scholarly journals Beneficial Effects of Alpha-Lipoic Acid on Hypertension, Visceral Obesity, UCP-1 Expression and Oxidative Stress in Zucker Diabetic Fatty Rats

Antioxidants ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 648 ◽  
Author(s):  
Adil El Midaoui ◽  
I. George Fantus ◽  
Ali Ait Boughrous ◽  
Réjean Couture
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Body Weight ◽  
Gastrocnemius Muscle ◽  
Antioxidant Properties ◽  
Visceral Obesity ◽  
Adipocyte Hypertrophy ◽  
Zdf Rats ◽  
Protein Staining ◽  
O2 Production

Evidence suggests that oxidative stress plays a major role in the development of metabolic syndrome. This study aims to investigate whether α-lipoic acid (LA), a potent antioxidant, could exert beneficial outcomes in Zucker diabetic fatty (ZDF) rats. Male 6-week-old ZDF rats and their lean counterparts (ZL) were fed for six weeks with a standard diet or a chow diet supplemented with LA (1 g/kg feed). At 12 weeks of age, ZDF rats exhibited an increase in systolic blood pressure, epididymal fat weight per body weight, hyperglycemia, hyperinsulinemia, insulin resistance (HOMA index), adipocyte hypertrophy and a rise in basal superoxide anion (O2•−) production in gastrocnemius muscle and a downregulation of epididymal uncoupled protein-1 (UCP-1) protein staining. Treatment with LA prevented the development of hypertension, the rise in whole body weight and O2•− production in gastrocnemius muscle, but failed to affect insulin resistance, hyperglycemia and hyperinsulinemia in ZDF rats. LA treatment resulted in a noticeable increase of pancreatic weight and a further adipocyte hypertrophy, along with a decrease in epididymal fat weight per body weight ratio associated with an upregulation of epididymal UCP-1 protein staining in ZDF rats. These findings suggest that LA was efficacious in preventing the development of hypertension, which could be related to its antioxidant properties. The anti-visceral obesity effect of LA appears to be mediated by its antioxidant properties and the induction of UCP-1 protein at the adipose tissue level in ZDF rats. Disorders of glucose metabolism appear, however, to be mediated by other unrelated mechanisms in this model of metabolic syndrome.

scholarly journals Caloric Restriction Reverses Hepatic Insulin Resistance and Steatosis in Rats with Low Aerobic Capacity

Endocrinology ◽  
2010 ◽  
Vol 151 (11) ◽  
pp. 5157-5164 ◽  
Author(s):  
Thomas A. Bowman ◽  
Sadeesh K. Ramakrishnan ◽  
Meenakshi Kaw ◽  
Sang Jun Lee ◽  
Payal R. Patel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Caloric Restriction ◽  
Visceral Obesity ◽  
Insulin Clearance ◽  
Hepatic Insulin Resistance ◽  
The Metabolic Syndrome ◽  
Cell Adhesion Molecule 1 ◽  
Muscle Triglyceride

Rats selectively bred for low aerobic running capacity exhibit the metabolic syndrome, including hyperinsulinemia, insulin resistance, visceral obesity, and dyslipidemia. They also exhibit features of nonalcoholic steatohepatitis, including chicken-wire fibrosis, inflammation, and oxidative stress. Hyperinsulinemia in these rats is associated with impaired hepatic insulin clearance. The current studies aimed to determine whether these metabolic abnormalities could be reversed by caloric restriction (CR). CR by 30% over a period of 2–3 months improved insulin clearance in parallel to inducing the protein content and activation of the carcinoembryonic antigen-related cell adhesion molecule 1, a main player in hepatic insulin extraction. It also reduced glucose and insulin intolerance and serum and tissue (liver and muscle) triglyceride levels. Additionally, CR reversed inflammation, oxidative stress, and fibrosis in liver. The data support a significant role of CR in the normalization of insulin and lipid metabolism in liver.

