Rat Model Of Diet-induced Obesity Research Articles

646 - Prostatic enlargement and chronic inflammation in association with downregulation of SQSTM1/p62 in high fat diet induced obesity rat model

646 - Prostatic enlargement and chronic inflammation in association with downregulation of SQSTM1/p62 in high fat diet induced obesity rat model

Whole Egg Consumption Decreases Cumulative Weight Gain in Diet-Induced Obese Rats

Whole egg (WE) consumption has been demonstrated to attenuate body weight (BW) gain and adiposity in genetic animal models of type 2 diabetes (T2D). This finding was accompanied by increased food consumption. This study aimed to examine the effects of long-term WE intake on BW gain, fat distribution, and food intake in a rat model of diet-induced obesity (DIO). Male Sprague Dawley rats (n=24) were obtained at 5 wk of age and were randomly weight-matched across 1 of 4 dietary intervention groups (6 rats per group): a casein-based diet (CAS), a high-fat high-sucrose CAS diet (HFHS CAS), a whole egg-based diet (EGG), or a high-fat high-sucrose EGG diet (HFHS EGG). All diets provided 20% (w/w) protein and were provided for 33 wk. HFHS diets provided ∼61% of kilocalories from fat and 10% from sucrose. Daily weight gain and food intake were recorded, biochemical parameters were measured via ELISA, and epididymal fat pad weights were recorded at the end of the study. At 33 wk, cumulative BW gain in DIO rats fed HFHS EGG resulted in 23% lower weight gain compared with DIO rats fed HFHS CAS (P <0.0001), but no significant differences in BW gain were observed between the HFHS EGG group and the control EGG and CAS groups (P=0.71 and P=0.61, respectively). Relative food intake (grams per kilogram BW) was 23% lower (P<0.0001) in rats fed HFHS CAS compared with CAS, whereas there was no difference in food intake within the EGG dietary groups. DIO rats fed HFHS EGG exhibited a 22% decrease in epididymal fat weight compared with their counterparts fed the HFHS CAS. Our data demonstrate that consumption of a WE-based diet reduced BW gain and visceral fat in the DIO rat, similar to our previous findings in a genetic rat model with T2D.

Liraglutide shows superior cardiometabolic benefits than lorcaserin in a novel free choice diet-induced obese rat model

Lorcaserin (LORCA) and liraglutide (LIRA) were evaluated in a novel diet-induced obese (DIO) rat model fed a free choice (FC) diet, that presents rats with the options between control chow (CC) or high fat/cholesterol (HFC) diet, and normal water (NW) or 10% fructose water (FW).After 8 weeks of FC diet-induced obesity/insulin resistance, rats were maintained on FC diet and treated daily for 5 weeks with vehicle, LORCA 18 mg/kg orally or LIRA 0.4 mg/kg subcutaneously.Compared to CC diet, FC diet resulted in higher intake of HFC and FW, and significantly higher caloric intake and overweight. LIRA induced a lower HFC/FW and higher CC/NW intake, a 12% body weight loss (P < 0.01 vs. FC) and 40% lower visceral fat mass (P < 0.001). LORCA only reduced HFC intake and body weight gain (P < 0.001 vs. FC).FC diet raised HOMA-IR index and plasma leptinemia by 66% and 165% (both P < 0.05 vs. CC), which were 50% and 70% lower with LIRA (both P < 0.05 vs. FC), but unchanged by LORCA.LIRA and LORCA significantly improved FC diet-induced glucose intolerance. Only LIRA reduced liver fatty acids, triglycerides, and cholesterol by 68, 71 and 51% (all P < 0.001). FC diet also induced a diastolic dysfunction with reduced E/A ratio (P < 0.01 vs. CC), which was improved by LIRA and LORCA (both P < 0.01 vs. FC). LIRA also raised fractional shortening (P < 0.01 vs. FC).Overall, LIRA showed superior cardiometabolic benefits than LORCA in DIO rats under the FC diet, a model that will be useful to evaluate novel drugs targeting obesity and co-morbidities.

