Rat Adipose Tissue Research Articles

Влияние сшивающих агентов на матриксные свойства гидрогелевых структур на основе альгината натрия

A comparative study of gelation processes in aqueous solutions of sodium alginate initiated by their chemical crosslinking with divalent ions Ca2+ or Ba2+ was carried out. 3D cryoprinted hydrogel scaffolds of certain architectonics were formed from the studied compositions containing various concentrations of crosslinking agents. It is shown that the increase in the crosslinking agent concentration from 2 to 10 wt. % leads to the improvement in the strength characteristics of alginate structures. At the same time, scaffolds crosslinked with 10 % aqueous solutions of both CaCl2 and BaCl2 retain their structural stability during 21 days of incubation in a culture medium at a temperature of 37 °C. During in vitro experiments on cultures of mesenchymal stem cells derived from rat adipose tissue, samples crosslinked with Ba2+ ions were found to demonstrate a moderate cytotoxic effect and showed their inability to maintain cell adhesion, unlike non-toxic scaffolds crosslinked in CaCl2 aqueous solutions. In vivo analysis of experimental samples on an intramuscular implantation model for male Wistar rats also confirmed moderate cytotoxicity of alginate scaffolds formed using Ba2+ ions as crosslinking agents. The results obtained allow us to assert that of all the studied by us materials, sodium alginate crosslinked with a 10% CaCl2 aqueous solution can be considered the most promising for various biomedical applications.

Edible and medicinal mushrooms (Pleurotus ostreatus, Ustilago maydis, Ganoderma lucidum) reduce endoplasmic reticulum stress and inflammation in adipose tissue of obese Wistar rats fed with a high fat plus saccharose diet.

Obesity is an increasing global public health problem. A strategy to treat obesity is the use of functional foods. Edible and medicinal mushrooms contain diverse bioactive compounds showing important antihyperlipidemic, antioxidant, and prebiotic properties. We analysed the effects of adding (10%) of Pleurotus ostreatus (Po, basidiomata), Ganoderma lucidum (Gl, basidiomata), or Ustilago maydis (Um, galls), milled, to a high fat plus saccharose diet (HFD + S) for 6 months in a model of obesity with Wistar rats. We assessed weight gain, body composition, lipid parameters, endoplasmic reticulum stress (proteins and inflammatory markers: BiP, XBP-1, JNK, p-JNK, TNF-α), and adiponectin in subcutaneous adipose tissue (SAT). The consumption of edible and medicinal mushrooms decreased weight gain (-17.2-30.1%) and fat mass (-23.7-43.1%), maintained fat-free mass, reduced levels of serum biochemical parameters (TC: -40.1-44.1%, TG: -37.7-51.6%, LDL-C: -64.5-71.1%), and prevented adipocyte hypertrophy (-30.9-36.9%) and collagen deposition (-70.9-73.7%) in SAT. Compared with the HFD + S group, mushroom consumption by Wistar rats significantly reduced the expression of proteins associated with endoplasmic reticulum stress and inflammation (BiP: -72.2-88.2%; XBP-1: -71.5-81.8%; JNK: -71.2-90.0%; p-JNK: -37.3-81.0%; TNF-α: -80.7-91.5%), whereas significantly increased adiponectin protein expression (246.4-654.2%) in SAT. These effects outperformed those obtained through the commercial lipid-lowering drug atorvastatin, contributing synergistically to prevent further obesity-related dysfunctions, such as insulin resistance derived from inflammation and ER stress in adipose tissue. Bioactive compounds from edible, functional and medicinal mushrooms represent new emerging therapies for obesity treatments using natural products.

Antiobesity Effect of Lacticaseibacillus paracasei LM-141 on High-Fat Diet-Induced Rats through Alleviation of Inflammation and Insulin Resistance.

