doi: 10.1007/978-3-319-48382-5_1, Fatani, S., Pickavance, L. C., Sadler, C. J., Harrold, J. EC, VdS, JC, LD, MdC, AL-L, and AL performed the experiments and data analysis. Thus, the aim of this study was to test the hypothesis that unsaturated high-fat diet-induced obesity does not generate endothelial dysfunction via increasing the vascular leptin/Akt/eNOS signaling. DOI: 10.1016/B978-0-12-409547-2.12509-0. Google has many special features to help you find exactly what you're looking for. On the other hand, Akt inhibition promoted reduction in the acetylcholine response only in C rats (Figure 4B). 518-524-7186 Jelayna Kerbaugh. Data are reported as the means ± SEM. The responses to these vasoconstrictor agonists may be related to the amount and the nature of the lipids in the diet, which are considered protective factors and/or atherogenic and are associated with the modulation of NOS activity (Santos et al., 2013). This result was in accordance with our previously published results (Bruder-Nascimento et al., 2011, 2017). ∗p < 0.05. At the end of the experimental protocol, the fat index was used as an indicator of obesity. Regulation of vascular tone by adipocytes. Biol. The presence of L-NAME blunted the response of leptin-induced relaxation in both groups (Figure 5A). In addition, it was verified that insulin potentiates this response by increasing the Akt phosphorylation at the sites of Ser473 and Thr308 (Vecchione et al., 2003). Antonopoulos, A. S., and Tousoulis, D. (2017). Med. Arq. Glucose tolerance test (A), area under the curve for glucose – AUC (B), insulin serum level (C) and (D) homeostatic model assessment index (HOMA-IR) from control (C; n = 9) and obese (Ob; n = 7) groups. Moreover, in rabbits fed a hyperlipidemic diet for 12 weeks, hyporeactivity was observed in the responses stimulated by the noradrenaline and angiotensin-II (Jerez et al., 2012). |, Creative Commons Attribution License (CC BY). 931-337-4589 Shell Schierer. Hypertension. 73, 368–375. Recently, a study verified that in eNOS knockout mice, leptin and a fat-rich diet induced an increase in the endothelial nNOS expression by phosphorylating JAK-2/STAT-3, thereby compensating for the reduction of NO and restoring the endothelial function in angiotensin-II-infused mice (Benkhoff et al., 2012). Diffential vascular dysfunction in response to diets of differing macronutrient composition: a phenomenonological study. On the other hand, Keita et al. Gut 63:262–271 (Epub 2013 Mar 8) Google Scholar In addition, obesity is often associated with metabolic and endocrine disorders, such as glucose intolerance, insulin resistance, hyperleptinemia, dyslipidemia, and hypertension. Keita Hibi, Kazuaki Amikura, Naoki Sugiura, Keiko Masuda, Satoshi Ohno, Takashi Yokogawa, Takuya Ueda and Yoshihiro Shimizu. URL. (2007). FE was defined as the ability of animals to convert feed energy consumed in body weight and was measured by dividing body weight gain (g) by the total caloric intake (kcal) and multiplying by 100. Vasc. doi: 10.1097/FJC.0b013e318235156a, Keita, H., Ramírez-San, J. E., Paniagua-Castro, N., Garduño-Siciliano, L., and Quevedo, L. (2013). AL-L, VR, and AL participated and conceived the research design. doi: 10.1016/S0014-2999(98)00535-4, Jerez, S., