Obese Male Rats Research Articles

Zinc Supplementation Partially Decreases the Harmful Effects of a Cafeteria Diet in Rats but Does Not Prevent Intestinal Dysbiosis.

Zinc (Zn) plays an important role in metabolic homeostasis and may modulate neurological impairment related to obesity. The present study aimed to evaluate the effect of Zn supplementation on the intestinal microbiota, fatty acid profile, and neurofunctional parameters in obese male Wistar rats. Rats were fed a cafeteria diet (CAF), composed of ultra-processed and highly caloric and palatable foods, for 20 weeks to induce obesity. From week 16, Zn supplementation was started (10 mg/kg/day). At the end of the experiment, we evaluated the colon morphology, composition of gut microbiota, intestinal fatty acids, integrity of the intestinal barrier and blood–brain barrier (BBB), and neuroplasticity markers in the cerebral cortex and hippocampus. Obese rats showed dysbiosis, morphological changes, short-chain fatty acid (SCFA) reduction, and increased saturated fatty acids in the colon. BBB may also be compromised in CAF-fed animals, as claudin-5 expression is reduced in the cerebral cortex. In addition, synaptophysin was decreased in the hippocampus, which may affect synaptic function. Our findings showed that Zn could not protect obese animals from intestinal dysbiosis. However, an increase in acetate levels was observed, which suggests a partial beneficial effect of Zn. Thus, Zn supplementation may not be sufficient to protect from obesity-related dysfunctions.

Extended treatment with (1→3)(1→6)-β-d-glucan (Botryosphaeran) reduces obesity and its comorbidities in high-fat/high-sugar diet-fed rats.

Obesity is associated with other diseases such as diabetes and cancer. Botryosphaeran, a fungal (1→3)(1→6)-β-d-glucan, is described to present antimutagenic, hypoglycemic, hypocholesterolemic, and antitumor activities when administered by gavage over 15 days in rats and mice. Thus, the present study aims to analyze the metabolic effects of Botryosphaeran (12 mg/kg body weight/day) treatment over 30 days in obese Wistar male rats. Obesity was induced in the rats by a high-fat/high-sugar diet for 8 weeks. Control rats received a standard diet. On the5th week, Botryosphaeran treatment commenced. Groups: control, obese, and obese+Botryosphaeran 30 days. In the8th week, obesity was characterized. Feed intake, glucose and lipid profiles, glucose tolerance, and insulin sensitivity were analyzed. Obese rats showed accumulation of visceral adipose tissue, reduction of muscle mass, glucose intolerance, insulin resistance, hyperglycemia, and dyslipidemia. Botryosphaeran effectively reduced weight gains and the accumulation of retroperitoneal adipose tissue, corrected the levels of glucose, triglycerides, and very low-density lipoprotein-cholestrol, and improved insulin sensitivity. Treatment for 30 days was effective in maintaining the beneficial effects demonstrated by this β-glucan when administered for 15 days without promoting side effects. Treatment with (1→3)(1→6)-β- d-glucan presented anti-obesogenic and beneficial metabolic effects in Wistar rats; important for the treatment of obesity and its comorbidities.

The effect of phenotype on development of brown and white adipose tissue cellularity and nonshivering thermogenesis in the wistar fatty rat

