scholarly journals Ameliorative Effect of Hexane Extract ofPhalaris canariensison High Fat Diet-Induced Obese and Streptozotocin-Induced Diabetic Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Rosa Martha Perez Gutierrez ◽  
Diana Madrigales Ahuatzi ◽  
Maria del Carmen Horcacitas ◽  
Efren Garcia Baez ◽  
Teresa Cruz Victoria ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
High Fat Diet ◽  
Serum Insulin ◽  
Body Weight Loss ◽  
Insulin Level ◽  
Hexane Extract ◽  
Diabetic Mice ◽  
High Fat ◽  
Obesity And Diabetes

Obesity is one of the major factors to increase various disorders like diabetes. The present paper emphasizes study related to the antiobesity effect ofPhalaris canariensisseeds hexane extract (Al-H) in high-fat diet- (HFD-) induced obese CD1 mice and in streptozotocin-induced mild diabetic (MD) and severely diabetic (SD) mice.AL-H was orally administered to MD and SD mice at a dose of 400 mg/kg once a day for 30 days, and a set of biochemical parameters were studied: glucose, cholesterol, triglycerides, lipid peroxidation, liver and muscle glycogen, ALP, SGOT, SGPT, glucose-6-phosphatase, glucokinase, hexokinase, SOD, CAT, GSH, GPX activities, and the effect on insulin level. HS-H significantly reduced the intake of food and water and body weight loss as well as levels of blood glucose, serum cholesterol, triglyceride, lipoprotein, oxidative stress, showed a protective hepatic effect, and increased HDL-cholesterol, serum insulin in diabetic mice. The mice fed on the high-fat diet and treated with AL-H showed inhibitory activity on the lipid metabolism decreasing body weight and weight of the liver and visceral adipose tissues and cholesterol and triglycerides in the liver. We conclude that AL-H can efficiently reduce serum glucose and inhibit insulin resistance, lipid abnormalities, and oxidative stress in MD and SD mice. Our results demonstrate an antiobesity effect reducing lipid droplet accumulation in the liver, indicating that its therapeutic properties may be due to the interaction plant components soluble in the hexane extract, with any of the multiple targets involved in obesity and diabetes pathogenesis.

scholarly journals Effect of endurance exercise on oxidative stress marker malondialdehyde in type 2 diabetic mice.

2020 ◽  
Vol 27 (07) ◽  
pp. 1493-1498
Author(s):  
Sana Akram ◽  
Maimona Tabssum ◽  
Maryam Rao ◽  
Hamid Javaid Qureshi
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Endurance Exercise ◽  
High Fat Diet ◽  
Exercise Program ◽  
Oxidative Stress Marker ◽  
Diabetic Mice ◽  
High Fat ◽  
Type 2 Diabetic

Diabetes is associated with oxidative stress and has a significant role in the pathophysiology of the disease and its complications. Exercise training is a powerful therapeutic approach in diabetes and has protective effects against the progress of its complications. Objectives: The aim of this study was to investigate the effect of an endurance exercise program on the oxidative stress marker malondialdehyde (MDA) in high fat diet-low dose streptozotocin induced type 2 diabetic mouse model. Study Design: Randomized Control trial. Setting: Department of Physiology, Akhtar Saeed Medical and Dental College, Lahore. Period: August 2017 to August 2018. Material & Methods: 60 male albino mice were fed a high fat diet containing 60% kCal as fat for 4 weeks. This was followed by intra peritoneal injection of 40mg/kg body weight streptozotocin, given on three consecutive days. Mice with fasting blood glucose more than 250mg/dl after a week were considered diabetic. Half the mice underwent an exercise program which comprised of a 20 minute swimming session per day, with a 6% body weight load attached to the tail of mice, 3 days a week, for 4 weeks. The level of MDA was estimated in both groups using TBARs method. Results: Mean malondialdehyde level was significantly (p˂0.05) reduced in diabetic mice that underwent endurance exercise training. Conclusion: This study highlights the important role of endurance exercise in reducing oxidative stress in diabetes.