scholarly journals Isolation, Characterization and Neuroprotective Activity of Folecitin: An In Vivo Study

Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 825
Author(s):  
Umar Farooq ◽  
Taous Khan ◽  
Shahid Ali Shah ◽  
Md. Sanower Hossain ◽  
Yousaf Ali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Nlrp3 Inflammasome ◽  
Interleukin 1 ◽  
Antioxidant Properties ◽  
Neuroprotective Activity ◽  
Bioactive Metabolites ◽  
Inflammasome Activation ◽  
Dependent Manner ◽  
Rat Pups

Neurodegenerative diseases (NDs) extend the global health burden. Consumption of alcohol as well as maternal exposure to ethanol can damage several neuronal functions and cause cognition and behavioral abnormalities. Ethanol induces oxidative stress that is linked to the development of NDs. Treatment options for NDs are yet scarce, and natural product-based treatments could facilitate ND management since plants possess plenty of bioactive metabolites, including flavonoids, which typically demonstrate antioxidant and anti-inflammatory properties. Hypericum oblongifolium is an important traditional medicinal plant used for hepatitis, gastric ulcer, external wounds, and other gastrointestinal disorders. However, it also possesses multiple bioactive compounds and antioxidant properties, but the evaluation of isolated pure compounds for neuroprotective efficacy has not been done yet. Therefore, in the current study, we aim to isolate and characterize the bioactive flavonoid folecitin and evaluate its neuroprotective activity against ethanol-induced oxidative-stress-mediated neurodegeneration in the hippocampus of postnatal day 7 (PND-7) rat pups. A single dose of ethanol (5 g/kg body weight) was intraperitoneally administered after the birth of rat pups on PND-7. This caused oxidative stress accompanied by the activation of phosphorylated-c-Jun N-terminal kinase (p-JNK), nod-like receptor family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein (ASC), and cysteine-aspartic acid protease-1 (caspase-1) proteins to form a complex called the NLRP3-inflammasome, which converts pro-interleukin 1 beta (IL-1B) to activate IL-1B and induce widespread neuroinflammation and neurodegeneration. In contrast, co-administration of folecitin (30 mg/kg body weight) reduced ethanol-induced oxidative stress, inhibited p-JNK, and deactivated the NLRP3-inflammasome complex. Furthermore, folecitin administration reduced neuroinflammatory and neurodegenerative protein markers, including decreased caspase-3, BCL-2-associated X protein (BAX), B cell CLL/lymphoma 2 (BCL-2), and poly (ADP-ribose) polymerase-1 (PARP-1) expression in the immature rat brain. These findings conclude that folecitin is a flavone compound, and it might be a novel, natural and safe agent to curb oxidative stress and its downstream harmful effects, including inflammasome activation, neuroinflammation, and neurodegeneration. Further evaluation in a dose-dependent manner would be worth it in order to find a suitable dose regimen for NDs.

scholarly journals Age-dependent increase in oxidative stress in gastrocnemius muscle with unloading

2008 ◽  
Vol 105 (6) ◽  
pp. 1695-1705 ◽  
Author(s):  
Parco M. Siu ◽  
Emidio E. Pistilli ◽  
Stephen E. Alway
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Young Adult ◽  
Gastrocnemius Muscle ◽  
Medial Gastrocnemius ◽  
Brown Norway ◽  
Aged Rats ◽  
Muscle Weight ◽  
Animal Body ◽  
Age Dependent