Anti-obesity activity of gold nanoparticles synthesized from Salacia chinensis modulates the biochemical alterations in high-fat diet-induced obese rat model via AMPK signaling pathway

Salacia chinensis (SC) is generally known as Saptrangi, which has been used as an herb in Ayurvedic medicine and has a broad range of biological applications. The current research was planned to develop Salacia chinensis-loaded gold nanoparticles (SC-AuNPs) and to assess the anti-obesity parameters in a high-fat diet (HFD) treated obese rats. SC-AuNPs were synthesized and characterized using UV–visible spectroscopy, SEM, FTIR, EDX, XRD, and TEM. Furthermore, the bodyweight changes, BMI, adipose index, leptin, resistin, adiponectin, AI, CRI, liver marker enzymes, inflammatory markers, lipid profile, AMPK signaling proteins, and liver histopathological changes were analyzed. We observed that the synthesized SC-AuNPs had a spherical shape, crystalline nature, and possessed a different functional group. The SC-AuNPs treatments also decreased body weight, BMI, adipose index, leptin, resistin, AI, CRI, liver marker enzymes, lipid profile, inflammatory markers, and AMPKα1. On the other hand, SC-AuNPs treatment increased adiponectin, HDL-C, and pAMPKα1. The histopathological findings showed improved result with reduced hepatocyte degradation under the influence of SC-AuNPs treatment.

Effect of electroacupuncture on silent information regulator 1, fork head transcription factor O1 and proopiomelanocortin in the hypothalamus of rats with obesity induced by high-fat diet

To investigate the effect of electroacupuncture (EA) on silent information regulator 1 (SIRT1), forkhead transcription factor O1 (FoxO1), and proopiomelanocortin (POMC) in the hypothalamus of rats with high-fat diet-induced obesity (DIO), as well as the mechanism of EA in regulating central appetite peptides to help lose weight. Male Wistar rats were randomly divided into normal group, model group, EA group, EA＋inhibitor group, inhibitor group, and sham-operation group, with 10 rats in each group. High-fat diet was used to establish a rat model of DIO. The rats in the EA group and EA＋inhibitor group were given EA at "Fenglong" (ST40), "Zhongwan "(CV12)，"Guanyuan "(CV4), and"Zusanli" (ST36) with continuous wave at a frequency of 2 Hz and an intensity of 1 mA, for 10 minutes each time. The rats in the EA＋inhibitor group and inhibitor group were given tube placement in the third ventricle and injection of the specific SIRT1 antagonist EX-527. The rats in the sham-operation group were given tube placement in the third ventricle and injection of artificial cerebrospinal fluid. The above treatment was given 3 times a week for 8 weeks in total. Body weight, food intake, and Lee's index were observed before and after treatment. An automatic biochemical analyzer was used to measure the serum levels of total cholesterol (TC), triglyceride (TG), and free fatty acid (FFA), and Western blot was used to measure the protein expression of SIRT1, FoxO1, acetylated FoxO1(AC-FoxO1), and POMC in the hypothalamus. Before treatment, the model group, the EA group, the EA＋inhibitor group, the inhibitor group, and the sham-operation group had significantly higher body weight and food intake than the normal group (P<0.01), and the model group and the sham-operation group had a significantly higher Lee's index than the normal group (P<0.05). Compared with the model group after treatment, the EA group and the EA＋inhibitor group had significant reductions in body weight, food intake, TC, and the protein expression of AC-FoxO1 (P<0.01, P<0.05) and significant increases in the protein expression of SIRT1, FoxO1 and POMC (P<0.01, P<0.05); the EA group had significant reductions in Lee's index and the levels of TG, FFA(P<0.05，P<0.01)；the inhibitor group had significant increases in food intake, the serum levels of TC, TG, FFA(P<0.01) and significant reductions in the protein expression of SIRT1, FoxO1 and POMC (P<0.01，P<0.05). Compared with the EA group, the EA＋inhibitor group and the inhibitor group had significant increases in body weight, food intake, Lee's index, the levels of TG, FFA and the protein expression of AC-FoxO1 (P<0.01, P<0.05) and significant reductions in the protein expression of SIRT1, FoxO1 and POMC (P<0.01); the inhibitor group had significant increases in the serum levels of TC (P<0.01). Compared with the EA＋inhibitor group, the inhibitor group had significant increases in body weight, food intake, the serum levels of TC, TG, FFA, and the protein expression of AC-FoxO1 (P<0.01), as well as significant reductions in the protein expression of SIRT1, FoxO1 and POMC (P<0.01). In rats with DIO, EA can effectively up-regulate the expression of SIRT1 in the hypothalamus, exert a deacetylation effect on FoxO1, and promote the expression of the downstream appetite-inhibiting peptide POMC, which may be one of the mechanisms of EA to help lose weight by regulating central appetite peptides in the obesity model.