scholarly journals Early Overnutrition Results in Early-Onset Arcuate Leptin Resistance and Increased Sensitivity to High-Fat Diet

Endocrinology ◽  
2010 ◽  
Vol 151 (4) ◽  
pp. 1598-1610 ◽  
Author(s):  
Maria M. Glavas ◽  
Melissa A. Kirigiti ◽  
Xiao Q. Xiao ◽  
Pablo J. Enriori ◽  
Sarah K. Fisher ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
High Fat Diet ◽  
Arcuate Nucleus ◽  
Leptin Resistance ◽  
Signal Transducer ◽  
High Fat ◽  
Insulin Tolerance ◽  
Obesity And Diabetes ◽  
Transcription 3

Childhood obesity increases the risk of adult obesity and diabetes, suggesting that early overnutrition permanently programs altered energy and glucose homeostasis. In the present studies, we used a mouse model to investigate whether early overnutrition increases susceptibility to obesity and insulin resistance in response to a high-fat diet (HFD). Litters from Swiss Webster dams were culled to three [chronic postnatal overnutrition (CPO)] or 10 (control) pups and then weaned onto standard chow at postnatal day (P) 23. At 6 wk of age, a subset of mice was placed on HFD, and glucose and insulin tolerance were examined at 16–17 wk of age. Leptin sensitivity was determined by hypothalamic phosphorylated signal transducer and activator of transcription-3 immunoreactivity at P16 and adulthood after ip leptin. CPO mice exhibited accelerated body weight gain and hyperleptinemia during the preweaning period but only a slightly heavier body weight and normal glucose tolerance in adulthood on standard chow diet. Importantly, CPO mice exhibited significant leptin resistance in the arcuate nucleus, demonstrated by reduced activation of phospho-signal transducer and activator of transcription-3, as early as P16 and throughout life, despite normalized leptin levels. In response to HFD, CPO but not control mice displayed insulin resistance in response to an insulin tolerance test. In conclusion, CPO mice exhibited early and persistent leptin resistance in the arcuate nucleus and, in response to HFD, rapid development of obesity and insulin resistance. These studies suggest that early overnutrition can permanently alter energy homeostasis and significantly increase susceptibility to obesity and insulin resistance.

scholarly journals The PYY/Y2R-Deficient Mouse Responds Normally to High-Fat Diet and Gastric Bypass Surgery

2019 ◽  
Author(s):  
Brandon Boland ◽  
Michael B. Mumphrey ◽  
Zheng Hao ◽  
Benji Gill ◽  
R. Leigh Townsend ◽  
...  
Keyword(s):  
Gastric Bypass ◽  
Body Composition ◽  
Body Weight ◽  
High Fat Diet ◽  
Body Weight Loss ◽  
Liver Weight ◽  
Receptor Subtypes ◽  
High Fat ◽  
Knockout Mouse Model ◽  
Gut Hormone

Background/Goals: The gut hormone PYY secreted from intestinal L-cells has been implicated in the mechanisms of satiation via Y2-receptor (Y2R) signaling in the brain and periphery and is a major candidate for mediating the beneficial effects of bariatric surgery on appetite and body weight. Methods: Here we assessed the role of Y2R signaling in the response to low- and high-fat diets and its role in the effects of Roux-en-Y gastric bypass (RYGB) surgery on body weight, body composition, food intake, energy expenditure and glucose handling, in global Y2R-deficient (Y2RKO) and wildtype mice made obese on high-fat diet. Results: Both male and female Y2RKO mice responded normally to low- and high-fat diet in terms of body weight, body composition, fasting levels of glucose and insulin, as well as glucose and insulin tolerance for up to 30 weeks of age. Contrary to expectations, obese Y2RKO mice also responded similarly to RYGB compared to WT mice for up to 20 weeks after surgery, with initial hypophagia, sustained body weight loss, and significant improvements in fasting insulin, glucose tolerance, HOMA-IR, and liver weight compared to sham-operated mice. Furthermore, non-surgical Y2RKO mice weight-matched to RYGB showed the same improvements in glycemic control as Y2RKO mice with RYGB that were similar to WT mice. Conclusions: PYY signaling through Y2R is not required for the normal appetite-suppressing and body weight-lowering effects of RYGB in this global knockout mouse model. Potential compensatory adaptations of PYY signaling through other receptor subtypes or other gut satiety hormones such as GLP-1 remain to be investigated.