In this study, we set out to evaluate the antiobesity activities of our newly isolated Lacticaseibacillus paracasei LM-141 (LPLM141) using a high-fat diet (HFD)-fed rat model. Male Sprague-Dawley rats were fed with a HFD with or without low-dosage (2 × 107 CFU/day per rat) or high-dosage (2 × 109 CFU/day per rat) LPLM141 for 14 weeks. The results showed that administration of LPLM141 significantly decreased body weight gain, liver weight, adipose tissue weight, and epididymal white adipocyte size increased by HFD feeding. The abnormal serum lipid profile induced by HFD feeding was normalized by administration of LPLM141. The enhanced chronic low-grade inflammation in HFD-fed rats was reduced by LPLM141 supplementation, as reflected by decreased serum lipopolysaccharide (LPS) and monocyte chemoattractant protein-1 (MCP-1) levels, reduced macrophage infiltration in adipose tissue, and increased serum adiponectin concentration. In addition, the elevations of proinflammatory cytokine genes and suppression of PPAR-γ mRNA in adipose tissues of rats fed with a HFD were markedly reversed by LPLM141 administration. Oral administration of LPLM141 induced browning of epididymal white adipose tissue (eWAT) and activation of interscapular brown adipose tissue (iBAT) in rats fed with HFD. Consumption of LPLM141 exhibited a significant amelioration in insulin resistance, which were mechanistically caused by downregulation of the serum leptin level and upregulation of hepatic IRS-1 and p-Akt protein expressions, in HFD treated rats. LPLM141 consumption significantly decreased hepatic lipogenic gene expressions and preserved liver function stimulated by HFD treatment. Administration of LPLM141 obviously mitigated hepatic steatosis observed in HFD feeding rats. Our current findings shed light on LPLM141 supplementation that exhibited an antiobesity effect in HFD-fed rats by alleviating inflammation and insulin resistance, which further highlighted the potential of utilizing LPLM141 as a preventive/therapeutic probiotic agent for obesity.

The Synergistic Protective Effect of γ-Oryzanol (OZ) and N-Acetylcysteine (NAC) against Experimentally Induced NAFLD in Rats Entails Hypoglycemic, Antioxidant, and PPARα Stimulatory Effects.

This study estimated that the combined effect of γ-Oryzanol and N-acetylcysteine (NAC) against high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) in rats also estimated some of their mechanisms of action. Adult male rats were divided into seven groups (n = 8 each) as control, control + NAC, control + γ-Oryzanol, HFD, HFD + NAC, HFD + γ-Oryzanol, and HFD + NAC + γ-Oryzanol. NAC was administered orally at a final concentration of 200 mg/kg, whereas γ-Oryzanol was added to diets at a concentration of 0.16. All treatments were conducted for 17 weeks and daily. Both NAC and γ-Oryzanol were able to reduce final body weights, fat weights, fasting glucose, fasting insulin, serum, and serum levels of liver function enzymes as well as the inflammatory markers such as tumor necrosis factor-α (TNF-α), interleukine-6 (IL-6), and leptin in HFD-fed rats. They also improved hepatic structure and glucose tolerance, increased adiponectin levels, and reduced serum and hepatic levels of triglycerides (TGs) and cholesterol (CHOL) in these rats. These effects were concomitant with a reduction in the hepatic levels of lipid peroxides (MDA) and serum levels of LDL-C, but also with an increment in the hepatic levels of superoxide dismutase (SOD) and glutathione (GSH). Interestingly, only treatment with γ-Oryzanol stimulated the mRNA levels of proliferator-activated receptor alpha (PPARα) and carnitine palmitoyltransferase 1 (CPT1) in the liver and white adipose tissue (WAT) of rats. Of note, the combination therapy of both drugs resulted in maximum effects and restored almost normal liver structure and basal levels of all the above-mentioned metabolic parameters. In conclusion, a combination therapy of γ-Oryzanol and NAC is an effective therapy to treat NAFLD, which can act via several mechanisms on the liver and adipose tissue.