Effects of dietary copper deficiency on adipocyte functions in a rat model of high-fructose diet-induced obesity

Background High fructose intake has been reported to impair copper (Cu) status, leading to low Cu availability with exacerbation of Cu-deficiency complications. These Cu–fructose interactions have been well documented in rats. Aims This experimental study was designed to evaluate the effects of dietary Cu deficiency on lipid profile in addition to adipocyte functions in the form of adiponutrin level and antioxidant capacity in a high-fructose diet-induced obesity rat model. Materials and methods The study was conducted on 60 male albino rats that were divided randomly into four equal groups as follows: group I (control group), group II (Cu-deficient group), group III (high fructose group), and group IV (Cu-deficient/high-fructose group). Plasma Cu level was measured by inductively coupled plasma optical emission spectrometry. Plasma ceruloplasmin and adipose tissue superoxide dismutase activities were assayed calorimetrically. Adiponutrin level in adipose tissue was measured by enzyme-linked immunosorbent assay. Results Plasma Cu level, ceruloplasmin activity, and adipose tissue superoxide dismutase activity were significantly decreased in Cu-deficient/high-fructose group when compared with other studied groups. However, adiponutrin level in adipose tissue was significantly increased in Cu-deficient/high-fructose group compared with other studied groups. Conclusion The modulated adiponutrin level, oxidative stress, dyslipidemia, and adipose tissue inflammation were highlighted as the principal culprits mediating Cu-deficiency and high-fructose diet complications such as nonalcoholic steatohepatitis.

Genome-Wide Regulation of Electroacupuncture and Treadmill Exercise on Diet-Induced Obese Rats.

Acupuncture has been widely used for obesity treatment, but its mechanism is still unclear. To investigate the molecular mechanisms, we applied electroacupuncture (EA) at the Zusanli (ST36) acupoint and treadmill exercise (TE) in a diet-induced obese (DIO) rat model and used RNA sequencing (RNA-seq) to identify molecular consequences. Forty Sprague-Dawley male rats were selected and randomly divided into five groups: control (C), DIO model (M), EA, TE, and EA + TE groups. According to the results, acupuncture reduced body weight and the ratio of retroperitoneal white adipose tissue (retro-WAT) to body weight. Total RNA was extracted from the retro-WAT from five groups for RNA-seq. Differentially expressed genes (DEG) analysis showed that there were obvious differences among the four comparisons of C vs. M, M vs. EA, M vs. TE, and M vs. EA + TE, followed by 1383, 913, 3324, and 2794 DE genes. Gene ontology (GO) term enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis were performed to further classify the DEGs. Several GO terms were commonly significantly enriched in both M vs. TE and M vs. EA, such as myofibril and muscle contraction. In addition, some pathways were regulated by EA and TE, such as the peroxisome proliferator activated receptor signaling pathway and calcium signaling pathway. This study is the first to compare and analyze the differences in gene expression profiles in the retro-WAT of rats in different groups, which provide a clue for further investigation into the molecular mechanisms of obesity treatment by EA and TE.