Oxidative stress increases during unloading in muscle from young adult rats. The present study examined the markers of oxidative stress and antioxidant enzyme gene and protein expressions in medial gastrocnemius muscles of aged and young adult (30 and 6 mo of age) Fischer 344 × Brown Norway rats after 14 days of hindlimb suspension. Medial gastrocnemius muscle weight was decreased by ∼30% in young adult and aged rats following suspension. When muscle weight was normalized to animal body weight, it was reduced by 12% and 22% in young adult and aged rats, respectively, after suspension. Comparisons between young adult and aged control animals demonstrated a 25% and 51% decline in muscle mass when expressed as absolute muscle weight and muscle weight normalized to the animal body weight, respectively. H2O2 content was elevated by 43% while Mn superoxide dismutase (MnSOD) protein content was reduced by 28% in suspended muscles compared with control muscles exclusively in the aged animals. Suspended muscles had greater content of malondialdehyde (MDA)/4-hydroxyalkenals (4-HAE) (29% and 58% increase in young adult and aged rats, respectively), nitrotyrosine (76% and 65% increase in young adult and aged rats, respectively), and catalase activity (69% and 43% increase in young adult and aged rats, respectively) relative to control muscles. Changes in oxidative stress markers MDA/4-HAE, H2O2, and MnSOD protein contents in response to hindlimb unloading occurred in an age-dependent manner. These findings are consistent with the hypotheses that oxidative stress has a role in mediating disuse-induced and sarcopenia-associated muscle losses. Our data suggest that aging may predispose skeletal muscle to increased levels of oxidative stress both at rest and during unloading.

scholarly journals Effects of the Angiotensin Receptor Blocker Olmesartan on Adipocyte Hypertrophy and Function in Mice with Metabolic Disorders

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Akinobu Maeda ◽  
Kouichi Tamura ◽  
Hiromichi Wakui ◽  
Masato Ohsawa ◽  
Kengo Azushima ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Adipose Tissue ◽  
Metabolic Disorders ◽  
Visceral Obesity ◽  
Pleiotropic Effects ◽  
Stress Axis ◽  
Therapeutic Effects ◽  
Kkay Mice ◽  
Adipocyte Hypertrophy

In the present study, we examined the therapeutic effects of olmesartan, an angiotensin II (Ang II) type 1 receptor (AT1R)-specific blocker, in genetically obese diabetic KKAy mice, a model of human metabolic disorders with visceral obesity, with a focus on an olmesartan effect on the adipose tissue. Olmesartan treatment (3 mg/kg per day) for 4 weeks significantly lowered systolic blood pressure but did not affect body weight during the study period in KKAy mice. However, there were three interesting findings possibly related to the pleiotropic effects of olmesartan on adipose tissue in KKAy mice: (1) an inhibitory effect on adipocyte hypertrophy, (2) a suppressive effect on IL-6 gene expression, and (3) an ameliorating effect on oxidative stress. On the other hand, olmesartan exerted no evident influence on the adipose tissue expression of AT1R-associated protein (ATRAP), which is a molecule interacting with AT1R so as to inhibit pathological AT1R activation and is suggested to be an emerging molecular target in metabolic disorders with visceral obesity. Collectively, these results suggest that the blood pressure lowering effect of olmesartan in KKAy mice is associated with an improvement in adipocyte, including suppression of adipocyte hypertrophy and inhibition of the adipose IL-6-oxidative stress axis. Further study is needed to clarify the functional role of adipose ATRAP in the pleiotropic effects of olmesartan.

Preventive effect of curcumin on inflammation, oxidative stress and insulin resistance in high-fat fed obese rats

2016 ◽  
Vol 13 (2) ◽  
Author(s):  
Nachimuthu Maithilikarpagaselvi ◽  
Magadi Gopalakrishna Sridhar ◽  
Rathinam Palamalai Swaminathan ◽  
Ramalingam Sripradha
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Body Weight ◽  
Density Lipoprotein ◽  
High Fat ◽  
Oxidative Stress Parameters ◽  
Tnf Α ◽  
Male Wistar Rats ◽  
Fat Feeding

