Obese Diabetic Rats Research Articles

Evaluating Anti-Diabetic Effect of Courmarin Derivative Aesculetin in Rats with Diet-Induced Obesity.

Obesity, modifiable and an avertable medical condition, has become a global threat due to rapid modernization and industrialization. Swift growth in modernization not only eases the day-to-day life, it also mandates sedentary lifestyle, which leads to various noncommunicable diseases. At present one in eight people in global population are obese, and these booming obese individuals are prone to various other micro- and macrovascular diseases such hyperglycemia, myocardial infraction, hypertension, stroke, and so forth. Ample research had unveiled an intricate association perceived between obesity and Type 2 diabetes mellitus pathogenesis. Although the intake of anti-obesity drugs along with anti-diabetic drugs had effectively regulated the hyperglycemic conditions in diabetic patients, it causes various side effects on long-term usage. Coumarins are phytochemicals that have demonstrated pharmacological properties including anti-inflammatory, antioxidant, anti-tumor, and so forth. In this analysis, we assessed anti-obesity and anti-diabetic potency of aesculetin, a courmarin derivative. The rats were induced obesity with high-fat diet and subjected to streptozotocin infusion to induce hyperglycemia. Obese diabetic induced rats were treated with aesculetin and assessed for its anti-diabetic effect. BMI were assessed in the rats to analyze the anti-obesity effect of aesculetin. Diabetic profile test and lipid profile test were performed to evaluate the anti-diabetic effect of aesculetin. Ameliorative effect of aesculetin in obese rats during hyperglycemic conditions was assessed with renal profile test, hepatic function biomarkers, and by histopathological analysis of cardiac tissue. The anti-inflammatory and antioxidant property were also assessed to determine the mechanism of action of aesculetin. To confirm the anti-obesity potency of aesculetin, adipokines levels were estimated. Aesculetin eminently decreased the BMI, HbA1c, cholesterol levels, and intensified secretion of insulin in obese diabetic rats. It also regulated the renal, hepatic functional markers and prevented cardiac tissue injury in obese diabetic rats. It regulated the adipokines, increased antioxidants, and decreased level of proinflammatory cytokines, thereby prevented obesity-induced hyperglycemic effects in rats. To conclude, our findings had confirmed the supplementary intake of aesculetin prevents obesity-induced hyperglycemic disorder in rats.

Melatonin induces fiber switching by improvement of mitochondrial oxidative capacity and function via NRF2/RCAN/MEF2 in the vastus lateralis muscle from both sex Zücker diabetic fatty rats.

The positive role of melatonin in obesity control and skeletal muscle (SKM) preservation is well known. We recently showed that melatonin improves vastus lateralis muscle (VL) fiber oxidative phenotype. However, fiber type characterization, mitochondrial function, and molecular mechanisms that underlie VL fiber switching by melatonin are still undefined. Our study aims to investigate whether melatonin induces fiber switching by NRF2/RCAN/MEF2 pathway activation and mitochondrial oxidative metabolism modulation in the VL of both sex Zücker diabetic fatty (ZDF) rats. 5-Weeks-old male and female ZDF rats (N=16) and their age-matched lean littermates (ZL) were subdivided into two subgroups: control (C) and orally treated with melatonin (M) (10mg/kg/day) for 12 weeks. Interestingly, melatonin increased oxidative fibers amounts (Types I and IIa) counteracting the decreased levels found in the VL of obese-diabetic rats, and upregulated NRF2, calcineurin and MEF2 expression. Melatonin also restored the mitochondrial oxidative capacity increasing the respiratory control ratio (RCR) in both sex and phenotype rats through the reduction of the proton leak component of respiration (state 4). Melatonin also improved the VL mitochondrial phosphorylation coefficient and modulated the total oxygen consumption by enhancing complex I, III and IV activity, and fatty acid oxidation (FAO) in both sex obese-diabetic rats, decreasing in male and increasing in female the complex II oxygen consumption. These findings suggest that melatonin treatment induces fiber switching in SKM improving mitochondrial functionality by NRF2/RCAN/MEF2 pathway activation.