Establishment of the diet-induced obese rat model for atrial fibrillation.

Establishment of the diet-induced obese rat model for atrial fibrillation.

Protective Effect of Indole-3-Carbinol on Sperm Morphometric Alteration in a High-Fat Diet-Induced Obese Rat Model

Protective Effect of Indole-3-Carbinol on Sperm Morphometric Alteration in a High-Fat Diet-Induced Obese Rat Model

Metformin Reduces Lipotoxicity-Induced Meta-Inflammation in β-Cells through the Activation of GPR40-PLC-IP3 Pathway.

Background and Purpose Metformin, a widely used antidiabetic drug, has been shown to have anti-inflammatory properties; nevertheless, its influence on β-cell meta-inflammation remains unclear. The following study investigated the effects of metformin on meta-inflammatory in β-cells and whether the underlying mechanisms were associated with the G protein-coupled receptor 40-phospholipase C-inositol 1, 4, 5-trisphosphate (GPR40-PLC-IP3) pathway. Materials and Methods Lipotoxicity-induced β-cells and the high-fat diet-induced obese rat model were used in the study. Results Metformin-reduced lipotoxicity-induced β-cell meta-inflammatory injury was associated with the expression of GPR40. GPR40 was involved in metformin reversing metabolic inflammation key marker TLR4 activation-mediated β-cell injury. Furthermore, downstream signaling protein PLC-IP3 of GPR40 was involved in the protective effect of metformin on meta-inflammation, and the above process of metformin was partially regulated by AMPK activity. In addition, the anti-inflammatory effects of metformin were observed in obese rats. Conclusion Metformin can reduce lipotoxicity-induced meta-inflammation in β-cells through the regulation of the GPR40-PLC-IP3 pathway and partially via the regulation of AMPK activity.

Metabolic Effects of the Sweet Protein MNEI as a Sweetener in Drinking Water. A Pilot Study of a High Fat Dietary Regimen in a Rodent Model.

Sweeteners have become integrating components of the typical western diet, in response to the spreading of sugar-related pathologies (diabetes, obesity and metabolic syndrome) that have stemmed from the adoption of unbalanced dietary habits. Sweet proteins are a relatively unstudied class of sweet compounds that could serve as innovative sweeteners, but their introduction on the food market has been delayed by some factors, among which is the lack of thorough metabolic and toxicological studies. We have tried to shed light on the potential of a sweet protein, MNEI, as a fructose substitute in beverages in a typical western diet, by studying the metabolic consequences of its consumption on a Wistar rat model of high fat diet-induced obesity. In particular, we investigated the lipid profile, insulin sensitivity and other indicators of metabolic syndrome. We also evaluated systemic inflammation and potential colon damage. MNEI consumption rescued the metabolic derangement elicited by the intake of fructose, namely insulin resistance, altered plasma lipid profile, colon inflammation and translocation of lipopolysaccharides from the gut lumen into the circulatory system. We concluded that MNEI could represent a valid alternative to fructose, particularly when concomitant metabolic disorders such as diabetes and/or glucose intolerance are present.

Anti-obesity effect of cocoa proteins (Theobroma cacao L.) variety “Criollo” and the expression of genes related to the dysfunction of white adipose tissue in high-fat diet-induced obese rats

Abstract The objective of this work was to evaluate if Cocoa Proteins (CP) from the cocoa-bean were able to reduce factors related to obesity and activated related gene targets against white adipose tissue (WAT) dysfunction in a rat model of hypercaloric diet-induced obesity. The results showed that the administration with 150 mg/kg/day of CP on a hypercaloric diet reduces body-weight gain, relative weight of WAT, serum triglycerides, NEFAs, insulin, and leptin levels, and pro-inflammatory factors, with an increase in serum HDL levels, activation (AMPK, PPAR-γ, PPAR-α, SIRT1, Plin1, and PGC-1α) and repression (TNF-α, SREBP-1c, Leptin and ACC) of the mRNA of transcription factors and proteins related to WAT dysfunction. The CP prevented dysfunction in WAT who is related to obesity by down-regulation of factors related to lipogenesis and up-regulation of those related to energy expenditure, lowering the release of triglycerides and NEFAs into peripheral tissues, thus decreasing pro-inflammatory processes.

Xiexin Tang ameliorates dyslipidemia in high-fat diet-induced obese rats via elevating gut microbiota-derived short chain fatty acids production and adjusting energy metabolism

Ethnopharmacological relevanceTraditional herbal medicine has been taken as a new and effective approach to treat many chronic diseases. Xiexin Tang (XXT), a compound recipe composed of Dahuang (Rheum palmatum L.), Huangqin (Scutellaria baicalensis Georgi) and Huanglian (Coptis chinensis Franch.), has been reported to have hypoglycemic and hypolipidemic effects, but its mechanism remains unclear. Our previous study found that Xiexin Tang markedly ameliorated the composition of the gut microbiota, especially for some short chain fatty acids (SCFAs) producing bacteria, and then notably increased SCFAs production. However, the mechanism of XXT on the fermentation of gut bacteria and further improvement of obesity is not yet clear. Aim of the studyThis study aimed to unravel the molecular mechanism of XXT on the amelioration of obesity. Materials and methodsHere, high-fat diet-induced obese rat model was established to investigate the intervention efficacy following oral administration of XXT. Additionally, the expressions of key enzymes of gut microbe-derived SCFAs biosynthesis and key targets in the signaling pathway of energy metabolism were investigated by ELISA and qPCR analysis. ResultsResults showed that XXT could notably correct lipid metabolism disorders, alleviate systematic inflammation, improve insulin sensitivity and reduce fat accumulation. Additionally, XXT could increase gut microbiota-derived SCFAs-producing capacity by enhancing mRNA levels and activities of SCFA-synthetic key enzymes such as acetate kinase (ACK), methylmalonyl-CoA decarboxylase (MMD), butyryl-CoA: acetate CoA transferase (BUT) and butyrate kinase (BUK), which markedly decreased the adenosine triphosphate (ATP) contents, elevated adenosine diphosphate (ADP) and adenosine monophosphate (AMP) levels and further lowered the energy charge (EC) in obese rats via activating peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)/uncoupling protein-2 (UCP-2) signaling pathway. What's more, XXT could notably ameliorate dyslipidemia via increasing the gene expression of 5′-AMP-activated protein kinase (AMPK) and blocking mammalian target of rapamycin (mTOR) signaling pathway. ConclusionsTaken together, our data provided a novel insight into the role of XXT in losing weight from energy metabolism regulation, which unraveled the molecular mechanism of XXT on the alleviation of dyslipidemia and fat heterotopic accumulation. The study provided useful information for XXT in clinical application to treat obesity.

The preprohormone expression profile of enteroendocrine cells following Roux-en-Y gastric bypass in rats

ObjectiveRoux-en-Y gastric bypass (RYGB) leads to rapid remission of type 2 diabetes (T2D) and sustained body weight loss, but the underlying molecular mechanisms are still not fully understood. To further elucidate these mechanisms and identify potentially novel preprohormone encoding genes with anti-diabetic and/or anti-obesity properties, we performed a comprehensive analysis of gene expression changes in enteroendocrine cells after RYGB in diet-induced obese (DIO) rats. MethodsThe mRNA expression profiles of enteroendocrine cell enriched samples were characterized at 9, 22 and 60 days after RYGB surgery in a DIO rat model. Enteroendocrine cells were identified by chromogranin A immunohistochemistry and isolated by laser capture microdissection (LCM) from five regions covering the full rostro-caudal extension of the gastrointestinal (GI) tract. RNA sequencing and bioinformatic analyses were subsequently applied to identify differentially expressed preprohormone encoding genes. ResultsFrom the analysis of enteroendocrine cell mRNA expression profiles, a total of 54 preprohormones encoding genes were found to be differentially regulated at one or more time-points following RYGB. These included well-known RYGB associated preprohormone genes (e.g. Gcg, Cck, Gip, Pyy and Sct) and less characterized genes with putative metabolic effects (e.g. Nmu, Guca2a, Guca2b, Npw and Adm), but also 16 predicted novel preprohormone genes. Among the list of gene transcripts, Npw, Apln and Fam3d were further validated using in situ mRNA hybridization and corresponding peptides were characterized for acute effects on food intake and glucose tolerance in mice. ConclusionWe present a comprehensive mRNA expression profile of chromogranin A positive enteroendocrine cells following RYGB in rats. The data provides a region-specific characterization of all regulated preprohormone encoding genes in the rat GI tract including 16 not hitherto known. The comprehensive catalogue of preprohormone expression changes may support our understanding of hormone mediated effects of RYGB on diabetes remission and body weight reduction.

2004-P: Liraglutide Shows Better Weight Loss and Cardiometabolic Benefits than Lorcaserin and Pioglitazone in a Novel Diet-Induced Obese Rat Model

To evaluate drugs targeting obesity/type 2 diabetes on weight loss and cardiometabolic benefits, and mimic human hyperenergetic nutritional behavior, we set-up a new diet-induced obese (DIO) rat model fed a free choice (FC) diet: control chow (CC) or high fat/cholesterol (HFC) diet, and normal water (NW) or 10% fructose water (FW). After an 8-week FC diet period, rats were treated with vehicle, liraglutide 0.4mg/kg s.c. QD (LIRA, a GLP-1 receptor agonist), lorcaserin 18mg/kg p.o. QD (LORCA, a 5-HT2C receptor agonist) and pioglitazone 10mg/kg p.o. QD (PIO, a PPARgamma agonist) for 5 weeks. FC diet induced high intake of HFC and FW, resulting in significantly higher caloric intake and overweight, as compared with rats fed a CC diet alone. LIRA induced a 12% body weight loss (p&amp;lt;0.01 vs. FC), with marked reduction in HFC and FW intake and lower visceral fat mass (p&amp;lt;0.001). LORCA induced lower body weight gain (p&amp;lt;0.001 vs. FC), while PIO showed higher body weight gain (p&amp;lt;0.01). FC diet raised HOMA-IR index by 66% (p&amp;lt;0.05 vs. CC), which was 50% lower with LIRA and PIO (both p&amp;lt;0.05 vs. FC), but unchanged by LORCA. Glucose intolerance induced by FC diet was significantly improved by LIRA, LORCA and PIO. During an insulin tolerance test, glucose area under the curve was 27% higher in FC rats (p&amp;lt;0.001 vs. CC) and was significantly reduced by LIRA and PIO, but not by LORCA. LIRA reduced liver fatty acids, triglycerides and cholesterol by 68, 71 and 51% (all p&amp;lt;0.001). PIO reduced liver triglycerides and LORCA had no effect on liver steatosis. Using echocardiography, we detected a diastolic dysfunction with reduced E/A ratio under FC diet (p&amp;lt;0.01 vs. CC), which was improved by both LIRA and LORCA (both p&amp;lt;0.01 vs. FC). LIRA also raised fractional shortening (p&amp;lt;0.01 vs. FC). In conclusion, LIRA showed superior cardiometabolic benefits than LORCA and PIO in our DIO rat fed a FC diet. This novel model mimicking human overfeeding will be useful to evaluate drugs targeting obesity/type 2 diabetes. Disclosure F. Briand: Employee; Self; Physiogenex. E. Brousseau: Employee; Self; Physiogenex. T. Sulpice: Employee; Self; Physiogenex.