Brown adipose tissue (BAT) has been noted in cadaveric specimens by anatomists for hundreds of years and is now known to be a primary peripheral tissue in the expression of non-shivering thermogenesis in response to perturbations in diet and environment in homeothermic species including man and animals. The Wistar Fatty Rat (WFR) is an animal model of obesity, insulin resistance (IR) and NIDDM and expresses the (-fa) obesity trait in an NIH/Wistar background. This stain has been reported to exhibit NIDDM and an impaired thermogenic response to parameters of diet and environment in the obese phenotype. Groups of lean and obese male WFR rats were maintained in hanging wire-bottomed steel cages and fed a nutritionally complete diet containing 54% CHO as equal parts cornstarch (ST) and sucrose (SUC) (50:60 w/w) plus vitamins, minerals, fiber, and essential micronutrients from 22 to 30 weeks of age. Measures of body weight were monitored and measures of resting, and norepinephrine stimulated VO2 determined. Animals were sacrificed by decapitation and the Interscapular BAT depot (IBAT) and primary white adipose tissue (WAT) depots excised in their entirety for measures of adiposity including adipocyte size and number per IBAT and WAT depots. The studies included measures of adipocyte lipid content and adipocyte number of WAT depots including the dorsal (DOR), epididymal (EPI) and visceral retroperitoneal (VRP) depots. Final Body weights, net weight gain and relative adiposity of obese were significantly greater than their lean littermates throughout the study with the greatest increase in WAT cell lipid content and adipocyte number in the VRP depot. IBAT cell number, cell lipid content of IBAT tissues and IBAT:BW ratio of obese >> lean littermates. Fasting glucose was similar in both phenotypes, but fasting insulin and the Insulin: Glucose (I: G) ratios were markedly elevated in obese+NIDDM animals. Resting VO2 and the thermic response to NE of lean >> Obese+NIDDM. A robust NE response in plasma glucose concentrations occurred in both phenotypes following NE with the greatest increase in the obese+NIDDM phenotype. The results of this study indicate that while the development of IBAT and WAT mass and cellularity became exaggerated via hyperplasia and hypertrophy in the obese-NIDDM animals, the superimposition of early hyperphagia and the NIDDM stigmata which likely includes the development of significant IR is a contributing factor. The elevations in I: G and IR of the Obese+NIDDM phenotype may further facilitate adipocyte hyperplasia and hypertrophy in both WAT and BAT depots and may further compromise the capacity of the obese diabetic animals to fully express BAT-mediated contributions to NST. Moreover, the increased BAT mass and cellularity in the Obese+NIDDM was not by itself a reliable predictor of the thermic responses to diet and environment.

Histological Study on The Effects of Orlistat on Left Ventricular Myocardium of High Fat Diet-Fed Adult Male Wistar Rats

Obesity-induced by a high-fat diet in animal studies recapitulates the human form of obesity. Obesity is a serious public health concern, a risk factor for many diseases, including cardiovascular disorders. Our study evaluated the impact of orlistat on the left ventricular myocardium in high fat diet-induced obese adult Wistar rats. Our study included fifteen adult male Wistar rats weighing between (130-150g). The rats following environmental acclimatization were assigned into three groups A-C (n=5 each), the control (standard rat diet), high-fat diet only, high-fat diet, and orlistat as A, B, and C, respectively. The rats were placed on diets for eight weeks, which performed the sacrifice and histological procedures. The heart and left ventricles were excised and fixed in 10% buffered formalin solution for histological studies. Body Mass Index (BMI) of the high-fat diet-only group markedly increased (P<0.05) relative to the control and the orlistat-treated groups. Heart weight and relative heart weights were not significantly different across the groups. Histological examination of the left ventricular myocardium with the hematoxylin and eosin stain revealed significant deviation from the regular pattern in the high-fat diet-only group. The orlistat-treated group showed a near-normal left ventricular myocardial histoarchitectural pattern. Orlistat ameliorated left ventricular myocardial alteration, restored elastic tissue component, and reversed increased collagen deposition in high fat diet-induced obese male Wistar rats.

Effects of the Anti-obesity Drugs Vita Slim and Green Tea on Certain Biochemical and Physiological Indices of Obese Adult Male Albino Rats

Effects of the Anti-obesity Drugs Vita Slim and Green Tea on Certain Biochemical and Physiological Indices of Obese Adult Male Albino Rats

Fecal Microbiota Transplantation During Lactation Programs the Metabolism of Adult Wistar Rats in a Sex-specific Way