The Role of Quercetin and Exercise in Modulating Apoptosis and Cardiomyopathy via PI3K/AKT/FOXO3 Pathways in Diabetic Obese Rats.

Quercetin and exercise both have antidiabetic effects through decreasing blood glucose while increasing insulin sensitivity. Therefore, the present study aimed to investigate the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) exercises along with quercetin administration on apoptosis and cardiomyopathy in diabetic obese rats. In this experimental study, 35 male Wistar rats [diabetic rats for experimental groups and normal rats for healthy control (HC)] were divided into seven groups (for each group n=5): HC, diabetic control (DC), diabetic quercetin control (DQC), diabetic HIIT (DHT), diabetic MICT (DMT), DHT with quercetin (DQHT) and DMT with quercetin (DQMT). The rats were fed a high-fat diet (HFD) for 8 weeks and a low dose of streptozotocin (STZ) was administered to create a model of type 2 diabetes mellitus (T2DM). Eight weeks of HIIT and MICT with or without quercetin treatment were performed. Quercetin was used at 15 mg/kg, as a suspension in carboxymethyl cellulose (CMC) at a concentration of 0.5%. One-way analysis of variance with LSD's post-hoc test with a significant level of P≤0.05 was used to analyze data. Just 8 weeks of HIIT and MICT protected the protein content of PI3K, AKT, and FOXO3 and caspase-8 (Casp- 8) gene expression in heart tissues (P<0.05). Quercetin and both training protocols decreased blood glucose, while improving inflammatory markers and the lipid profile (P<0.05). Reduction in blood glucose along with improvements in the inflammatory markers and the lipid profile by quercetin injection may be a promising approach for the development of new antidiabetic medications. In addition, both training protocols showed potentially successful diabetic cardiomyopathy treatments through modulating the FOXO3 and PI3K/AKT pathways.

Melatonin Ameliorates Organellar Calcium Homeostasis, Improving Endoplasmic Reticulum Stress-Mediated Apoptosis in the Vastus Lateralis Muscle of Both Sexes of Obese Diabetic Rats.

Endoplasmic reticulum (ER) stress is a crucial factor in the progression of obesity-related type 2 diabetes (diabesity), contributing to skeletal muscle (SKM) dysfunction, calcium imbalance, metabolic inflexibility, and muscle atrophy. The ER and mitochondria together regulate intracellular calcium levels, and melatonin, a natural compound with antioxidant properties, may alleviate these challenges. Our previous research showed that melatonin raises intracellular calcium and preserves muscle structure by enhancing mitochondrial function in obese diabetic rats. This study further explores melatonin's potential to reduce ER stress in the vastus lateralis (VL) muscle by modulating the unfolded protein response (UPR) and restoring calcium levels disrupted by diabesity. Five-week-old Zücker diabetic fatty (ZDF) rats and lean littermates of both sexes were divided into control and melatonin-treated groups (10 mg/kg/day for 12 weeks). Flame atomic absorption spectrometry results showed that melatonin restored VL intraorganellar calcium homeostasis, increasing calcium levels in mitochondria and reducing them in the ER by raising the activity and expression of calcium transporters in both sexes of ZDF rats. Melatonin also decreased ER stress markers (GRP78, ATF6, IRE1α, and PERK) and reduced pro-apoptosis markers (Bax, Bak, P-JNK, cleaved caspase 3 and 9) while increasing Bcl2 levels and melatonin receptor 2 (MT2) expression. These findings suggest that melatonin may protect against muscle atrophy in obese and diabetic conditions by mitigating ER stress and calcium imbalance, highlighting its therapeutic potential.

The Use of Maca (Lepidium meyenii) to Improve Semen Quality in Diabetic Obese Male Rats

The Use of Maca (Lepidium meyenii) to Improve Semen Quality in Diabetic Obese Male Rats

Modification of adipogenesis and oxidative stress by quercetin: positive or negative impact on adipose tissue metabolism of obese diabetic Zucker rats?

Reactive oxygen species (ROS) play a key role in the regulation of adipogenesis. The aim of our study was to investigate the effect of quercetin (QCT) supplement on obese adipose tissue metabolism of 30-week-old diabetic Zucker rats (ZDF), not well examined yet. QCT was administered orally at dose of 20mg/kg body weight/day for 6 weeks. Adipocytes from subcutaneous adipose tissue (ScWAT) were isolated and their size was evaluated by light microscopy. Gene expression of adipogenic markers in subcutaneous and visceral adipose tissue was determined by real-time PCR and expression of proteins involved in lipid and glucose metabolism was determined in ScWAT by immunoblotting. Obese ZDF rats suffered from diabetes, hyperinsulinemia and had higher index HOMA-IR (Homeostatic Model Assessment for Insulin Resistance). Treatment with QCT had no significant impact on these metabolic disorders in genetic model of obesity and type 2 diabetes used in our study. Nevertheless, QCT reduced expression of inflammatory cytokine tumour necrosis factor alpha in ScWAT and also visceral adipose tissue and up-regulated expression of anti-inflammatory adiponectin in ScWAT. A shift in redox equilibrium was detected via inhibition of pro-oxidant genes by QCT. Furthermore, QCT reduced adipocyte size in ScWAT, down-regulated expression of fatty acid synthase and adipogenic markers, and moreover stimulated expression of proteolytic enzymes. These changes likely resulted in reduced fat deposition in ScWAT, which was reflected in the elevated circulated levels of free fatty acids in QCT-treated obese ZDF rats compared with obese untreated controls. This increase could, at least in part, explain why we did not observe an improvement in systemic metabolic health by QCT in our model. In conclusion, our study suggests that preventive treatment with QCT might be more effective than its administration in the stage of fully developed diabetes, and further research in this area is needed.

The adipose tissue melanocortin 3 receptor is targeted by ghrelin and leptin and may be a therapeutic target in obesity

ObjectiveObesity is linked to perturbations in energy balance mechanisms, including ghrelin and leptin actions at the hypothalamic circuitry of neuropeptide Y (NPY) and melanocortin. However, information about the regulation of this system in the periphery is still scarce. Our objective was to study the regulation of the NPY/melanocortin system in the adipose tissue (AT) and evaluate its therapeutic potential for obesity and type 2 diabetes. MethodsThe expression of the NPY/melanocortin receptors’ levels was assessed in the visceral AT of individuals with obesity and altered metabolism. Protein levels of these receptors were evaluated in cultured adipocytes incubated with ghrelin (30 and 100 ng/mL) and leptin (1 and 10 nM) and in the AT of an animal model with a mutation in the leptin receptor (ZSF1 rat), to understand their regulation by leptin and ghrelin. The vertical sleeve gastrectomy animal model was used to evaluate the putative therapeutic potential of the NPY/melanocortin system. ResultsIn this study, we unravelled that leptin (1 nM and 10 nM) selectively reduced the levels of NPY5R and MC3R but no other NPYR/MCRs in cultured adipocytes. In turn, acylated ghrelin (100 ng/mL) significantly increased NPY1R, but the inhibition of its receptor also abrogates MC3R levels. However, in the Lepr-deficient ZSF1 rat, both NPY5R and MC3R levels were reduced, along with other NPYRs and MCRs, suggesting that leptin resistance negatively affects NPY and melanocortin signalling. In human adipose tissue, we found a downregulation of genes encoding the NPY and melanocortin receptors in the visceral AT of individuals with obesity and insulin resistance, being correlated with genes regulating metabolic activity. Additionally, diabetic obese rats submitted to vertical sleeve gastrectomy showed increased levels of NPY, melanocortin, ghrelin, and leptin receptors in the AT, including MC3R, suggesting it may constitute a therapeutic target in obesity. ConclusionsOur results suggest that the AT NPY/melanocortin system, particularly the MC3R, may be involved in the neuroendocrine regulation of adipocyte metabolism. Altogether, our work shows MC3R is under the control of the ghrelin/leptin duo, is reduced in patients with obesity and prediabetes, and may constitute a therapeutic target in obesity.

Combination of Metformin and Epigallocatechin-3-Gallate Lowers Cortisol, 11β-Hydroxysteroid Dehydrogenase Type 1, and Blood Glucose Levels in Sprague Dawley Rats with Obesity and Diabetes.