scholarly journals In vivo antidiabetic activities of green and black tea polysaccharides using streptozotocin- induced diabetic mice fed with a high-fat diet

2019 ◽  
Vol 8 ◽  
Author(s):  
Kübra Akalın ◽  
Arzu Taş Ekiz ◽  
Fatih Karakaya ◽  
Ayse Karadag ◽  
Ebru Pelvan ◽  
...  
Keyword(s):  
Body Weight ◽  
Treatment Period ◽  
High Fat Diet ◽  
Black Tea ◽  
High Energy ◽  
Diabetic Mice ◽  
High Fat ◽  
Tea Polysaccharides ◽  
Green And Black Tea

Type-2 diabetes (T2D) is the most common type of chronic disease in adults and accounts for around 90% of all cases of diabetes. Therefore, developing dietary supplements from natural sources, such as teas, is of great interest. Seven diet groups together with a parallel control group were used for three periods of 16 weeks in total [stabilization period (W-2-W0), model period (W0-W8), and treatment period (W8-W14)]. The primary aim of this study was to investigate the in vivo antidiabetic activities of green and black tea polysaccharides (GTPS and BTPS, respectively) using streptozotocin induced diabetic mice fed with either a high-fat diet (HFD) or normal diet (ND). Streptozotocin and HFD induced T2D in vivo model was developed during the model period (W0-W8) in C57BL/6J male mice. Both GTPS and BTPS groups were administrated for 6 weeks (daily 400 mg/kg body weight) by oral gavage throughout the treatment period (W8-W14). The results showed that BTPS group significantly (P < 0.05) decreased the fasting blood glucose level in diabetic mice even fed with a HFD and improved the insulin resistance. Similar effect was not obtained when GTPS group fed with a HFD. In addition, BTPS group fed with a HFD effectively suppressed the body weight gain despite high energy intake and was more successful than its GTPS counterpart group in healing pathologies of liver and affected plasma blood lipid levels due to streptozotocin and HFD-induced diabetes. The present work suggests that BTPS can be used as an antidiabetic dietary supplement without posing any potential health risk.

scholarly journals Effects of Omega-3 Fatty Acids on Insulin Resistance in an Ovariectomized Mouse Model of Diet-Induced Obesity Treated with Chemotherapy

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 345-345
Author(s):  
Kate Ormiston ◽  
Zihan Zhang ◽  
Kelly Murphy ◽  
A Courtney DeVries ◽  
Maryam Lustberg ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Blood Glucose ◽  
Body Fat ◽  
High Fat Diet ◽  
Serum Insulin ◽  
Model Assessment ◽  
Omega 3 ◽  
High Fat ◽  
Body Weights

