Effect of Ventromedial Hypothalamus on Food Intake, Body Weight, Insulin Resistance, Lipid Profile and Thyroid Profile in High-Fat Diet Obese Female Wistar Rats

2019 ◽  
Vol 7 (4) ◽  
pp. 27
Author(s):  
T. Archana Gaur ◽  
G.K. Pal ◽  
Pravati Pal
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Food Intake ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Ventromedial Hypothalamus ◽  
High Fat ◽  
Obese Female ◽  
Female Wistar Rats ◽  
Thyroid Profile

scholarly journals Protective role of melatonin against adipose-hepatic metabolic comorbidities in experimentally induced obese rat model

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0260546
Author(s):  
Mary J. Obayemi ◽  
Christopher O. Akintayo ◽  
Adesola A. Oniyide ◽  
Ayodeji Aturamu ◽  
Olabimpe C. Badejogbin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Food Intake ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Liver Lipid ◽  
Control Group ◽  
Metabolic Dysfunction ◽  
High Fat ◽  
Male Wistar Rats

Background Adipose and hepatic metabolic dysfunctions are critical comorbidities that also aggravate insulin resistance in obese individuals. Melatonin is a low-cost agent and previous studies suggest that its use may promote metabolic health. However, its effects on some comorbidities associated with obesity are unknown. Herein, we investigated the hypothesis that melatonin supplementation would attenuate adipose-hepatic metabolic dysfunction in high fat diet (HFD)-induced obesity in male Wistar rats. Materials and methods Twenty-four adult male Wistar rats (n = 6/group) were used: Control group received vehicle (normal saline), obese group received 40% high fat diet, melatonin-treated group received 4 mg/kg of melatonin, and obese plus melatonin group received 40% HFD and melatonin. The treatment lasted for 12 weeks. Results HFD caused increased food intake, body weight, insulin level, insulin resistance and plasma and liver lipid but decreased adipose lipid. In addition, HFD also increased plasma, adipose and liver malondialdehyde, IL-6, uric acid and decreased Glucose-6-phosphate dehydrogenase, glutathione, nitric oxide and circulating obestatin concentration. However, these deleterious effects except food intake were attenuated when supplemented with melatonin. Conclusion Taken together, the present results indicate that HFD exposure causes adipose-hepatic metabolic disturbance in obese animals, which are accompanied by oxidative stress and inflammation. In addition, the present results suggest that melatonin supplementation attenuates adipose-hepatic metabolic dysfunction, accompanying obesity by suppression of oxidative stress/inflammation-dependent mechanism and increasing circulating obestatin.

scholarly journals Effects of treatment with leptin-like peptides on factors related to body fat control in Wistar rats fed a high-fat diet*

2011 ◽  
pp. 61-71
Author(s):  
Elpidia Poveda ◽  
Francisco Ruiz ◽  
María Carlina Castillo
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Dna Fragmentation ◽  
Body Fat ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Biological Action ◽  
High Fat ◽  
Modified Peptides ◽  
Cellular Medium

Introduction: The results of administering recombinant leptin, as well as the 116-130 peptide of mouse leptin in ob/ob mice have shown the probability of discovering more efficient leptin-based therapeutic methods to treat obesity. Objective: To demonstrate in Wistar rats fed with high-fat diet if the administration of synthetic peptides corresponding to the 116-130 peptide of mouse leptin (SR 116), its human homologue peptide (SH 95: sequence 95-109 from the 1AX8 protein) and five modified peptides (P80 to P84) similar to these two peptides, produces effects related to regulation of body fat. Materials and methods: Nine-week old Wistar rats were fed a high-fat diet for fifteen weeks. On the fifteenth week, and for five consecutive days, they were treated with the peptides to be evaluated. During the days of treatment, body weight and food intake were evaluated. After the last peptide administration, lipid profile, glycerol in the cellular medium, and DNA fragmentation in adipocytes were analyzed. Results: The results revealed that: the SR116 peptide affects the regulation of adiposity in rats fed a high-fat diet. The SH 95 is the human peptide with biological activity similar to SR 116 to lower weight, lessen food intake, and increase free glycerol in the cellular medium. The P80 and P81 peptides had a similar effect on SR 116 and SH 95 regarding body weight and food intake. The SR 116, SH 95 and three of the modified peptides (P80, P81, and P82) caused DNA fragmentation. Conclusion: The results suggest that peptides analogous to leptin are potentially viable to achieve effects of adiposity reduction in Wistar rats with obesity associated to high-fat diet; more research is rendered to explain the differences among peptides and the biological action mechanisms.