Intrauterine androgen exposure impairs gonadal adipose tissue functions of adult female rats

Prenatal androgen exposure induces fetal programming leading to alterations in offspring health and phenotypes that resemble those seen in women with Polycystic Ovary Syndrome. It has been described that prenatal androgenization affects the reproductive axis and leads to metabolic and endocrine disorders. Adipose tissue plays a crucial role in all these functions and is susceptible to programming effects. Particularly, gonadal adipose tissue is involved in reproductive functions, so dysfunctions in this tissue could be related to fertility alterations. We aimed to investigate the extent to which prenatal hyperandrogenization is able to alter the functionality of gonadal adipose tissue in female adult rats, including lipid metabolism, adipokines expression, and de novo synthesis of steroids. Pregnant rats were treated with 1 mg of testosterone from day 16 to day 19 of pregnancy, and female offspring were followed until 90 days of age, when they were euthanized. The prenatally hyperandrogenized (PH) female offspring displayed two phenotypes: irregular ovulatory (PHiov) and anovulatory (PHanov). Regarding lipid metabolism, both PH groups displayed disruptions in the main lipid pathways with altered levels of triglyceride and increased lipid peroxidation levels. In addition, we found that Peroxisome Proliferator-Activated Receptors (PPARs) alpha protein expression was decreased in both PH phenotypes (p < 0.05), but no changes were found in PPARγ protein levels. Furthermore, regarding adipokines, no changes were found in Leptin and Adiponectin protein levels, but Chemerin protein levels were decreased in the PHiov group (p < 0.05). Regarding de novo synthesis of steroids, the PHanov group showed increased protein levels of Cyp17a1 and Cyp19, while the PHiov group only showed decreased protein levels of Cyp19 (p < 0.05). These results suggest that prenatal androgen exposure affects females’ gonadal adipose tissue in adulthood, disturbing different lipid pathways, Chemerin expression, and de novo synthesis of steroids.

Anti-obesity effect of simvastatin and omega-3 and its combination on obese model male Wistar rats

Strategies to reduce obesity have become main priority for many health institution and health staff around the world, as the prevalence of obesity has risen and exacerbated in most of the world mainly because of the modern life style which tend to be more sedentary with an increase eating unhealthy fast western food. Many years ago, the lipid-lowering drug simvastatin; and omega-3 were considered as a traditional lipid-lowering drug that have been well-documented to possess anti-inflammatory, cardioprotective and triglyceride-lowering properties; and their co-administration may demonstrate a complementary effect in lowering patients' triglycerides and total cholesterol to treat atherosclerosis. Many previous studies have been found other beneficial effects for simvastatin, and omega-3; since, simvastatin can be used for the treatment of Alzheimer's disease; and for prevention of prostate cancer; while omega 3 can reduce the risk of sudden cardiac death in addition to preventing obesity that has been documented by recent studies. But, the effect of simvastatin alone or its combination with omega-3 as potential anti-obesity therapy and /or protection against obesity is not yet known through their effects on thermogenic factors. Aim of the study is to evaluate the effect of simvastatin on thermogenic genes including (UCP1) using quantitative real time PCR, while the expression of uncoupling protein 1 (UCP1) protein was detected in iBAT and iWAT adipocyte by immunohistochemistry. Method One hundred twenty (120) male Wistar rats (five-six week age and weighing 100-150g) were allocated into five groups: treated with two different doses of simvastatin, omega-3 and mixed treatment, in addition to high fat diet group which considered as a control group. Treatments were given for eight weeks. Three rats from each group were weekly-authenticated along the 60 days interscapular brown adipose tissue (iBAT) and inguinal white adipose tissues (iWAT) were obtained. Results; showed that simvastatin and omega-3 have an obvious activation of UCP1genes, this reflects an increase in thermogenic process in adipose tissue in obese high fat diet rats and their combination exert a synergistic increase in the thermogenic mechanism when compared to simvastatin 9mg/ kg /day alone. Conclusion this study gives a hope for the utilization of simvastatin either alone or in combination with omega-3 as anti-obesity therapy; through their enhancement of thermogenic in white and brown adipose tissues with a consequent weight loss.

