Effects of topical capsaicin combined with moderate exercise on insulin resistance, body weight and oxidative stress in hypoestrogenic obese rats

2017 ◽  
Vol 41 (5) ◽  
pp. 750-758 ◽  
Author(s):  
J M L Medina-Contreras ◽  
J Colado-Velázquez ◽  
N L Gómez-Viquez ◽  
P Mailloux-Salinas ◽  
I Pérez-Torres ◽  
...  
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 ◽  
...  

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.


Author(s):  
Basiru Olaitan Ajiboye ◽  
Babatunji Emmanuel Oyinloye ◽  
Jennifer Chidera Awurum ◽  
Sunday Amos Onikanni ◽  
Adedotun Adefolalu ◽  
...  

Abstract Objectives The current study evaluates the protective role of aqueous extract of Sterculia tragacantha leaf (AESTL) on pancreatic gene expressions (insulin, PCNA, PDX-1, KI-67 and GLP-1R) and oxidative stress parameters in streptozotocin-induced diabetic rats. Methods Diabetes mellitus was induced into the experimental Wistar animals via intraperitoneal (IP) injection of streptozotocin (35 mg/kg body weight) and 5% glucose water was given to the rats for 24 h after induction. The animals were categorized into five groups of 10 rats each as follows normal control, diabetic control, diabetic rats administered AESTL (150 and 300 mg/kg body weight) and diabetic rats administered metformin (200 mg/kg) orally for two weeks. Thereafter, the animals were euthanized, blood sample collected, pancreas harvested and some pancreatic gene expressions (such as insulin, PCNA, PDX-1, KI-67, and GLP-1R)s as well as oxidative stress parameters were analyzed. Results The results revealed that AESTL significantly (p<0.05) reduced fasting blood glucose level, food and water intake, and lipid peroxidation in diabetic rats. Diabetic rats administered different doses of AESTL showed a substantial upsurge in body weight, antioxidant enzyme activities, and pancreatic gene expressions (insulin, PCNA, PDX-1, KI-67, and GLP-1R). Conclusions It can therefore be concluded that AESTL has the ability to protect the pancreas during diabetes mellitus conditions.


Animals ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 703
Author(s):  
Jae-Cheol Jang ◽  
Kwang Kim ◽  
Young Jang ◽  
Yoo Kim

The experiment aimed to investigate the effects of dietary β-mannanase supplementation on growth performance, apparent total tract digestibility (ATTD) of nutrients, intestinal integrity, and the immunological and oxidative stress parameters in weaning pigs. A total of 64 newly weaning pigs (initial body weight: 6.96 ± 0.70 kg) were allotted to two dietary treatments in eight replicates per treatment with four pigs per pen based on body weight and sex. Dietary treatments were 1.) CON (control: corn-soybean meal based basal diet) and 2.) β-mannanase (basal diet +0.06% β-mannanase). The β-mannanase supplementation did not affect growth performance, concentrations of acute phase protein, superoxide dismutase and glutathione peroxidase. However, the pigs fed the β-mannanase-supplemented diet had greater ATTD of ether extract, jejunum villus height, and villus height-to-crypt depth ratio, and lower crypt depth compared with those fed the CON diet (p < 0.05). The pigs fed the β-mannanase-supplemented diet tended to have the lower count of E. coli in cecum than those fed the CON diet (p = 0.08). In conclusion, dietary β-mannanase supplementation did not affect growth performance, immune response and oxidative stress of weaning pigs, whereas it increased fat digestibility and had positive effects on intestinal integrity and cecum microflora by reducing the count of E.coli.


2009 ◽  
Vol 23 (1) ◽  
pp. 59-67 ◽  
Author(s):  
Régine Debin ◽  
Benjamin Lauzier ◽  
Pierre Sicard ◽  
Stéphanie Delemasure ◽  
Sébastien Amoureux ◽  
...  