The Effect of Exercise and Protein Source on Food Intake Regulation and Characteristics of Metabolic Syndrome in Obese Female Wistar Rats

2019 ◽  
Vol 15 (2) ◽  
pp. 175-184
Author(s):  
Alireza Jahan-Mihan ◽  
Peter Magyari ◽  
Shawna Jenkins ◽  
Valeria Palamidy ◽  
Lindsay Pappas ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Body Weight ◽  
Food Intake ◽  
Whey Protein ◽  
Soy Protein ◽  
Wistar Rats ◽  
Protein Diet ◽  
Obese Female ◽  
Female Wistar Rats

Background: Beneficial effects of dietary proteins and exercise in treatment of obesity is well-recognized. The effect of exercise and protein source on food intake, body weight and characteristics of metabolic syndrome in obese female Wistar rats was examined. Female Wistar rats received an obesogenic diet for 12 weeks. Then, rats were allocated to four groups and received one of the following treatments for eight weeks: 1- Whey protein Diet + Exercise (WPE), 2- Soy protein diet + exercise (SPE), 3- Whey protein diet, no exercise (WPN), 4- Soy protein diet, no exercise (SPN). The exercise comprised of 30 minutes on a treadmill, three times/week. Body weight (BW) and food intake (FI), blood pressure, pulse, glucose and intake regulatory hormones were measured. Results: FI and plasma ghrelin (2.7 times) were higher in exercise groups compared with non-exercise groups. BW was lower (6.7%) in groups fed a whey protein diet compared with those fed a soy protein diet. Abdominal fat (% BW) was lower (22.8%) in WPE compared with other groups. Diastolic blood pressure (11.1%) and pulse (6%) were lower in groups fed a soy protein diet compared with groups fed a whey protein diet. Conclusion: While exercise affects food intake, source of protein determines BW and BC. Whey protein showed more favorable effect on BW and body composition.

Abstract 6260: Up-Regulated Expression of MicroRNA-143 in Association with Obesity in the Adipose Tissue of Mice Fed High Fat Diet

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Rieko Takanabe ◽  
Koh Ono ◽  
Tomohide Takaya ◽  
Takahiro Horie ◽  
Hiromichi Wada ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Control Cell ◽  
High Fat ◽  
Expression Levels ◽  
Mesenteric Fat ◽  
Regulated Expression

Obesity is the result of an expansion and increase in the number of individual adipocytes. Since changes in gene expression during adipocyte differentiation and hypertrophy are closely associated with insulin resistance and cardiovascular diseases, further insight into the molecular basis of obesity is needed to better understand obesity-associated diseases. MicroRNAs (miRNAs) are approximately 17–24nt single stranded RNA, that post-transcriptionally regulate gene expression. MiRNAs control cell growth, differentiation and metabolism, and may be also involved in pathogenesis and pathophysiology of diseases. It has been proposed that miR-143 plays a role in the differentiation of preadipocytes into mature adipocytes in culture. However, regulated expression of miR-143 in the adult adipose tissue during the development of obesity in vivo is unknown. To solve this problem, C57BL/6 mice were fed with either high-fat diet (HFD) or normal chow (NC). Eight weeks later, severe insulin resistance was observed in mice on HFD. Body weight increased by 35% and the mesenteric fat weight increased by 3.3-fold in HFD mice compared with NC mice. We measured expression levels of miR-143 in the mesenteric fat tissue by real-time PCR and normalized with those of 5S ribosomal RNA. Expression of miR-143 in the mesenteric fat was significantly up-regulated (3.3-fold, p<0.05) in HFD mice compared to NC mice. MiR-143 expression levels were positively correlated with body weight (R=0.577, p=0.0011) and the mesenteric fat weight (R=0.608, p=0.0005). We also measured expression levels in the mesenteric fat of PPARγ and AP2, whose expression are deeply involved in the development of obesity, insulin resistant and arteriosclerosis. The expression levels of miR-143 were closely correlated with those of PPARγ (R=0.600, p=0.0040) and AP2 (R=0.630, p=0.0022). These findings provide the first evidence for up-regulated expression of miR-143 in the mesenteric fat of HFD-induced obese mice, which might contribute to regulated expression of genes involved in the pathophysiology of obesity.