L-Arginine supplementation regulates energy-substrate metabolism in skeletal muscle and adipose tissue of diet-induced obese rats.

Dietary supplementation with l-arginine has been reported to reduce white fat mass in diet-induced obese rats and in obese humans. This study was conducted to test the hypothesis that the arginine treatment regulates glucose and fatty acid metabolism in insulin-sensitive tissues. Male Sprague-Dawley rats (4-week-old) were fed either low- or high-fat diets for 15 weeks (n = 16/diet). Thereafter, lean or obese rats were fed their respective diets and received drinking water containing either 1.51% l-arginine-HCl or 2.55% alanine (isonitrogenous control) (n = 8/treatment group). After 12 weeks of treatment, rats were euthanized and tissue samples were collected for biochemical assays. High-fat feeding increased the size of adipocytes isolated from retroperitoneal (RP) adipose tissue, while arginine treatment reduced their size. The total number of adipocytes in the adipose tissue did not differ among the four groups of rats. Glucose oxidation in extensor digitorum longus (EDL) muscle, soleus muscle, and RP adipose tissue were reduced in response to high-fat feeding. On the contrary, oleic acid oxidation in RP adipose tissue was enhanced in rats fed the high-fat diet. Arginine treatment stimulated both glucose and oleic acid oxidation in EDL and soleus muscles, while having no effect on glucose oxidation, oleic acid oxidation, or basal lipolysis per 106 adipocytes in RP adipose tissue. Collectively, these results indicate that oral supplementation with arginine to diet-induced obese rats promoted the oxidation of energy substrates in skeletal muscle, thereby reducing white fat in the body.

An obesogenic diet impairs uncoupled substrate oxidation and promotes whitening of the brown adipose tissue in rats.

Brown adipose tissue (BAT) is richin mitochondria containing uncoupling protein 1 (UCP1), and dissipates energy through thermogenesis. However, even though BAT mass and its UCP1 content increase in rodents chronically fed a high-fat sucrose-enriched (HFS) diet, marked expansion of adiposity still occurs in these animals, suggesting insufficient BAT-mediated HFS diet-induced thermogenesis. Thus, the objective of this study was to investigate the metabolic and molecular mechanisms that regulate BAT thermogenesis in HFS-induced obesity. To accomplish this, rats were fed either a standard chow or HFS diet for 8weeks. Subsequently, glucose and fatty acidmetabolism and the molecular mechanisms underlying these processes were assessed in freshly isolated primary BAT adipocytes. Despite increasing BAT mass and its UCP1 content, the HFS diet reduced uncoupled glucose and palmitate oxidation in BAT adipocytes. It also markedly diminished tyrosine hydroxylase content and lipolysis in these cells. Conversely, glucose uptake, lactate production, glycerol incorporation into lipids, palmitate incorporation into triacylglycerol (TAG), phosphoenolpyruvate carboxykinase and glycerol kinase levels, and lipoprotein lipase and cluster of differentiation 36 gene expression were increased. In summary, a HFS diet enhanced glyceroneogenesis and shifted BAT metabolism toward TAG synthesis by impairing UCP1-mediated substrate oxidation and by enhancing fatty acid esterification inintact brown adipocytes. These adaptive metabolic responses to chronic HFS feeding attenuated BAT thermogenic capacity and favoured the development of obesity. KEY POINTS: Despite increasing brown adipose tissue (BAT) mass and levels of thermogenic proteins such as peroxisome proliferator-activated receptor γ coactivator 1α, carnitine palmitoyltransferase 1B and uncoupling protein 1 (UCP1), an obesogenic high-fat sucrose-enriched (HFS) diet attenuated uncoupled glucose and fatty acid oxidation in brown adipocytes. Brown adipocytes diverted glycerol and fatty acids toward triacylglycerol (TAG) synthesis by elevating the cellular machinery that promotes fatty acid uptake along with phosphoenolpyruvate carboxykinase and glycerol kinase levels. The HFS diet increased glucose uptake that supported lactate production and provided substrate for glyceroneogenesis and TAG synthesis in brown adipocytes. Impaired UCP-1-mediated thermogenic capacity and enhanced TAG storage in BAT adipocytes were consistent with reduced adipose triglyceride lipase and tyrosine hydroxylase levels in HFS diet-fed animals.