Abstract: The present study investigated the beneficial effects of curcumin on inflammation, oxidative stress and insulin resistance in high-fat fed male Wistar rats.: Five-month-old male Wistar rats (n=20) were divided into two groups (10 rats in each group). Among the two groups, one group received 30 % high-fat diet (HFD) and another group received 30 % HFD with curcumin (200 mg/kg body weight). Food intake, body weight and biochemical parameters were measured at the beginning and at the end of the study. After 10 weeks, oxidative stress parameters in skeletal muscle and hepatic triacylglycerol (TAG) content were estimated. Histological examinations of the liver samples were performed at the end of the experiment.: High-fat feeding caused increase in body weight, liver and adipose tissue mass. Rats fed with HFD showed increased levels of fasting plasma glucose, insulin, Homeostasis Model Assessment for Insulin resistance (HOMA-IR), total cholesterol (TC), TAG, very low density lipoprotein cholesterol (VLDL-c) and decreased high-density lipoprotein cholesterol (HDL-c). There was also increase in the plasma inflammatory markers [tumor necrosis factor-α (TNF-α), C-reactive protein (CRP)] and skeletal muscle oxidative stress parameters [malondialdehyde (MDA), total oxidant status (TOS)] in these rats. In addition, high-fat feeding increased liver TAG content and caused fat accumulation in the liver. Treatment with curcumin significantly reduced body weight, relative organ weights (liver, adipose tissue), glucose, insulin and HOMA-IR. Curcumin supplementation decreased plasma levels of TC, TAG, VLDL-c, TNF-α and increased HDL-c. Administration of curcumin also reduced MDA, TOS in skeletal muscle, hepatic TAG content and liver fat deposition.: Curcumin supplementation improved HFD-induced dyslipidemia, oxidative stress, inflammation and insulin resistance.

scholarly journals Effects of Concurrent Training on Oxidative Stress and Insulin Resistance in Obese Individuals

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Niara da Silva Medeiros ◽  
Fabiana Guichard de Abreu ◽  
Alana Schraiber Colato ◽  
Leandro Silva de Lemos ◽  
Thiago Rozales Ramis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Body Weight ◽  
Oxidative Damage ◽  
Body Fat ◽  
Moderate Intensity ◽  
Concurrent Training ◽  
Tbars Level ◽  
Anthropometric Parameters ◽  
And Oxidative Stress

Obesity is associated with insulin resistance (IR) and increased oxidative stress. Thus, the present study aimed to evaluate anthropometric parameters, IR, and oxidative stress in obese individuals subjected to two types of concurrent training at the same intensity but differing in frequency. Accordingly, 25 individuals were divided into two groups: concurrent training 1 (CT1) (5 d/wk) and concurrent training 2 (CT2) (3 d/wk), both with moderate intensity. Anthropometric parameters, IR, and oxidative stress were analyzed before and after 26 sessions of training. Both groups had reduced body weight and body mass index (P<0.05), but only CT1 showed lower body fat percentage and increased basal metabolic rate (P<0.05). Moreover, CT1 had increased HOMA-IR and decreased protein damage (carbonyl level), and CT2 had decreased HOMA-IR and increased lipid peroxidation (TBARS level) (P<0.05). On the other hand, both training protocols reduced the GPx activity. It can be concluded that both types of concurrent training could be an alternative for lowering body weight and BMI. Also, it was observed that concurrent training, depending on the frequency, can contribute to reducing body fat, oxidative damage (protein oxidation), and IR but can induce oxidative damage to lipids. More studies are needed to elucidate the mechanisms involved.

scholarly journals Role of the Neutral Amino Acid Transporter Slc7a10 in Adipocyte Lipid Storage, Obesity and Insulin Resistance

2021 ◽  
Author(s):  
Ada Admin ◽  
Regine Å. Jersin ◽  
Divya Sri Priyanka Tallapragada ◽  
André Madsen ◽  
Linn Skartveit ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Amino Acid ◽  
Lipid Accumulation ◽  
Lipid Storage ◽  
Ros Generation ◽  
Neutral Amino Acid Transporter ◽  
Adipocyte Hypertrophy