Abstract Objectives Our objective was to examine effects of dietary enrichment of eicosapentaenoic acid + docosahexaenoic acid (EPA + DHA) on high fat diet-induced insulin resistance during chemotherapy. Methods Adult, female C57Bl/6 mice (n = 48) were assigned to 1 of 3 diets; low-fat diet (LF; 10% kcals fat), high-fat diet (HF; 45% kcals fat), or HF diet with omega-3 s (HF n-3; 2% kcals EPA + DHA) for 7 weeks. Mice received vehicle or chemotherapy injections (doxorubicin + cyclophosphamide), by tail vein at week 4 and 6. Food intake and body weights were recorded. Fasted blood glucose and serum insulin were measured weekly.  Homeostatic model assessment of insulin resistance (HOMA-IR) was calculated. Body composition was measured using Echo MRI. Data were analyzed using ANOVA; p &lt; 0.05 was considered significant. Results Total kilocalories significantly differed by group (p &lt; 0.001); HF and HF n-3 groups consumed more than the LF group (p &lt; 0.001, p &lt; 0.0001; respectively). Obesity was induced prior to first injection with body weights being significantly different (p &lt; 0.01); the LF group weighed less than the HF n-3 group (p &lt; 0.01), and there was a similar trend between LF and HF groups (p = 0.0519). Body weights at sacrifice significantly differed (p &lt; 0.0001); chemotherapy mice weighed less than vehicle (p &lt; 0.0001). Percent body fat at sacrifice significantly differed (p &lt; 0.0001); chemotherapy mice had less fat than vehicle (p &lt; 0.0001), and the LF group had less fat than HF  (p &lt; 0.01) and HF n-3 group (p &lt; 0.01). Blood glucose significantly differed at sacrifice (p &lt; 0.01); chemotherapy mice had lower glucose than vehicle (p &lt; 0.05) and HF group had higher glucose than LF group (p &lt; 0.01). HOMA-IR scores at sacrifice significantly differed (p &lt; 0.05); chemotherapy mice had lower scores than vehicle  (p &lt; 0.05) and mice on the LF and HF n-3 diets had lower scores than the HF diet (p &lt; 0.01; p &lt; 0.05 respectively). Conclusions Chemotherapy lowered body weight and body fat in mice, potentially contributing to decreases in blood glucose and insulin resistance. EPA + DHA enrichment of a HF diet reduced insulin resistance in mice comparable to a LF diet group. This occurred in both chemotherapy and vehicle treated mice, despite LF diet-fed mice having lower body weight and adiposity. Underlying mechanisms are being investigated. Funding Sources NIH #5R01CA18994.

scholarly journals Replacing Part of Glucose with Galactose in the Postweaning Diet Protects Female But Not Male Mice from High-Fat Diet–Induced Adiposity in Later Life

2019 ◽  
Vol 149 (7) ◽  
pp. 1140-1148 ◽  
Author(s):  
Lianne M S Bouwman ◽  
José M S Fernández-Calleja ◽  
Inge van der Stelt ◽  
Annemarie Oosting ◽  
Jaap Keijer ◽  
...  
Keyword(s):  
Body Weight ◽  
Insulin Receptor ◽  
High Fat Diet ◽  
Serum Insulin ◽  
Later Life ◽  
Partial Replacement ◽  
Model Assessment ◽  
High Fat ◽  
Female Mice ◽  
Subcutaneous White Adipose Tissue