The combined effects of metformin and epigallocatechin-3-gallate (EGCG) on cortisol, 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), and blood glucose levels have not been investigated. This study evaluated the effectiveness of combining EGCG with metformin in regulating those levels in a rat model of diet-induced diabetes and obesity. Thirty diabetic and obese rats on a high-fat diet were treated daily for 28 days with EGCG (100 mg/kg of body weight/day), metformin (200 mg/kg of body weight/day), or both. Control groups comprised lean rats, untreated obese diabetic rats, and metformin-only-treated rats. Blood samples were collected to measure cortisol and fasting blood glucose (FBG) levels and liver tissue samples were examined for 11β-HSD1 levels. Rats receiving combination therapy had significantly reduced cortisol levels (from 36.70±15.13 to 31.25±7.10 ng/mL) compared with the untreated obese diabetic rats but not the rats receiving monotherapy. Rats receiving combination therapy and EGCG monotherapy had significantly lower 11β-HSD1 levels compared with the untreated obese diabetic rats (92.68±10.82 and 93.74±18.11 ng/L vs. 120.66±14.00 ng/L). Combination therapy and metformin monotherapy significantly reduced FBG levels (440.83±133.30 to 140.50±7.36 mg/dL and 480.67±86.32 to 214.17±102.78 mg/dL, respectively) by approximately 68.1% and 55.4% compared with rats receiving EGCG monotherapy and untreated obese diabetic rats. Combining EGCG with metformin exhibited synergistic effects compared with monotherapy for managing diabetes, leading to improved outcomes in reduction of baseline cortisol levels along with reduction in 11β-HSD1 and blood glucose levels.

Exercise training and spexin ameliorate thyroid changes in obese type 2 diabetic rats: the possible interlaying mechanisms.

Thyroid dysfunction and diabetes mellitus are prevalent endocrine disorders that often coexist and influence each other. The role of spexin (SPX) in diabetes and obesity is well documented, but its connection to thyroid function is less understood. This study investigates the influence of exercise (EX) and SPX on thyroid hypofunction in obese type 2 diabetic rats. Rats were divided into normal control, obese diabetic sedentary, obese diabetic EX, and obese diabetic SPX groups, with subdivisions for M871 and HT-2157 treatment in the latter two groups. High-fat diet together with streptozotocin (STZ) injection induced obesity and diabetes. The EX group underwent swimming, and the SPX group received SPX injections for 8 wk. Results showed significant improvements in thyroid function and metabolic, oxidative, and inflammatory states with EX and SPX treatment. The study also explored the involvement of galanin receptor isoforms (GALR)2/3 in SPX effects on thyroid function. Blocking GALR2/3 receptors partially attenuated the beneficial effects, indicating their interaction. These findings underscore the importance of EX and SPX in modulating thyroid function in obesity and diabetes. Comprehending this interplay could enable the development of new treatment approaches for thyroid disorders associated with obese type 2 diabetes. Additional research is necessary to clarify the exact mechanisms connecting SPX, EX activity, and thyroid function.NEW & NOTEWORTHY This study proves, for the first time, the beneficial effects of SPX on thyroid dysfunction in obese diabetic rats and suggests that SPX mediates the EX effect on thyroid gland and exerts its effect mainly via GALR2.

Effects of Delayed Carbohydrate Digestion on Energy Intake, Adiposity and Weight Gain in Congenic Lean and Obese-Diabetic Rats