The intestinal microbiota is involved in many physiological processes. However, the effects of microbiota in metabolic programming still unknow. We evaluated whether the transplantation of fecal microbiota during early life can program health or disease during adulthood in a model of lean and obese male and female Wistar rats. Parental obesity were induced using a small litter (SL, 3 pups/dam) model. At 90 d old, normal litter (NL, 9 pups/dam) and SL males and females (parents) from different litters were mated: NL male vs. NL female; SL male vs. SL female. After birth, male and female offspring rats were also standardized in normal litters or small litters . From the 10th until 25th d of life, the NL and SL male and female offspring received via gavage of a solution containing the diluted feces of the opposite dam (fecal microbiota, M) or saline solution (S). At 90 d of age, biometric and biochemical parameters were assessed. NLM male rats transplanted with obese microbiota showed increased body weight, and fat pad deposition, hyperinsulinemia, glucose intolerance and dyslipidemia. SLM male rats transplanted with lean microbiota had decreased retroperitoneal and mesenteric fat, triglycerides and VLDL levels and improvement of glucose tolerance. Despite SLM female rats showed higher visceral fat, microbiota transplantation in female rats caused no changes in these parameters compared with control groups. Fecal microbiota transplantation during lactation induces long-term effects on the metabolism of male Wistar rats. However, female rats were resistant to metabolic alterations caused by the treatment.

Histopathological alterations in liver, kidney, and testis of obese male albino rats following thunder god vine roots extract treatment

Histopathological alterations in liver, kidney, and testis of obese male albino rats following thunder god vine roots extract treatment

Correlation between Intermittent Fasting and Mental and Physical Fatigue in High‐fat‐induced Obese and Non‐obese Rats

Intermittent fasting (IF) is an alternate pattern of eating and restricting food intake. This study evaluated mental and physical fatigue secondary to IF in high‐fat diet‐induced (HFD) obese male rats. Fifty‐four rats were randomly assigned to a HFD (n=28) or a standard diet (SD; n=26). After six weeks, the HFD rats were divided into one of four groups: obese HFD ad libitum (OB‐HFD‐AL), obese HFD intermittent fasting (OB‐HFD‐IF), obese SD ad libitium (OB‐SD‐AL), and obese SD IF (OB‐SD‐IF). Similarly, non‐obese controls were grouped into HFD ad libitum (C‐HFD‐AL), non‐obese HFD IF (C‐HFD‐IF), non‐obese SD ad libitum (C‐SD‐AL), and non‐obese SD IF (C‐SD‐IF). The IF groups fasted for 18 hours per day, seven days a week. After two weeks, their physical and mental fatigue was measured using open field (OF) and novel object recognition (NOR) paradigms. Regardless of the diet type, rats on IF gained weight at a slower pace (p< 0.05) and had lower glucose levels (p < 0.01) compared to the AL group. In non‐obese rats, ketone levels were higher in the IF‐HFD group compared to the IF‐SD (p<0.05) and AL‐SD (p<0.01) groups. Obese rats exhibited higher ketones in IF‐SD conditions versus AL‐SD rats (p<0.01). In both obese and non‐obese groups, AL‐HFD rats had higher ketone levels than AL‐SD rats (p<0.05). Increased ketone levels could be correlated with greater distance traveled during OF. IF protected against recognition memory deficit during NOR. Overall, this study demonstrates that increased ketone levels, whether caused by diet type or IF, correlate to decreased physical fatigue and protect against mental fatigue.

Effectiveness of high-intensity interval training and high-protein diet on TNF-α protein level in colon tissue of obese male rats: The importance of diet modifying