Renin-angiotensin System (RAS)-mediated Antiobesity and Antihypertensive Effects of Korean Traditional Soybean Paste (Doenjang) in Rat Model of Diet-induced Obesity (P08-097-19)

ObjectivesHypertension is becoming more prevalent and one of the main cause is found in the increase of excessive dietary sodium intake. It is also risk factors for cardiovascular and kidney disease. Korean Traditional Fermented Food, doenjang, is made with high salt, so many of them are thinking that there is a lot of relation to hypertension despite reporting many health benefits. Our previous studies reported that doenjang have been associated effect of anti-obesity in human and animal study. Therefore, we expected that doenjang may have different effects on blood pressure and lipid metabolism compared to same concentrations of salt. MethodsIn this study, Sprague-Dawley rats divided into four groups, normal diet (ND), high fat diet (HD), high fat diet with 8% table salt (HDS), high fat diet with Doenjang contains 8% table salt (HDJ) for 13 weeks. The systolic blood pressure (SBP), serum chemistry, Na+ and K+ concentrations, liver and renal gene expressions were measured. ResultsDoenjang decreased systolic blood pressure (SBP), body weight and hepatic lipids. Serum chemistry, leptin and aldosterone levels were increased in HD and HDS groups while decreased in HDJ group. Results from analysing feces and urine, Na+, Ca+ and K+concentrations were changed by Doenjang. Furthermore, fatty acid synthesis-related genes expression was decreased in liver and downregulated the renin, AT1 receptor and ACE in renal cortex of doenjang treatment group. ConclusionsThese results suggest that doenjang may have anti-obesity and anti-hypertension through regulation of the renin angiotensin system. We believed that it is an important result of demonstrating that doenjang has health benefits regardless of salt content. Funding SourcesThis work was supported by the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MEST) (No. 2018R1A2B6006477).

A histomorphometric study on the hepatoprotective effects of a green rooibos extract in a diet-induced obese rat model

Obesity, type two diabetes mellitus and insulin resistance are associated with increased oxidative stress and inflammation. Unfermented green rooibos is an aspalathin rich variant of traditional fermented rooibos (Aspalathus linearis) and has a high polyphenol content. The present study aimed to determine the histologically observable effects of a commercially produced, aspalathin-rich green rooibos extract, Afriplex GRT™ (GRE) in a diet-induced obese rat model. Male Wistar rats (N = 28) were randomly assigned to four study groups (n = 7): control (C), green rooibos (GRT), high-fat diet (HFD) and experimental (HFD-GRT) group. Body mass was determined prior to euthanasia and liver mass was determined after death. The left lateral lobe of the liver was processed to wax and stained using haematoxylin and eosin (H & E), Masson’s trichrome stain, Gordons and Sweet’s reticulin impregnation and periodic acid-Schiff stain. Frozen liver tissue sections were used for Oil red O staining. Morphometric quantification of steatosis, semiquantitative pathology grading and scoring were performed and verified by a veterinary histopathologist. A significant increase in body and liver mass was observed in the HFD groups while co-treatment with green rooibos significantly reduced both. The volume and area of steatosis were significantly increased in the HFD groups while the area of steatosis significantly reduced with green rooibos co-treatment. The percentage, location and type of steatosis as well as presence of inflammation and hepatocellular injury were reduced in the HFD group co-treated with GRE. These findings suggest that a GRE has potential as an anti-steatotic, anti-inflammatory and weight reducing agent in vivo.