The burgeoning prevalence of obesity and overweight conditions including NIDDM and dysregulation of energy balance are rapidly approaching epidemic proportions in much of Western society and imposing a significant burden on available health care resources. Once diagnosed, treatment is typically a life-long effort to attenuate the continued progression of pathophysiologic sequela of the disorders. Since the predominate proportion of macronutrient energy source in most Western diets is often carbohydrate, typically more than 50% by weight at ~4 kcals/gram, efforts to modulate the impact of dietary CHO on parameters of adiposity and weight gain were investigated. This study determined the effects of delayed carbohydrate digestion on energy intake and consequent weight gain groups of young adult, obese-NIDDM rats that were fed a USDA-formulated, hyperinsulinemic diet consisting of 54% sucrose plus essential fats, proteins, micronutrients and fiber for up to 8 weeks, or the same diet containing 150 mg/kg of (1,5 dideoxy-1,5-[(2-hydroxyethyl) imino]-D glucitol; generic miglitol). Measures of daily energy intake and weight gain were determined at weekly intervals. Adiposity was determined by dissecting major fat depots at the end of the study and determining adipose tissue mass and cellularity. Miglitol resulted in 20% less energy intake and weight gain, and corresponding decreases in adiposity after 8 weeks of study. The results of this study indicate that delayed carbohydrate digestion via the α-glucosidase inhibitor miglitol or other similar agents may be a useful adjunct in the regulation of food intake and in attenuating weight gain in man and animals in addition to their well-established effects as an adjunct in the treatment of impaired glycemic responses in obesity and NIDDM.

The Significance of Bile in the Biliopancreatic Limb on Metabolic Improvement After Duodenal-Jejunal Bypass

IntroductionDuodenal-jejunal bypass (DJB) is an experimental procedure in metabolic surgery that does not have a restrictive component. Changes in bile acid (BA) dynamics and intestinal microbiota are possibly related to metabolic improvement after DJB. Our previous studies involving obese diabetic rats showed the crucial role of the biliopancreatic limb (BPL) in metabolic improvement after DJB caused by BA reabsorption. We established a new DJB procedure to prevent bile from flowing into the BPL and aimed to elucidate the importance of bile in the BPL after DJB.MethodsOtsuka Long-Evans Tokushima Fatty rats with diabetes were divided into three groups: two DJB groups and a sham group (n = 11). Duodenal-jejunal anastomosis was performed proximal to the papilla of Vater in the DJB group (n = 11). However, the DJB-D group (n = 11) underwent a new procedure with duodenal-jejunal anastomosis distal to the papilla of Vater for preventing bile flow into the BPL.ResultsGlucose metabolism improved and weight gain was suppressed in the DJB group, but not in the DJB-D and sham groups. Serum BA level and conjugated BA concentration were elevated in the DJB group. The gut microbiota was altered only in the DJB group; the abundance of Firmicutes and Bacteroidetes decreased and that of Actinobacteria increased. However, the DJB-D group exhibited no apparent change in the gut microbiota, similar to the sham group.ConclusionBAs are essential in the BPL for metabolic improvement after DJB; they can improve the gut microbiota in these processes.Graphical

Blood Sugar; Lipid Profile and Bone Health of Obese Diabetic Rats fed on Bread Supplemented with Chia and Quinoa Flours

Blood Sugar; Lipid Profile and Bone Health of Obese Diabetic Rats fed on Bread Supplemented with Chia and Quinoa Flours

Impact of High-Intensity Interval Training on GLP-1R/ PKBα Axis in Pancreatic Tissue of Diabetes Rats Induced by High-Fat Diet and STZ

Objective: Apart from hormonal factors and oxidative stress, insulin synthesis is strongly dependent on transcription factors in the pancreas. The aim of the present study was to assess the impact of high-intensity interval training (HIIT) on genes affecting insulin synthesis in diabetic obese rats.&#x0D; Materials and Methods: Type 2 diabetes (T2D) was induced by a 6-week high-fat diet (HFD) and intraperitoneal injection of streptozotocin (25 mg /kg) in 14 male Wistar rats (10 week old, 220±10 g). Rats with fasting glucose levels between 400 and 150 were considered T2D. The diabetic rats were randomly assigned to exercise (HIIT: 6 weeks/5 sessions weekly, n= 7) or control (n= 7) groups. Forty-eight hours after the intervention, fasting GLP-1R and PKBα gene expression in pancreatic tissue and plasma insulin and glucose levels were compared between the groups. Data were compared by independent t-test used to compare variables, version 22 between groups. A P&lt; 0.05 was considered significant.&#x0D; Results: HIIT led to significant increase in PKBα gene expression (P: 0.001) and insulin (P: 0.031) and decreases in glucose concentration (P: 0.001) compared with the control group. No change was observed in the GLP-1R gene expression response to HIIT (P: 0.093).&#x0D; Conclusion: HIIT is associated with increased serum insulin levels in T2D obese rats. Despite no change in GLP-1R, this improvement is probably rooted in increased expression PKBα in pancreas in response to this type of exercise training