High-fat diets (HFDs) are a risk factor for obesity, insulin resistance, non-alcoholic fatty liver disease, hypertension, inflammatory bowel disease, and atherosclerosis. The present study aimed to investigate the effect of high-intensity interval training (HIIT) and high-protein diet (HPD) on interleukin-37 (IL-37) and tumor necrosis factor-alpha (TNF-α) protein levels in the colon tissue of obese male rats fed a high-fat diet (HFD). Forty obese male Wistar rats were randomly assigned into six equal groups: 1) HIIT, 2) HPD, 3) HIIT+ HPD, 4) Obese control 1 with HFD (Ct1), and 5) obese control 2 with breaking a HFD at the start of the study (Ct2). Eight rats were given a standard diet in the normal control group (NCt). Rats were sacrificed 48 h after the last intervention session and colon tissue was removed. The protein level of TNF-α was significantly lower in the HIIT, HPD, HIIT+ HPD, and Ct2 groups compared with the Ct1, with more lowering effects in the HPD and HIIT+ HPD and almost similar effects between the HIIT and Ct2 groups. No significant difference was observed in the IL-37 protein level between experimental groups. These findings suggest that HIIT, HPD, and HIIT+HPD may reduce colon inflammation through lowering of TNF-α inflammatory marker in colon tissue of obese rats receiving HFD. Although, the HPD alone and along with HIIT represent a more reducing effect than HIIT alone. However, breaking the HFD and replacing it with the standard diet was similar to the HIIT for reducing TNF-α. • HIIT, HPD, and HIIT+HPD led to a reduction in TNF-α protein levels in colon tissue of obese rats receiving HFD. • Replacing a HFD with the standard diet and HIIT without cessation of HFD had same effects on decreasing the TNF-α in rat colon. • A HPD alone and along with HIIT was more effective than HIIT without cessation of HFD on reducing the colon levels of TNF-α.

Soluble Isoform of ST2 is a Cardiac Inducer of Collagen Deposition in an Ex Vivo Model of Obesity

IntroductionOne of the main cardiac mechanosensor is the IL‐33/ST2L complex composed by the allarmin IL‐33 released into extracellular space by damaged cells during cardiac overload and its receptor, ST2L, which their binding promotes cell survival and anti‐fibrotic signaling. After damage, to stop IL‐33/ST2L signal, resident cardiac cells release sST2, the soluble isoform of transmembrane receptor of ST2, which sequesters IL‐33, functioning as a decoy receptor and blocking its signal. In obesity, the sST2 become over express especially by hypertrophic fat cells. The aim of our study is to evaluate in an ex vivo model of obesity the role of sST2 in the promotion of collagen production by cardiac cells.MethodsTen obese nondiabetic male Zucker rats (OB) (fa/fa‐, 10 weeks of age) and 10 lean littermates (L) (Fa/+) at the age of 25 weeks were weighted and scarified according to Italian Ministry of Health Authorization (N°325/2015PR of 2015/04/05) and their heart and visceral adipose tissue (VAT) were collected for the analysis. VAT biopsies were cut in 30mg pieces and added into a co‐culture system with H9C2 for 6‐24 and 48 hours. At each time points, cells and culture medium were collected. In all samples were evaluated ST2 by ELISA and collagen were quantified by quantitative Sircol assay for measurement of both acid‐soluble and pepsin‐soluble collagens.ResultsOB cardiac biopsies showed higher protein level of both ST2 and collagen than L rats (p<0.02 and p<0.002 respectively) and the rat weight positively correlates with ST2 cardiac protein level (p<0.05). Co‐culture data demonstrated that OB VAT promotes ST2 releases in both cardiac and fat cells, resulting an incremental increase of sST2 release in cell culture medium than L VAT in time. sST2 quantification in correspondent H9C2 co‐cultured lysate is more incremented in OB than L H9C2 after 48h.total collagen quantification in co‐culture medium resulted higher in OB than L (p<0.05).ConclusionOur results demonstrated in a co‐culture system that obesity promotes sST2 increase in the heart and this promotes collagen releases by cardiac cells, suggesting sST2 role in activation of pro‐fibrotic signaling and detrimental heart remodeling.