Elucidation of mechanisms that govern lipid storage, oxidative stress and insulin resistance may lead to improved therapeutic options for type 2 diabetes and other obesity-related diseases. Here, we find that adipose expression of the small neutral amino acid transporter SLC7A10, also known as alanine-serine-cysteine transporter 1 (ASC-1), shows strong inverse correlates with visceral adiposity, insulin resistance and adipocyte hypertrophy across multiple cohorts. Concordantly, loss of Slc7a10 function in zebrafish <i>in vivo</i> accelerates diet-induced body weight gain and adipocyte enlargement. Mechanistically, SLC7A10 inhibition in human and murine adipocytes decreases adipocyte serine uptake and total glutathione levels and promotes reactive oxygen species (ROS) generation. Conversely, SLC7A10 overexpression decreases ROS generation and increases mitochondrial respiratory capacity. RNA-sequencing revealed consistent changes in gene expression between human adipocytes and zebrafish visceral adipose tissue following loss of SLC7A10, e.g., upregulation of <i>SCD</i> (lipid storage) and downregulation of <i>CPT1A</i> (lipid oxidation). Interestingly, ROS scavenger reduced lipid accumulation and attenuated the lipid-storing effect of SLC7A10 inhibition. These data uncover adipocyte SLC7A10 as a novel important regulator of adipocyte resilience to nutrient and oxidative stress, in part by enhancing glutathione levels and mitochondrial respiration, conducive to decreased ROS generation, lipid accumulation, adipocyte hypertrophy, insulin resistance and type 2 diabetes.

scholarly journals Cardioprotective Effects of Metformin and Vildagliptin in Adult Rats with Insulin Resistance Induced by a High-Fat Diet

Endocrinology ◽  
2012 ◽  
Vol 153 (8) ◽  
pp. 3878-3885 ◽  
Author(s):  
Nattayaporn Apaijai ◽  
Hiranya Pintana ◽  
Siriporn C. Chattipakorn ◽  
Nipon Chattipakorn
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Body Weight ◽  
Mitochondrial Dysfunction ◽  
Cardiac Dysfunction ◽  
High Fat Diet ◽  
Plasma Insulin ◽  
High Fat ◽  
Antidiabetic Drug ◽  
Sympathovagal Imbalance

Insulin resistance has been shown to be associated with cardiac sympathovagal imbalance, myocardial dysfunction, and cardiac mitochondrial dysfunction. Whereas metformin is a widely used antidiabetic drug to improve insulin resistance, vildagliptin is a novel oral antidiabetic drug in a group of dipeptidyl peptidase-4 inhibitors in which its cardiac effect is unclear. This study aimed to determine the cardiovascular effects of metformin and vildagliptin in rats with insulin resistance induced by high-fat diet. Male Wistar rats were fed with either a normal diet or high-fat diet (n =24 each) for 12 wk. Rats in each group were divided into three subgroups to receive the vehicle, metformin (30 mg/kg, twice daily), or vildagliptin (3 mg/kg, once daily) for another 21 d. Heart rate variability (HRV), cardiac function, and cardiac mitochondrial function were determined and compared among these treatment groups. Rats exposed to a high-fat diet developed increased body weight, visceral fat, plasma insulin, cholesterol, oxidative stress, depressed HRV, and cardiac mitochondrial dysfunction. Metformin and vildagliptin did not alter body weight and plasma glucose levels but decreased the plasma insulin, total cholesterol, and oxidative stress levels. Although both metformin and vildagliptin attenuated the depressed HRV, cardiac dysfunction, and cardiac mitochondrial dysfunction, vildagliptin was more effective in this prevention. Furthermore, only vildagliptin prevented cardiac mitochondrial membrane depolarization caused by consumption of a high-fat diet. We concluded that vildagliptin is more effective in preventing cardiac sympathovagal imbalance and cardiac dysfunction, as well as cardiac mitochondrial dysfunction, than metformin in rats with insulin resistance induced by high-fat diet.