Effect of eight weeks of high-intensity interval training and moderate-intensity continuous training with quercetin supplementation on the gene expression of FOXO1 and ATG5 in the liver of diabetic obese rats

Effect of eight weeks of high-intensity interval training and moderate-intensity continuous training with quercetin supplementation on the gene expression of FOXO1 and ATG5 in the liver of diabetic obese rats

Impact of Bariatric Surgery on Subtilisin/Kexin Type 9 (PCSK9) Gene Expression and Inflammation in the Adipose Tissue of Obese Diabetic Rats.

Bariatric surgery improves dyslipidaemia and reduces body weight, but it remains unclear how bariatric surgery modulates gene expression in fat cells to influence the proprotein convertase subtilisin/kexin type 9 (PCSK-9) and low-density lipoprotein receptor (LDLR) gene expression. The expression of the PCSK9/LDLR/tumor necrosis factor-alpha (TNFα) gene in adipose tissue was measured in two groups of Zucker Diabetic Sprague Dawley (ZDSD) rats after Roux-en-Y gastric bypass (RYGB) surgery or 'SHAM' operation. There was lower PCSK9 (p = 0.02) and higher LDLR gene expression (p = 0.02) in adipose tissue in rats after RYGB. Weight change did not correlate with PCSK9 gene expression (r = -0.5, p = 0.08) or TNFα gene expression (r = -0.4, p = 0.1). TNFα gene expression was positively correlated with PCSK9 gene expression (r = 0.7, p = 0.001) but not correlated with LDLR expression (r = -0.3, p = 0.3). Circulating triglyceride levels were lower in RYGB compared to the SHAM group (1.1 (0.8-1.4) vs. 1.5 (1.0-4.2), p = 0.038) mmol/L with no difference in cholesterol levels. LDLR gene expression was increased post-bariatric surgery with the potential to reduce the number of circulating LDL particles. PCSK9 gene expression and TNFα gene expression were positively correlated after RYGB in ZDSD rats, suggesting that the modulation of pro-inflammatory pathways in adipose tissue after RYGB may partly relate to PCSK9 and LDLR gene expression.

Garcinia Mangostana Pericarp Extract Protection on Reproductive Function of Obese-Diabetic Rats Model

Background: Type 2 diabetes mellitus (T2DM) in obese has been considered a risk factor for male infertility. Garcinia mangostana pericarp extract (GMPE) is known to have anti-hyperglycemic, anti-diabetic, and anti-inflammatory effects. This study aimed to evaluate the effect of GMPE therapy on reproductive function in obese T2DM rats by examining testosterone level, testicular histopathological features, and hs-CRP level.Methods: Thirty-six male Wistar rats, aged 2-3 months, were randomly divided into 6 groups and treated with a standard diet (NC), high-fat diet (HFD) with GMPE 200 mg/kgBW (obese GMPE control/OGC200), HFD with 45 mg/kgBW STZ-NA (obese-diabetic control/ODC), obese-diabetic rats with GMPE 100 (DG100); 200 (DG200); and 400 mg/kgBW (DG400). STZ-NA was administered after 8 weeks of HFD treatment and followed by GMPE for 8 weeks after T2DM was confirmed. The level of hs-CRP and testosterone were measured in the serum using an enzyme-linked immunosorbent assay. Testicular histopathological examination was measured after 8 weeks of treatment by using Modified Jonhson Score (MJS) with HE staining.Results: ODC rats significantly showed increased hs-CRP level compared to NC (8.76±0.27 vs 0.30±0.07 ng/mL, P&lt;0.001) and reduced testosterone level and MJS compared to NC (73.69±2.22 vs170.14±1.34 ng/dL, 4.57±0.93 vs 9.87±0.16 MJS, respectively, P&lt;0.001). Testosterone and hs-CRP levels showed a negative and significant correlation (r=-0.974 and P&lt;0.001). On the treatment group, GMPE significantly reduced hs-CRP and increased testosterone levels in a dose-dependent manner.Conclusion: GMPE effectively protects reproductive function in obese DM rats by increasing testosterone levels and advanced spermatogenesis, as well as decreasing hs-CRP level.