ABSTRACT Background Duration of breastfeeding is positively associated with decreased adiposity and increased metabolic health in later life, which might be related to galactose. Objective The aim of this study was to investigate if partial replacement of glucose with galactose in the postweaning diet had a metabolic programming effect. Methods Male and female mice (C57BL/6JRccHsd) received an isocaloric diet (16 energy% fat; 64 energy% carbohydrates; 20 energy% protein) with either glucose (32 energy%) (GLU) or glucose + galactose (GLU + GAL, 16 energy% each) for 3 wk postweaning. Afterwards, all mice were switched to the same 40 energy% high-fat diet (HFD) for 9 wk to evaluate potential programming effects in an obesogenic environment. Data were analyzed within sex. Results Female body weight (−14%) and fat mass (−47%) were significantly lower at the end of the HFD period (both P < 0.001) among those fed GLU + GAL than among those fed GLU; effects in males were in line with these findings but nonsignificant. Food intake was affected in GLU + GAL–fed females (+8% on postweaning diet, −9% on HFD) compared with GLU-fed females, but not for hypothalamic transcript levels at endpoint. Also, in GLU + GAL–fed females, serum insulin concentrations (−48%, P  < 0.05) and the associated homeostasis model assessment of insulin resistance (HOMA-IR) were significantly lower ( P < 0.05) at endpoint, but there were no changes in pancreas morphology. In GLU + GAL–fed females, expression of insulin receptor substrate 2 (Irs2) (−27%, P  < 0.01 ; −44%, P  < 0.001) and the adipocyte size markers leptin (Lep) (−40%, P  < 0.05; −63% , P  < 0.05) and mesoderm-specific transcript homolog protein (Mest) (−80%, P < 0.05; −72%, P  < 0.05) was lower in gonadal and subcutaneous white adipose tissue (WAT), respectively. Expression of insulin receptor substrate1 (Irs1) (−24%, P  < 0.05) was only lower in subcutaneous WAT in GLU + GAL–fed females. Conclusions Partial replacement of glucose with galactose, resulting in a 1:1 ratio mimicking lactose, in a 3-wk postweaning diet lowered body weight, adiposity, HOMA-IR, and expression of WAT insulin signaling in HFD-challenged female mice in later life. This suggests that prolonged galactose intake may improve metabolic and overall health in later life.

scholarly journals The PYY/Y2R-Deficient Mouse Responds Normally to High-Fat Diet and Gastric Bypass Surgery

Nutrients ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 585 ◽  
Author(s):  
Brandon Boland ◽  
Michael Mumphrey ◽  
Zheng Hao ◽  
Benji Gill ◽  
R. Townsend ◽  
...  
Keyword(s):  
Gastric Bypass ◽  
Body Composition ◽  
Body Weight ◽  
High Fat Diet ◽  
Peptide Yy ◽  
Body Weight Loss ◽  
Receptor Subtypes ◽  
High Fat ◽  
Knockout Mouse Model ◽  
Gut Hormone

Background/Goals: The gut hormone peptide YY (PYY) secreted from intestinal L-cells has been implicated in the mechanisms of satiation via Y2-receptor (Y2R) signaling in the brain and periphery and is a major candidate for mediating the beneficial effects of bariatric surgery on appetite and body weight. Methods: Here we assessed the role of Y2R signaling in the response to low- and high-fat diets and its role in the effects of Roux-en-Y gastric bypass (RYGB) surgery on body weight, body composition, food intake, energy expenditure and glucose handling, in global Y2R-deficient (Y2RKO) and wildtype (WT) mice made obese on high-fat diet. Results: Both male and female Y2RKO mice responded normally to low- and high-fat diet in terms of body weight, body composition, fasting levels of glucose and insulin, as well as glucose and insulin tolerance for up to 30 weeks of age. Contrary to expectations, obese Y2RKO mice also responded similarly to RYGB compared to WT mice for up to 20 weeks after surgery, with initial hypophagia, sustained body weight loss, and significant improvements in fasting insulin, glucose tolerance, insulin resistance (HOMA-IR), and liver weight compared to sham-operated mice. Furthermore, non-surgical Y2RKO mice weight-matched to RYGB showed the same improvements in glycemic control as Y2RKO mice with RYGB that were similar to WT mice. Conclusions: PYY signaling through Y2R is not required for the normal appetite-suppressing and body weight-lowering effects of RYGB in this global knockout mouse model. Potential compensatory adaptations of PYY signaling through other receptor subtypes or other gut satiety hormones such as glucagon-like peptide-1 (GLP-1) remain to be investigated.

scholarly journals EXPLORATION OF IN VIVO ANTIOXIDANT ACTIVITY OF 50% ETHANOLIC EXTRACT OF SESAMUM INDICUM L. SEED AGAINST HIGH FAT DIET INDUCED RATS