scholarly journals IN VIVO HEPATOPROTECTIVE EFFECT OF CAFFEIC ACID ON MERCURIC CHLORIDE-INDUCED BIOCHEMICAL CHANGES IN ALBINO WISTAR RATS

2019 ◽  
pp. 119-124
Author(s):  
MANOGARAN MANJU ◽  
GANESAN JAGASEESAN
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Caffeic Acid ◽  
Liver Tissue ◽  
Wistar Rats ◽  
Control Level ◽  
Antioxidant Properties ◽  
Sublethal Dose ◽  
Mercury Chloride

Objective: Mercury (Hg) is a highly dangerous and also one of the harmful heavy metals which induces oxidative stress in the animal body. The present study is planned to examine the possible defensive result of caffeic acid (CA) against mercury chloride (HgCl2)-induced hepatotoxicity in male albino Wistar rats, Rattus norvegicus. Methods: Sublethal dose of HgCl2 (1.29 mg/kg body weight) was administrated in rats for 15 days through oral dose and the CA was administrated for another 15 days on mercuric-intoxicated rats. After completing the scheduled exposure time, the rats were sacrificed and the whole liver organ was removed immediately from the animal, and it was used to carry out for biochemical and bioenzymological studies to observe. Results: The level of lipid peroxidation (LPO) content reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in the liver tissue. CA is an energetic component in the phenolic propolis extract and also in a wide variety of plants, and a strong antioxidant helps to prevent oxidative damage and to reduce oxidative stress. The antioxidants such as GPx, CAT, and SOD and non-antioxidant GSH were significantly decreased, and also, the LPO level was increased in mercury toxicity rats. The treatment of CA (5 mg/kg body weight) in the liver tissue shows considerable declining in the level of oxidant content and along with an increase in the level of antioxidant properties by the way of improvement in liver tissues. Antioxidant and non-antioxidant enzyme (LOP, GSH, GPx, SOD, and CAT) activities were also significantly decreased to near untreated control level when compared to Hg-treated group. The CA acid alone treatment showed the enhanced antioxidant levels and not any alteration in the levels of biochemical parameters when compared with control. Conclusion: These observations of the present experimental study clearly explained the detoxify effects and protective effect of CA against HgCl2 toxicity in liver tissue.

scholarly journals Chronic Inflammation in Obesity and the Metabolic Syndrome

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Rosário Monteiro ◽  
Isabel Azevedo
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Stress Reactions ◽  
The Metabolic Syndrome ◽  
Inflammatory Status ◽  
Adipose Tissue Development ◽  
Adipocyte Hypertrophy ◽  
Physical Reasons ◽  
New Hypothesis

The increasing incidence of obesity and the metabolic syndrome is disturbing. The activation of inflammatory pathways, used normally as host defence, reminds the seriousness of this condition. There is probably more than one cause for activation of inflammation. Apparently, metabolic overload evokes stress reactions, such as oxidative, inflammatory, organelle and cell hypertrophy, generating vicious cycles. Adipocyte hypertrophy, through physical reasons, facilitates cell rupture, what will evoke an inflammatory reaction. Inability of adipose tissue development to engulf incoming fat leads to deposition in other organs, mainly in the liver, with consequences on insulin resistance. The oxidative stress which accompanies feeding, particularly when there is excessive ingestion of fat and/or other macronutrients without concomitant ingestion of antioxidant-rich foods/beverages, may contribute to inflammation attributed to obesity. Moreover, data on the interaction of microbiota with food and obesity brought new hypothesis for the obesity/fat diet relationship with inflammation. Beyond these, other phenomena, for instance psychological and/or circadian rhythm disturbances, may likewise contribute to oxidative/inflammatory status. The difficulty in the management of obesity/metabolic syndrome is linked to their multifactorial nature where environmental, genetic and psychosocial factors interact through complex networks.

Sign in / Sign up

Export Citation Format

Share Document