Evaluation of Proinflammatory Cytokines in Adipose Tissue of Hypertensive Lyon Rats

Evaluation of Proinflammatory Cytokines in Adipose Tissue of Hypertensive Lyon Rats

Lycopene Improves Metabolic Disorders and Liver Injury Induced by a Hight-Fat Diet in Obese Rats.

Epidemiological studies have shown that the consumption of a high-fat diet (HFD) is positively related to the development of obesity. Lycopene (LYC) can potentially combat HFD-induced obesity and metabolic disorders in rats. This study aimed to investigate the effect of LYC on metabolic syndrome and assess its anti-inflammatory and antioxidant effects on the liver and adipose tissue in rats fed an HFD. Thirty-six male Wistar albino rats were divided into three groups. Group Ι (the control group) was fed a normal diet, group ΙΙ (HFD) received an HFD for 16 weeks, and group ΙΙΙ (HFD + LYC) received an HFD for 12 weeks and then LYC (25 mg/kg b.wt) was administered for four weeks. Lipid peroxidation, antioxidants, lipid profile, liver function biomarkers, and inflammatory markers were determined. The results showed that long-term consumption of an HFD significantly increased weight gain, liver weight, and cholesterol and triglyceride levels. Rats on an HFD displayed higher levels of lipid peroxidation and inflammatory markers. Moreover, liver and white adipose tissue histopathological investigations showed that LYC treatment mended the damaged tissue. Overall, LYC supplementation successfully reversed HFD-induced changes and shifts through its antioxidant and anti-inflammatory activity. Therefore, LYC displayed a therapeutic potential to manage obesity and its associated pathologies.

Detection of brown adipose tissue in rats with acute cold stimulation using quantitative susceptibility mapping.

Detection of brown adipose tissue in rats with acute cold stimulation using quantitative susceptibility mapping.

Evaluation of the proliferative activity of cell cultures on nanostructured coatings for dental implants

The success of implantation treatment largely depends on osseointegration – a stable connection of bone tissue cells with the implant surface. One of the key technical factors on which successful osseointegration depends is the biocompatible surface of the implant.Materials and methods. The authors investigated three series of coatings on prototypes (samples) of titanium implants for biological compatibility: titanium dioxide (TiO2) films obtained by plasma activated atomic layer deposition (PEALD); titanium dioxide (TiO2) films obtained by sol-gel method; diamond-like carbon (DLC) films. Primary cultures of MSCs – mesenchymal stromal cells of rat adipose tissue were used to study proliferative activity.Results. A total of 30 samples were examined, samples made of titanium grade VT6 without coating served as a control. Samples, TiO2 ALD 25 nm, DLC 100 nm and DLC 200 nm, on which cellular elements showed significantly high levels of proliferative activity showed high biological compatibility.

Dexamethasone-Induced Adipose Tissue Redistribution and Metabolic Changes: Is Gene Expression the Main Factor? An Animal Model of Chronic Hypercortisolism.