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 Main and Interactive Effects of Fat and Sodium Contents of the Diet on Characteristics of Metabolic Syndrome in Male Wistar Rats (P08-038-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Alireza Jahan-Mihan ◽  
Kea Schwarz ◽  
Leila Nynia ◽  
Tatyana Kimble
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
High Fat Diet ◽  
Sodium Content ◽  
Fat Content ◽  
High Fat ◽  
High Sodium ◽  
Sodium Diet ◽  
Male Wistar Rats ◽  
High Sodium Diet

Abstract Objectives The objective of this study was to investigate the main and interactive effects of fat and sodium content of the diet on food intake, body weight and composition, glucose metabolism and blood pressure in male Wistar rats. Methods Male Wistar Rats (n = 48, initial body weight: 115.30 ± 1.73 g) were allocated into 4 groups (n = 12/group) and received one of the following diets: Normal sodium normal fat (NSNF), normal sodium high fat (NSHF), high sodium normal fat (HSNF), high sodium high fat (HSHF) diet for 12 weeks. Body weight (BW) and food intake (FI) were measured weekly. Short-term food intake (1, 2 and 12 hours food intake after 12 hours fasting) was measured at week 6. Body composition and organs’ weight were measured at week 12. Systolic (SBP) and diastolic (DBP) blood pressure, pulse and fasting blood glucose (FBG) were measured and oral glucose tolerance test (OGTT) was conducted at weeks 1, 4, 8 and 12. Results Regardless of sodium content, a greater FI (both gram and cal) was observed in rats fed normal fat diet compared with those fed high fat diet. Consistently, FI (g) at 1, 2 and 12 hours was higher in rats fed a normal fat diet. However, no difference in calorie intake was observed at any time point. Higher BW and fat (%) was observed in high fat diet groups. Moreover, greater kidneys’ weights was observed in high sodium diet groups. Fasting blood glucose was higher in rats fed a normal sodium diet compared with those fed a high sodium diet while the tAUC glucose response to glucose preload was higher in rats fed a high fat diet compared with those fed a normal fat diet which is consistent with higher body weight in high fat diet groups. Regardless of fat content of the diet, pulse was higher in rats fed a high sodium diet compared with those fed a normal sodium diet. No effect of either dietary sodium or fat content of the diet on SBP or DBP was observed. Conclusions Fat but not sodium content of the diet is a determining factor in regulation of FI and BW. Moreover, both fat and sodium content of the diet influence the glucose metabolism potentially through different mechanisms. While pulse is influenced by sodium content, the results of this study do not support the effect of sodium or fat content of the diet on either SBP or DBP. Funding Sources UNF, Brooks College of Health internal grant.