Protective effect of prebiotic and exercise intervention on knee health in a rat model of diet-induced obesity

Obesity, and associated metabolic syndrome, have been identified as primary risk factors for the development of knee osteoarthritis (OA), representing nearly 60% of the OA patient population. In this study, we sought to determine the effects of prebiotic fibre supplementation, aerobic exercise, and the combination of the two interventions, on the development of metabolic knee osteoarthritis in a high-fat/high-sucrose (HFS) diet-induced rat model of obesity. Twelve-week-old male Sprague-Dawley rats were randomized into five groups: a non-exercising control group fed a standard chow diet, a non-exercising group fed a HFS diet, a non-exercising group fed a HFS diet combined with prebiotic fibre supplement, an exercise group fed a HFS diet, and an exercise group fed a HFS diet combined with prebiotic fibre supplement. Outcome measures included knee joint damage, percent body fat, insulin sensitivity, serum lipid profile, serum endotoxin, serum and synovial fluid cytokines and adipokines, and cecal microbiota. Prebiotic fibre supplementation, aerobic exercise, and the combination of the two interventions completely prevented knee joint damage that is otherwise observed in this rat model of obesity. Prevention of knee damage was associated with a normalization of insulin resistance, leptin levels, dyslipidemia, gut microbiota, and endotoxemia in the HFS-fed rats.

Alteration in iron efflux affects male sex hormone testosterone biosynthesis in a diet-induced obese rat model.

This study was motivated by clinical observations that dysmetabolic iron overload syndrome (DIOS) and an androgen deficiency are common features observed in obese adult men; however, the molecular mechanism underlying the effects of DIOS on androgen deficiency remains to be elucidated. We established a DIOS animal model by feeding Sprague-Dawley rats an iron/fat-enriched diet (50% fat plus 0.25, 1, or 2 g ferric iron per kg diet) for 12 weeks to induce iron dysfunction (indicated by decreased tissue iron efflux) in obese rats. Obese rats fed an iron/fat-enriched diet showed decreased levels of testicular total Testosterone (T) and iron exporter ferroportin but increased levels of testicular iron and hepcidin, and these effects were more evident with a >1 g ferric iron per kg diet. A western blot analysis showed that an iron/fat-enriched diet triggered testicular endoplasmic reticular (ER) stress but decreased mitochondrion biogenesis proteins (PGC1α and TFAM) and T-converting proteins (StAR, CYP11A, and 17β-HSD). TUNEL staining showed that >1 g ferric iron induced apoptosis mainly in germ cells and Leydig's cells. Uncontrolled testicular iron efflux may cause mitochondrial-ER dysfunction and affect T biosynthesis. Future study targeting the testicular hepcidin-ferroportin axis may offer a therapeutic tool to alleviate testicular iron retention and mitochondrial-ER stress in Leydig's cells.

Anti-Obesity, Anti-Atherosclerotic and Anti-Oxidant Effects of Pu-Erh Tea on a High Fat Diet-Induced Obese Rat Model

Pu-erh tea, a traditional Chinese beverage, has been believed to have many benefits to human health and without side effects. In this study, we systematically analyzed the main active components of Pu-erh tea and investigated its anti-obesity, anti-atherosclerotic and anti-oxidant effects using an obese rat model. Obesity was induced by feeding a high-fat diet and subsequently the experimental obese mice were fed with high-fat diet supplemented with low (2.5%), medium (5%) or high (7.5%) doses of Pu-erh tea powder for 6 weeks respectively. As result, the body weight gain of the rats was decreased by medium and high doses of Pu-erh tea treatments. Furthermore, the levels of serum total cholesterol (TC), triglyceride (TG) and atherosclerosis index (AI) were significantly lowered by Pu-erh tea compared to the control group. Conversely, high density lipoproteincholesterol (HDL-C) level of the rats was significantly elevated by Pu-erh tea treatments. In addition, Pu-erh tea treatments increased the activities of anti-oxidative enzymes such as superoxide dismutase (SOD) and glutathione peroxides (GSH-Px), whereas reduced the level of lipid peroxidation product malondialdehyde (MDA) in obese rats. Collectively, our find-ings revealed that Pu-erh tea exerts comprehensive benefits in anti-obesity, anti-atherosclerotic and anti-oxidant effects, therefore can be used as a promising functional food in obesity management.