Differential remodelling of visceral and pericardial adipose tissue in response to stress and exercise

Obesity is driven by an imbalance between caloric intake and energy expenditure, causing excessive storage of nutrients in adipose tissue at different sites around the body. Increased visceral adipose tissue (VAT) is associated with diabetes, whilst pericardial adipose tissue (PAT) is associated with cardiac pathology. Adipose tissue can expand either through cellular hypertrophy or hyperplasia, with the former correlating with decreased metabolic health in obesity. The aim of this study was to determine how VAT and PAT remodel in response to obesity, stress and exercise.Here we have used the obese Zucker rats which develop hyperphagia with reduced energy expenditure, resulting in morbid obesity as a result of leptin resistance. At 9 weeks of age lean (LZR) and obese (OZR) Zucker male rats were treated with or without unpredictable chronic mild stress or exercise for 8 weeks. To determine the phenotype for PAT and VAT, tissue cellularity and gene expression were analyzed. Tissue cellularity was determined following haematoxylin and eosin staining, whilst qPCR was used to examine gene expression.PAT adipocytes were significantly smaller than those from VAT and had a more biege‐like appearance. In the OZR group, VAT adipocyte cell size increased significantly compared with LZR, whilst PAT showed no change. Exercise and stress resulted in a significant reduction in VAT cellularity in OZR, whilst PAT showed no change. This suggests that PAT cellularity does not remodel significantly compared with VAT. Picro sirus red staining indicated that PAT had significantly more fibrosis than VAT. However, this fibrosis was decreased following stress treatment. This data indicate that the extracellular matrix of PAT is able to remodel more readily than in VAT.Gene expression analysis showed that PAT expressed higher levels of UCP1 compared with VAT, indicating that it has a more brown‐like phenotype. In the LZR group, exercise increased insulin receptor substrate 1 (IRS1) in PAT, but was decreased in the OZR group. On the other hand, in VAT, exercise decreased IRS1 in LZR, whilst increasing it in the OZR. This suggests that in obesity, VAT is more responsive to exercise and subsequently becomes less insulin resistant compared with PAT. In VAT, stress increased PPAR‐γ expression in the OZR group but decreased it in the PAT. This suggests that in obesity, stress increases adipogenesis more significantly in the VAT compared with PAT.Taken together, our data suggest that VAT is considerably more plastic than PAT and remodels rapidly in response to obesity, exercise and psychological stress.

Effect of a chromium‐fructooligosaccharide complex on glycemic parameters in obese and obese‐NIDDM rats

The incidence and odds ratio of obesity and Type 2 diabetes, a common sequela of obesity, are increasing in incidence to the point of becoming epidemic in Western society. To determine the potential beneficial effects of a chromium‐fructooligosaccharide complex (FCC) on glycemic responses of male obese and obese NIDDM rats, groups of 3 ‐ 4 month old lean and obese LA/Ntul//‐cp and SHR/Ntul//‐cp rats (NIDDM‐rats, n= 6 rats/group) reared normally on Purina #5012 chow from the time of weaning, were subjected to an oral glucose tolerance (OGT) after a brief 4‐hour fast. A second group of NIDDM rats (n=5) aged one year were also administered the OGT and FCC challenges. NIDDM rats develop IGT by adolescence and renal disease, cataracts, and impaired nerve conduction velocity typical of DM by adulthood. Animals were administered a glucose solution equivalent to 2.5 grams/kg BW via intragastric gavage, or the same glucose plus the FCC (2.5 g/kg BW, containing 200µg Cr and 2.25 mg/serving) or the FCC alone over a brief (1‐2 minute) duration. Measures of blood glucose (BG) were determined at 30‐minute intervals from zero to +120 minutes post gavage via tail bleeding, and the area under the curve (AUC) of each group determined. Final body weights (BW) of obese were greater than lean (p=0.05), and obese‐NIDDM > Obese rats (p=<0.05) and increased in NIDDM rats with older age. OGT of lean rats remained normal throughout, and FCC resulted in minor decreases in AUC and in BG concentrations at all time points (p= n.s.) The OGT of obese rats demonstrated significant increases in BG at +60, +90‐, and +120‐minutes post gavage but remained non‐diabetic, and FCC decreased the glycemic increase and AUC by ~50%, similar to the glycemic response off lean littermates. The OGT of young NIDDM was significantly impaired and FCC resulted in a 32% reduction in the AUC. The OGT and AUC of OLD NIDDM rats was greater than in young rats and was decreased by 25% with FCC. OGT and OGG+FCC were similar at both ages in NIDDM rats. These results are consistent with an FCC‐mediated improvement in glycemic control in congenic animal models for obesity and obesity+NIDDM and suggest that the FCC complex may be a useful nutraceutical adjunct in the dietary treatment of obesity and other glucose intolerant states as they occur in man and animals.