Effects of chia (Salvia hispanica L.) on oxidative stress and inflammation in ovariectomized adult female Wistar rats

2019 ◽  
Vol 10 (7) ◽  
pp. 4036-4045 ◽  
Author(s):  
Bárbara Pereira da Silva ◽  
Renata Celi Lopes Toledo ◽  
Marcella Duarte Villas Mishima ◽  
Maria Eliza de Castro Moreira ◽  
Christiane Mileib Vasconcelos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adult Female ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Lipid Profiles ◽  
Ovariectomized Rats ◽  
High Fat ◽  
Salvia Hispanica ◽  
Female Wistar Rats ◽  
Salvia Hispanica L

The study investigated the influence of chia consumption on inflammation, oxidative stress, and lipid profiles in female ovariectomized rats fed a high-fat diet.

SO023HEPATOCYTE GROWTH FACTOR (HGF) PRECLUDE HIGH-FAT DIET-INDUCED OBESITY AND IMPROVED INSULIN RESISTANCE IN MICE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Jun Muratsu ◽  
Yoshiaki Taniyama ◽  
Fumihiro Sanada ◽  
Atsuyuki Morishima ◽  
Katsuhiko Sakaguchi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
Growth Factor ◽  
Inflammatory Mediators ◽  
High Fat Diet ◽  
Neutralizing Antibody ◽  
Mrna Levels ◽  
Wild Type ◽  
High Fat

Abstract Background and Aims Obesity and its associated chronic inflammation in adipose tissue initiate insulin resistance, which is related to several pathologies including hypertension and atherosclerosis. Previous reports demonstrated that circulating hepatocyte growth factor (HGF) level was associated with obesity and type 2 diabetes. However, its precise role in obesity and related-pathology is unclear. Method In this experiment, cardiac-specific over-expression of human HGF in mice (HGF-Tg mice) which showed 4-5 times higher serum HGF levels than wild-type mice were used. We chose cardiac specific HGF overexpression, as other strain of HGF transgenic mice such as liver and kidney specific HGF overexpression mice develop cancer and cystic diseases, which are rare in the heart. In the present study, using HGF-Tg mice and anti-HGF neutralizing antibody (HGF-Ab), we explored the role of HGF in obese and insulin resistance induced by high fat diet (HFD) for 14 weeks (200 or 400ug/week). Results With normal chow diet (ND), there were no significant changes in body weight between WT and HGF-Tg mice. While body weight in wild-type mice fed with HFD for 14 weeks was significantly increased accompanied with insulin resistance, HGF-Tg mice prevented body weight gain and insulin resistance. Insulin resistance in obesity arises from the combination of altered functions of insulin target cells (e.g., liver, skeletal muscle, and adipose tissue) and the accumulation of macrophages that secrete pro-inflammatory mediators in adipose tissue. The accumulation of macrophages and elevated levels of inflammatory mediators in adipose tissue were significantly inhibited in HGF-Tg mice as compared to wild-type mice. In the gWAT, the mRNA levels of the mature macrophage marker F4/80, the chemoattractants, MCP-1 and CXCL2, and the inflammatory cytokines, such as TNF-α and iNOS, were significantly increased in WT mice fed with HFD. However, these levels were markedly reduced in HGF-Tg mice fed with HFD. Additionally, activation of Akt by insulin administration was significantly reduced in the gWAT SM, and liver by HFD; however, this activation was restored in HGF-Tg mice. Moreover, insulin-induced Akt signaling was decreased in HGF-Ab groups as compared to saline group under HFD condition. Importantly, HFD significantly increased the level of HGF mRNA by approximately 2 fold in gWAT, SM, and liver without changing cMet expression. All together, these data indicate that the HGF as one of the systemic gWAT, SM, and liver-derived growth factor plays a role in compensatory mechanism against insulin-resistance through the at least anti-inflammatory effect in adipose tissue. The HFD-induced obesity in wild-type mice treated with HGF-neutralizing antibody showed an exacerbated response to the glucose tolerance test. Conclusion HGF suppresses inflammation in adipose tissue induced by a high-fat diet, and as a result improves systemic insulin resistance. These gain-of-function and loss-of-function studies demonstrated that the elevated HGF level induced by HFD have protective role against obesity and insulin resistance.

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