Chronic hypercortisolism has been associated with the development of several metabolic alterations, mostly caused by the effects of chronic glucocorticoid (GC) exposure over gene expression. The metabolic changes can be partially explained by the GC actions on different adipose tissues (ATs), leading to central obesity. In this regard, we aimed to characterize an experimental model of iatrogenic hypercortisolism in rats with significant AT redistribution. Male Wistar rats were distributed into control (CT) and GC-treated, which received dexamethasone sodium phosphate (0.5 mg/kg/day) by an osmotic minipump, for 4 weeks. GC-treated rats reproduced several characteristics observed in human hypercortisolism/Cushing’s syndrome, such as HPA axis inhibition, glucose intolerance, insulin resistance, dyslipidemia, hepatic lipid accumulation, and AT redistribution. There was an increase in the mesenteric (meWAT), perirenal (prWAT), and interscapular brown (BAT) ATs mass, but a reduction of the retroperitoneal (rpWAT) mass compared to CT rats. Overexpressed lipolytic and lipogenic gene profiles were observed in white adipose tissue (WAT) of GC rats as BAT dysfunction and whitening. The AT remodeling in response to GC excess showed more importance than the increase of AT mass per se, and it cannot be explained just by GC regulation of gene transcription.

Chronic nitrate administration increases the expression the genes involved in the browning of white adipose tissue in female rats.

Nitrate, a nitric oxide (NO) donor, has antiobesity effect in female rats. This study hypothesized that the antiobesity effect of nitrate in female rats is due to the browning of white adipose tissue (WAT). Female Wistar rats (aged 8 months) were divided into two groups (n = 10/group): the control group received tap waterand the nitrate group received water containing 100 mg/L of sodium nitrate for 9 months. At months 0, 3, 6, and 9, obesity indices were measured. At month 9, gonadal adipose tissue was used to measure messenger RNA (mRNA) and protein levels of peroxisome proliferator-activated receptor-γ (PPAR-γ), PPAR-γ coactivator 1-α (PGC1-α), uncoupling protein 1 (UCP1), and adipocyte density and area. After the 9-month intervention, nitrate-treated rats had lower body weight, body mass index, thoracic circumference, and abdominal circumference by 6.4% (p = .012), 9.1% (p = .029), 6.0% (p = .056), and 5.7% (p = .098), respectively. In addition, nitrate-treated rats had higher PPAR-γ (mRNA: 1.78-fold, p = .016 and protein: 19%, p = .076), PGC1-α (mRNA: 1.69-fold, p = .012 and protein: 68%, p = .001), and UCP1 (mRNA: 2.50-fold, p = .001 and protein: 81%, p = .001) in gonadal adipose tissue. Nitrate also reduced adipocyte area by 35% (p = .054) and increased adipocyte density by 31% (p = .086). In conclusion, antiobesity effect of nitrate in female rats is associated with increased browning of gonadal adipose tissue as indicated by higher expression of PPAR-γ, PGC1-α, and UCP1 and reduced adipocyte area and increased adipocyte density.

Glucocorticoids decrease thermogenic capacity and increase triacylglycerol synthesis by glycerokinase activation in the brown adipose tissue of rats.

Although it is well established that glucocorticoids inactivate thermogenesis and promote lipid accumulation in interscapular brown adipose tissue (IBAT), the underlying mechanisms remain unknown. We found that dexamethasone treatment (1 mg/kg) for 7 days in rats decreased the IBAT thermogenic activity, evidenced by its lower responsiveness to noradrenaline injection associated with reduced content of mitochondrial proteins, respiratory chain protein complexes, noradrenaline, and the β3 -adrenergic receptor. In parallel, to understand better how dexamethasone increases IBAT lipid content, we also investigated the activity of the ATP citrate lyase (ACL), a key enzyme of de novo fatty acid synthesis, glucose-6-phosphate dehydrogenase (G6PD), a rate-limiting enzyme of the pentose phosphate pathway, and the three glycerol-3-P generating pathways: (1) glycolysis, estimated by 2-deoxyglucose uptake, (2) glyceroneogenesis, evaluated by phosphoenolpyruvate carboxykinase activity and pyruvate incorporation into triacylglycerol-glycerol, and (3) direct phosphorylation of glycerol, investigated by the content and activity of glycerokinase. Dexamethasone increased the mass and the lipid content of IBAT as well as plasma levels of glucose, insulin, non-esterified fatty acid, and glycerol. Furthermore, dexamethasone increased ACL and G6PD activities (79% and 48%, respectively). Despite promoting a decrease in the incorporation of U-[14 C]-glycerol into triacylglycerol (~54%), dexamethasone increased the content (~55%) and activity (~41%) of glycerokinase without affecting glucose uptake or glyceroneogenesis. Our data suggest that glucocorticoid administration reduces IBAT thermogenesis through sympathetic inactivation and stimulates glycerokinase activity and content, contributing to increased generation of glycerol-3-P, which is mostly used to esterify fatty acid and increase triacylglycerol content promoting IBAT whitening.