The Role of CD44v6 in Vascular Rarefaction and Left Ventricular Diastolic Dysfunction in HFpEF

CD44 is differentially spliced to form specific CD44 variants, but little is known regarding their specific contribution to cardiovascular pathologies. Specifically, CD44 variant 6 (CD44v6) is involved in abnormal angiogenesis. The hypothesis tested was that CD44v6 leads to coronary microvascular rarefaction whereby it contributes to left ventricle (LV) diastolic function in heart failure with preserved ejection fraction (HFpEF, also known as diastolic heart failure). The obese ZSF1 rat model of human HFpEF was employed and using transthoracic echocardiography, it was found that 21‐week‐old male obese ZSF1 rats exhibited diastolic dysfunction, accompanied with increased myocardial expression of CD44v6. Coronary arteriolar and capillary trees were labeled using Tomato Lectin (Lycopersicon esculentum) DyLight®594 and were imaged by fluorescent confocal microscopy to generate image stacks for 3D reconstruction. Unbiased automated tracing of the microvasculature was done using VesselLucida360 software (MBF) followed by a morphometric analysis (VesselLucida Explorer). It was found that total vessel length and the number of vessel’s branching nodes were reduced in the obese ZSF1 rats, whereas the total vessel’s volumes remained unchanged, when compared to the lean ZSF1 controls. These changes in the microvasculature were accompanied by decreased angiogenesis in the coronary arteries in the obese ZSF1 rats when compared to the lean ZSF1 rats. From these results, it was concluded that upregulation of CD44v6 plays a role in the impaired angiogenesis underlying the development of LV diastolic dysfunction in HFpEF.

Physiological, histological, anatomical and biochemical effects of a 2-months marked carbohydrate deprivation dietary program in obese male albino rats

Marked-carbohydrate deprivation diets are commonly used for weight loss based on the belief that carbohydrates cause weight gain. This work aimed to study the effect of marked carbohydrate deprivation (for two months) on the body weight, body mass index, protein, fat metabolism and insulin and leptin levels, and to clarify the mechanism by which marked carbohydrate deprivation can cause reduction of body weight and to clear possible side effects for this type of food regimen used increasingly to reduce weight. Twenty obese male albino rats were included in this study. All rats were chosen obese and were fed for one month each on 150 grams normal chow containing high carbohydrates, proteins and fats to make this content their normal daily intake and assure obesity Rats were divided into two groups. The first group was the control group. It contained ten rats, and they were fed on (half the daily regular intake) 75 grams normal chow containing carbohydrates, proteins and fats for two months. The second group contained ten rats and they were fed on 150 grams of food containing proteins and fats with minimal carbohydrates for two months. Rat groups were weighed and body mass index was calculated at the beginning and end of the study. Insulin, leptin levels and pH of blood were measured at the beginning and end of the study. Change in values in weight, BMI, pH of blood, insulin, and leptin levels were compared at the beginning of the study and at its end. Rate of change for all parameters in group two was compared to that of group one. There were significant decrease in weight, and BMI, in both groups at end of the study compared to the results obtained at the beginning. The rate of change decreased more significantly for the previously mentioned parameters in group two compared to group one. There were significant increase in insulin level in group one at end of the study compared to its level at the beginning of the study. While there were significant decrease in the insulin level in group two at end of the study compared to the level recorded at the beginning. There were significant decrease in the rate of change for the insulin in group two compared to that for group one at end of the study. Non-significant change in the pH at the end of the study was recorded in both groups compared to the results obtained at the beginning, The rate of change for pH in group two showed significant decrease compared to that of group one at end of the study. Leptin level showed non-significant decrease at the end of the study in group one compared to the results at the beginning. While it showed significant increase in group two at end of the study compared to the results obtained at the beginning. There was significant increase in the rate of change for leptin in group two compared to that in group one at end of the study.