2019 ◽  
pp. 55-61
Author(s):  
ZAFAR JAVED KHAN ◽  
NAEEM AHMAD KHAN
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Body Weight ◽  
High Fat Diet ◽  
Ethanolic Extract ◽  
Sesamum Indicum ◽  
Control Group ◽  
High Fat ◽  
Lipid Peroxidase

Objective: The aim of the present study was to investigate the in vivo antioxidant potential of 50% ethanolic extract of Sesamum indicum against high-fat diet-induced rats. Methods: Animals were treated with plant extract for 30 d, and a high-fat diet was given to all groups except plain control, throughout, out the study. And alpha-tocopherol acetate (Vit, E) was used as standard. Pre-treatment with 16 mg/100 gm of body weight of 50% ethanolic extract of Sesamum indicum improved the Superoxide dismutase, catalase, glutathione, and lipid peroxidation levels significantly as compared to control group. Results: The present studies revealed that Sesamum indicum has significant in vivo antioxidant activity and can be used to protect tissue from oxidative stress. The result showed that the activities of SOD, catalase, lipid peroxidase, and glutathione, in the group treated with high-fat diet declined significantly than that of normal group. Conclusion: 50% ethanolic extract of in the dose of Sesamum indicum 16 mg/100 gm of body weight, has improved the SOD, catalase, glutathione, and lipid peroxidase levels significantly, which were comparable with high-fat-diet-induced rats. Based on this study we conclude that the 50% ethanolic extract of Sesamum indicum possesses in vivo antioxidant activity and can be employed in protecting tissue from oxidative stress.

High-fat diet induces site-specific unresponsiveness to LPS-stimulated STAT3 activation in the hypothalamus

2014 ◽  
Vol 306 (1) ◽  
pp. R34-R44 ◽  
Author(s):  
Beatriz de Carvalho Borges ◽  
Rodrigo Rorato ◽  
Ernane Torres Uchoa ◽  
Paula Marangon ◽  
Glauber S. F. da Silva ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Brain Stem ◽  
High Fat Diet ◽  
Control Diet ◽  
Body Weight Loss ◽  
Hypothalamic Nucleus ◽  
High Fat

Hypophagia induced by inflammation is associated with Janus kinase (JAK)-2/signal transducer and activator of transcription (STAT) 3 signaling pathway, and leptin-mediated hypophagia is also mediated by JAK2-STAT3 pathway. We have previously reported that lipopolysaccharide (LPS) did not reduce food intake in leptin-resistant high-fat diet (HFD) rats but maintained body weight loss. We investigated whether changes in p-STAT3 expression in the hypothalamus and brain stem could account for the desensitization of hypophagia in HFD animals after a low LPS dose (100 μg/kg). Wistar rats fed standard diet (3.95 kcal/g) or HFD (6.3 kcal/g) for 8 wk were assigned into control diet-saline, control diet-LPS, HFD-saline, and HFD-LPS groups. LPS reduced feeding in the control diet but not HFD. This group showed no p-STAT3 expression in the paraventricular nucleus (PVN) and ventromedial hypothalamic nucleus (VMH), but sustained, though lower than control, p-STAT3 in the nucleus of the solitary tract (NTS) and raphe pallidus (RPa). LPS decreased body weight in HFD rats and increased Fos expression in the NTS. LPS increased body temperature, oxygen consumption, and energy expenditure in both control diet and HFD rats, and this response was more pronounced in HFD-LPS group. Brown adipose tissue (BAT) thermogenesis and increased energy expenditure seem to contribute to body weight loss in HFD-LPS. This response might be related with increased brain stem activation. In conclusion, LPS activates STAT3-mediated pathway in the hypothalamus and brain stem, leading to hypophagia, however, LPS effects on food intake, but not body weight loss, are abolished by leptin resistance induced by HFD. The preserved STAT3 phosphorylation in the brain stem suggests that unresponsiveness to LPS on STAT3 activation under HFD might be selective to the hypothalamus.

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