Effects Of Exercise On PPARγ Protein-protein Interaction In Subcutaneous Adipose Tissue Of High-fat Diet Rats

PPARγ is an important transcription factor in regulating the lipid metabolism of adipose tissue in exercise. However, the PPARγ-centered network is still unclear. PURPOSE: To explore the effects of exercise on the PPARγ protein-protein interaction network (PPI) in subcutaneous adipose tissue of high-fat diet rats. METHODS:24 4-week-old male SD rats were randomly divided into standard quiet group (C), high-fat quiet group (HC), high-fat training group (HE), each of eight. Rats of the C group were fed a normal diet (D12450B), while HC and HE groups were fed a high-fat diet (D12451). Rats in each group were subjected to 8 weeks of the experimental intervention. HE group also received the exercise intervention for 5 days every week and underwent 60%-70% VO2max intensity treadmill training for 50 minutes per day. After an 8-week intervention, the body weight of the rats was weighed, the body composition was measured by DEXA scanning. 3 rats from each group who completed the intervention process were randomly selected for the PPI work of PPARγ in subcutaneous adipose tissue, which consists of COIP-MS experiment and bioinformatics analysis. RESULTS:1.After the intervention, there was no significant difference in body weight among the three groups. However, the body fat percentage in the HC group was significantly higher than in the C group (43.71 ± 9.06% vs. 36.36 ± 6.19%, P < 0.01). And the body fat percentage in the HE group was significantly lower than the HC group (35.34 ± 2.99% vs. 43.71 ± 9.06%, P < 0.01).2. The protein expression of PPARγ in group H was significantly reduced vs. group C (0.59 ± 0.16 vs. 1.00 ± 0.00, P < 0.05); the total number of differential proteins was 33, 11 were up-regulated and 22 were down-regulated. The expression of PPARγ in the HE group was significantly increased vs. group H (0.94 ± 0.13 vs. 0.59 ± 0.16, P < 0.05); the total number of differential proteins was 25, 6 were up-regulated, and 19 were down-regulated. CONCLUSIONS:1. The 8-week high-fat diet may inhibit the body's inflammatory response by down-regulating the expression of PPARγ and its direct interaction protein Crp, and regulate lipid metabolism.2.In the 8-week high-fat diet rat model under the intervention of exercise, the differential protein function is enriched in amino acid metabolism, etc., and the energy metabolism process is closely related.

EFFECTS OF PROGENITOR CELL CONDITIONED MEDIA ON THE AMOUNT OF BRAIN CORTEX NEURONS IN A RAT MODEL OF TRAUMATIC BRAIN INJURY

Aim. The purpose of the study was to examine beneficial effect of conditioned media (CM) of progenitor cells of different origin (neurogenic progenitor cells, or NPCs, and adipose-derived mononuclear cells, or AMCs) as a source of mesenchymal multipotent stromal cells (MMSCs) on brain cortex neurons in rats with traumatic brain injury (TBI). Methods. TBI was reproduced in outbred sexually mature male rats by developing the model of free-falling load (50 g) with damage to the left hemisphere of the brain. The rats were injected 3 times with an interval of every other day intraperitoneally with NPCs CM and AMCs CM (dose 0.8 mg by total protein) that were obtained from cell cultures of fetal rat brain and adult rat adipose tissue. On the 5th day after TBI, the morphologic study of brain tissue was performed. Results. The number of neurons in the cortex of rats on the 5th day after TBI in damaged hemisphere as well as in contralateral hemisphere compared to control group decreased by half. Three i.p. injections of NPCs CM or AMCs CM increased the number of neurons in the cortex in both hemispheres in rats of corresponding groups compared to the rats with TBI without additional treatment. Conclusion. Obtained results indicate that CM obtained from NPCs and AMCs have noticeable neuroprotective effect on the damaged neurons and might be considered as an additional mode to treatment of TBI.

