characterized by gain in tumor number and sizes, and body weight loss. Citation Format: Kelly L. Harris, Stephanie R. Pulliam, Mohammad S. Niaz, Mary K. Washington, Samuel E. Adunyah, Aramandla Ramesh. Western diet enhances benzo(a)pyrene [B(a)P]-induced colon tumorigenesis in the PIRC rat model via proinflammatory mechanisms. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1583. doi:10.1158/1538-7445.AM2014-1583