1970 ◽  
Vol 36 (1) ◽  
pp. 14-19
Author(s):  
Md. Zakirul Islam ◽  
Md. Sayedur Rahman

The study was conducted to evaluate the anti-atherogenic potential of losartan and to assess the effects of hydrochlorothiazide and indapamide on losartan activity in rat. Cholesterol diet (0.5%) for 12 weeks led to significant hyperlipidemia, increased body weight and oxidative stress in erythrocyte. While, losartan, hydrochlorothiazide and indapamide treatment continued for next 12 weeks, losartan showed anti-atherogenic activity reflected by hypolipidemic effect and antioxidant effect in erythrocyte. This activity was abolished by addition of hydrochlorothiazide with losartan but remained unaltered by addition of indapamide with losartan. Atherosclerotic change and oxidative stress were not found in rat aorta, which may be due to short duration and low dose of cholesterol feeding. Hydrochlorothiazide treatment was associated with hypokalemia, which was not present in losartan or indapamide treatment. This study suggests that indapamide might be co-administered with losartan conserving the essential anti-atherogenic potential of losartan.Online: 13 July 2010DOI: http://dx.doi.org/10.3329/bmrcb.v36i1.5447Bangladesh Med Res Counc Bull 2010; 36: 14-19   


2000 ◽  
Vol 278 (4) ◽  
pp. E677-E683 ◽  
Author(s):  
Asako Suga ◽  
Tsutomu Hirano ◽  
Haruaki Kageyama ◽  
Toshimasa Osaka ◽  
Yoshio Namba ◽  
...  

To determine the influence of dietary fructose and glucose on circulating leptin levels in lean and obese rats, plasma leptin concentrations were measured in ventromedial hypothalamic (VMH)-lesioned obese and sham-operated lean rats fed either normal chow or fructose- or glucose-enriched diets (60% by calories) for 2 wk. Insulin resistance was evaluated by the steady-state plasma glucose method and intravenous glucose tolerance test. In lean rats, glucose-enriched diet significantly increased plasma leptin with enlarged parametrial fat pad, whereas neither leptin nor fat-pad weight was altered by fructose. Two weeks after the lesions, the rats fed normal chow had marked greater body weight gain, enlarged fat pads, and higher insulin and leptin compared with sham-operated rats. Despite a marked adiposity and hyperinsulinemia, insulin resistance was not increased in VMH-lesioned rats. Fructose brought about substantial insulin resistance and hyperinsulinemia in both lean and obese rats, whereas glucose led to rather enhanced insulin sensitivity. Leptin, body weight, and fat pad were not significantly altered by either fructose or glucose in the obese rats. These results suggest that dietary glucose stimulates leptin production by increasing adipose tissue or stimulating glucose metabolism in lean rats. Hyperleptinemia in VMH-lesioned rats is associated with both increased adiposity and hyperinsulinemia but not with insulin resistance. Dietary fructose does not alter leptin levels, although this sugar brings about hyperinsulinemia and insulin resistance, suggesting that hyperinsulinemia compensated for insulin resistance does not stimulate leptin production.


2019 ◽  
Vol 5 (3) ◽  
pp. 145-150
Author(s):  
Subathra Thiruchengodu Ammaiyappan ◽  
Gopal Krushna Pal ◽  
Dhanalakshmi Yerrabelli ◽  
Pravati Pal ◽  
Nivedita Nanda

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Qian Zhang ◽  
Xinhua Xiao ◽  
Jia Zheng ◽  
Ming Li ◽  
Miao Yu ◽  
...  

Increasing evidence shows that diabetes causes cardiac dysfunction. We hypothesized that a glucagon-like peptide-1 (GLP-1) analog, liraglutide, would attenuate cardiac dysfunction in diabetic rats. A total of 24 Sprague–Dawley (SD) rats were divided into two groups fed either a normal diet (normal, n=6) or a high-fat diet (HFD, n=18) for 4 weeks. Then, the HFD rats were injected with streptozotocin (STZ) to create a diabetic rat model. Diabetic rats were divided into three subgroups receiving vehicle (diabetic, n=6), a low dose of liraglutide (Llirag, 0.2 mg/kg/day, n=6), or a high dose of liraglutide (Hlirag, 0.4 mg/kg/day, n=6). Metabolic parameters, systolic blood pressure (SBP), heart rate (HR), left ventricular (LV) function, and whole genome expression of the heart were determined. Diabetic rats developed insulin resistance, increased blood lipid levels and oxidative stress, and impaired LV function, serum adiponectin, nitric oxide (NO). Liraglutide improved insulin resistance, serum adiponectin, NO, HR, and LV function and reduced blood triglyceride (TG), total cholesterol (TC) levels, and oxidative stress. Moreover, liraglutide increased heart nuclear receptor subfamily 1, group H, member 3 (Nr1h3), peroxisome proliferator activated receptor (Ppar) α (Pparα), and Srebp expression and reduced diacylglycerol O-acyltransferase 1 (Dgat) and angiopoietin-like 3 (Angptl3) expression. Liraglutide prevented cardiac dysfunction by activating the PPARα pathway to inhibit Dgat expression and oxidative stress in diabetic rats.


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