Physiological, histological, anatomical and biochemical effects of a 2-months marked carbohydrate deprivation dietary program in obese male albino rats

Physiological, histological, anatomical and biochemical effects of a 2-months marked carbohydrate deprivation dietary program in obese male albino rats

The effect of training on mitochondrial mitophagy factors in obese male rats

هدف: میتوفاژی می­تواند به کنترل کیفیت میتوکندری کمک کند. هدف از مطالعه حاضر، بررسی تأثیر یک دوره تمرین بر عوامل میتوفاژی میتوکندری در موش های صحرایی نر چاق بود.روش‌ها: در این مطالعه تجربی، 40 سر موش صحرایی نر (میانگین وزن20±120 گرم) پس از القاء چاقی با رژیم غذایی پرچرب (به مدت 10 هفته)، 8 سر موش صحرایی از گروه رژیم غذایی پرچرب (O) و 8 سر موش صحرایی گروه رژیم غذایی استاندارد (C) برای بررسی القای چاقی تشریح شدند و سایر موش‌های صحرایی چاق به‌طور تصادفی به 3 گروه کنترل چاق (OC)، تمرین تداومی با شدت متوسط (MICT) و تمرین تناوبی با شدت بالا (HIIT) تقسیم شدند. HIIT شامل 10 مرتبه‌ فعالیت 4 دقیقه‌ای با شدت 90-85 درصد VO2max و دفعه های استراحت فعال 2 دقیقه‌ای و برنامه MICT نیز 5 جلسه در هر هفته با شدت 70-65 درصد VO2max به مدت 12 هفته اجرا شد. سطوح bcl2 و پارکین با استفاده از روش الکتروفورز ژل و وسترن بلات اندازه­گیری شد. داده­ها با استفاده از آزمون‌های تحلیل واریانس یک‌طرفه و آزمون تعقیبی توکی در سطح معنا‌داری 05/0P≤ تجزیه و تحلیل شد.نتایج: نتایج نشان داد هر دو مداخله تمرین HIIT و MICT به افزایش معنا دار bcl2 و پارکین عضله نعلی نسبت به گروه کنترل منجر شدند (05/0P<). تفاوت معنا‌داری بین دو گروه HIIT و MICT در سطوح bcl2و پارکین رت‌های چاق وجود نداشت (05/0<P).نتیجه‌گیری: با توجه به نتایج، به نظر می‌رسد که HIIT و MICT می­توانند به کاهش تخریب و اختلال میتوکندری در عضله اسکلتی طی چاقی کمک کنند.

Interplay of Obesity, Ethanol, and Contaminant Mixture on Clinical Profiles of Cardiovascular and Metabolic Diseases: Evidence from an Animal Study

Obesity, ethanol, and contaminants are known risk factors of cardiovascular and metabolic diseases (CMD). However, their interplay on clinical profiles of these diseases remains unclear, and thus were investigated in this study. Male lean or obese JCR rats were given water or 10% ethanol and orally treated with or without a contaminant mixture (CM) dissolved in corn oil and loaded on two cookies at 0, 1.6, or 16 mg/kg BW/day dose levels for 4 weeks. The CM consisted 22 environmental contaminants found in human blood or serum of Northern populations. Over 60 parameters related to CMD were examined. The results revealed that obesity in JCR rats resembles the clinical profiles of non-alcoholic fatty liver disease in humans. Obesity was also associated with increased serum and organ retention of mercury, one of the chemical components of CM. Exposure to ethanol lightened hyperlipidemia, increased liver retention of mercury, and increased risk for hypertension in the obese rats. CM lessened hyperlipidemia and hyperenzymemia, worsened systemic inflammation and increased the risk for hypertension in the obese rats. CM markedly increased serum ethanol levels with or without ethanol exposure. Tissue total mercury contents significantly correlated with clinical parameters with altered profiles by both ethanol and obesity. These results suggest that obese individuals may be more prone to contaminant accumulation. Ethanol and CM exposure can alter clinical profiles associated with obesity, which may lead to misdiagnosis of CMD associated with obesity. CM can alter endogenous production and/or metabolism of ethanol, further complicating disease progression, diagnosis, and treatment.