Effect of Aronia melanocarpa fruit juice on glucose tolerance, lipid metabolism, and obesity in a rat model of metabolic syndrome

Abstract Metabolic syndrome (MS) is a serious health condition. The purpose of this study was to investigate the effects of polyphenol-rich Aronia melanocarpa fruit juice (AMFJ) on glucose tolerance, triglyceride levels, and adipose tissue in rats with MS induced by high-fat high-fructose (HFHF) diet. Fifty rats were allocated in 5 groups: control, MS, MS+AMFJ2.5, MS+AMFJ5, and MS+AMFJ10. In the course of 10 weeks, the control group was on a regular rat diet while the other groups received HFHF diet. During the experiment, control and MS groups were treated daily orally with distilled water (10.0 mL kg−1) and the other three groups – with AMFJ at doses of 2.5, 5.0, and 10.0 mL kg−1, respectively. In MS rats, glucose intolerance, hypertriglyceridemia, visceral obesity, and increased adipocyte size were observed. In AMFJ-treated groups, the serum glucose and triglycerides, as well as visceral fat and adipocyte size decreased significantly and did not differ from those of the control group. AMFJ at doses 2.5 and 5.0 mL kg−1 showed an anti-apoptotic activity in adipocytes, while at the dose of 10 mL kg−1 a pro-apoptotic effect was detected. In conclusion, AMFJ could antagonise most of the negative consequences of HFHF diet on carbohydrate and lipid metabolism in a rat MS model.

Isolation of Rat Adipose Tissue Mesenchymal Stem Cells for Differentiation into Insulin-producing Cells.

Mesenchymal stem cells (MSCs)-especially those isolated from adipose tissue (Ad-MSCs)-have gained special attention as a renewable, abundant source of stem cells that does not pose any ethical concerns. However, current methods to isolate Ad-MSCs are not standardized and employ complicated protocols that require special equipment. We isolated Ad-MSCs from the epididymal fat of Sprague-Dawley rats using a simple, reproducible method. The isolated Ad-MSCs usually appear within 3 days post isolation, as adherent cells display fibroblastic morphology. Those cells reach 80% confluency within 1 week of isolation. Afterward, at passage 3-5 (P3-5), a full characterization was carried out for the isolated Ad-MSCs by immunophenotyping for characteristic MSC cluster of differentiation (CD) surface markers such as CD90, CD73, and CD105, as well as inducing differentiation of these cells down the osteogenic, adipogenic, and chondrogenic lineages. This, in turn, implies the multipotency of the isolated cells. Furthermore, we induced the differentiation of the isolated Ad-MSCs toward the insulin-producing cells (IPCs) lineage via a simple, relatively short protocol by incorporating high glucose Dulbecco's modified Eagle medium (HG-DMEM), β-mercaptoethanol, nicotinamide, and exendin-4. IPCs differentiation was genetically assessed, firstly, via measuring the expression levels of specific β-cell markers such as MafA, NKX6.1, Pdx-1, and Ins1, as well as dithizone staining for the generated IPCs. Secondly, the assessment was also carried out functionally by a glucose-stimulated insulin secretion (GSIS) assay. In conclusion, Ad-MSCs can be easily isolated, exhibiting all MSC characterization criteria, and they can indeed provide an abundant, renewable source of IPCs in the lab for diabetes research.

Isolation of Rat Adipose Tissue Mesenchymal Stem Cells for Differentiation into Insulin-producing Cells

Isolation of Rat Adipose Tissue Mesenchymal Stem Cells for Differentiation into Insulin-producing Cells