Impact of bariatric surgery on glucose and lipid metabolism and liver and kidney function in food-induced obese diabetic rats.

Obesity usually causes diabetes mellitus (DM) and is a serious danger to human health. Type 2 DM (T2DM) mostly occurs along with obesity. Foodborne obesity-induced DM is caused by an excessive long-term diet and surplus energy. Bariatric surgery can improve the symptoms of T2DM in some obese patients. But different types of bariatric surgery may have different effects. To investigate the effect of bariatric surgery on glucose and lipid metabolism and liver and kidney function in rats. Male Sprague-Dawley rats aged 6-8 wk underwent Roux-en-Y gastric bypass surgery (RYGB), sleeve gastrectomy (SG), or gastric banding (GB). Glucose and insulin tolerance tests, analyses of biochemical parameters, histological examination, western blot, and quantitative real-time polymerase chain reaction were conducted. In comparison to the sham operation group, the RYGB, SG, and GB groups had decreased body weight and food intake, reduced glucose intolerance and insulin insensitivity, downregulated biochemical parameters, alleviated morphological changes in the liver and kidneys, and decreased levels of protein kinase C β/ P66shc. The effect in the RYGB group was better than that in the SG and GB groups. These results suggest that RYGB, SG and GB may be helpful for the treatment of foodborne obesity-induced DM.

Effects of High-Intensity Interval Training on Transcription Factor 7-Like 2 / Glucagon-Like Peptide-1 Axis in Pancreatic Tissue of Obese Diabetic Ratsobese diabetic rats

Effects of High-Intensity Interval Training on Transcription Factor 7-Like 2 / Glucagon-Like Peptide-1 Axis in Pancreatic Tissue of Obese Diabetic Ratsobese diabetic rats

Insulin resistance, the unbrowning of brown adipose tissue and beige adipose tissue development in obese and obese-diabetic rats: Is there a link?

Insulin resistance, the unbrowning of brown adipose tissue and beige adipose tissue development in obese and obese-diabetic rats: Is there a link?

Effects of antidiabetics and exercise therapy on suppressors of cytokine signaling-1, suppressors of cytokine signaling-3, and insulin receptor substrate-1 molecules in diabetes and obesity.

Pathological destruction of insulin signaling molecules such as insulin receptor substrate, especially due to the increase in suppressors of cytokine signaling molecules, has been demonstrated in experimental diabetes. The contribution of suppressors of cytokine signaling proteins to the development of insulin resistance and the effects of antidiabetic drugs and exercise on suppressors of cytokine signaling proteins are not clearly known. A total of 48 Wistar albino adult male rats were divided into six groups: control group, obese group with diabetes, obese diabetic rats treated with metformin, obese diabetic rats treated with pioglitazone, obese diabetic rats treated with exenatide, and obese diabetic rats with applied exercise program. Immunohistochemical staining was performed in both the liver and adipose tissue. There was a statistically significant decrease in suppressors of cytokine signaling-1, a decrease in suppressors of cytokine signaling-3, an increase in insulin receptor substrate-1, and a decrease in immunohistochemical staining in the obese group treated with metformin and exenatide compared to the obese group without treatment in the liver tissue (p<0.05). A statistically significant decrease in immunohistochemical staining of suppressors of cytokine signaling-1 and suppressors of cytokine signaling-3 was found in the obese group receiving exercise therapy compared to the obese group without treatment in visceral adipose tissue (p<0.05). Likewise, no significant immunohistochemistry staining was seen in diabetic obese groups. Metformin or exenatide treatment could prevent the degradation of insulin receptor substrate-1 protein by reducing the effect of suppressors of cytokine signaling-1 and suppressors of cytokine signaling-3 proteins, especially in the liver tissue. In addition, exercise can play a role as a complementary therapy by reducing suppressors of cytokine signaling-1 and suppressors of cytokine signaling-3 proteins in visceral adipose tissue.