Effects of the Antiobesity Drugs Aplex and Venera on Certain Biochemical and Physiological Indices in Obese Adult Male Albino Rats.

Background Because of the growing incidence of obesity, the use of synthetic antiobesity medicines as weight-loss agents has grown in popularity, although their usefulness has yet to be established. Two of such medicines are Aplex and Venera. This study is designed to determine the potential dangers of Aplex and Venera on certain biochemical and physiological indicators in obese adult male rats. Methods Twenty-one obese male albino rats (9 weeks old and having a body mass of 220 ± 20 g) were divided into three equal groups: the control group (vehicle treatment), the Aplex group (0.1 mg/kg/day) for 30 days, and the Venera group (0.1 mg/kg/day) for 30 days. Results The values of serum glucose, insulin, homeostatic model assessment of insulin resistance (HOMA-IR), total protein, total cholesterol (TC), high-density lipoprotein (HDL), very-low-density lipoprotein (VLDL), TC/HDL ratio, testosterone, thyroxine (T4), and leptin did not differ significantly between the treated and control groups. In contrast, the treated groups had substantial changes in bodyweight, serum alanine aminotransaminase (ALT), aspartate aminotransaminase (AST), albumin, globulin, albumin/globulin ratio (A/G ratio), triglycerides (TG), low-density lipoproteins (LDL), LDL/HDL ratio, urea, creatinine, and triiodothyronine (T3) levels. Conclusion The findings indicate that Aplex and Venera have negative impacts on crucial biochemical and physiological indicators, particularly liver and kidney functioning.

Long-Term Diabetes Improvement After Duodenal Exclusion in Zucker Diabetic Fatty Rats Is Associated with Prevention of Strain-Specific Pancreatic Remodeling and Increased Beta Cell Proliferation.

BackgroundResponse to metabolic surgery is heterogeneous and the metabolic states that underpin weight loss and metabolic improvement are still unclear. In this study, we investigate parameters of post-bariatric fasting glucoregulation and leverage artificial intelligence-assisted whole-slide image analyses to characterize associated immunohistologic features of the pancreas.Materials and MethodsWe performed either loop duodeno-jejunostomy (DJOS) with exclusion of 1/3 of total intestinal length, loop duodeno-ileostomy with exclusion of 2/3 of total intestinal length (DiOS), or a sham operation on 8-week-old male obese ZDF rats. Six months post-operative, we measured blood metabolites and hormones. Subsequently, pancreatic and intestinal tissue was removed, formalin fixed, and paraffin embedded. Immunohistologic (IHC) analyses included proliferating cell nuclear antigen (PCNA) to visualize the proliferation fraction and pancreatic and duodenal homeobox 1 (PDX 1) as a measure of pancreatic cell differentiation. For IHC quantification, all slides were digitalized and analyzed using QuPath. All analyzed slides were reviewed by two independent pathologists for correctness.ResultsDJOS and DiOS were associated with preserved fasting insulin production compared to sham. Histopathologic evaluation showed significantly higher numbers of beta cells and specifically of clustered cell organization in DJOS and DiOS compared to sham. Cell proliferation (PCNA) was significantly elevated in DJOS and DiOS compared to sham.ConclusionIn this interventional model of bariatric surgery in severe genetic diabetes, we demonstrate post-operative histologic and immunohistologic features of the pancreas associated with improved fasting glucose homeostasis.Graphical abstract

Impact of Green Coffee Extract on Body Weight and Physiological Indicators of Metabolic State in Obese Male Rats

Impact of Green Coffee Extract on Body Weight and Physiological Indicators of Metabolic State in Obese Male Rats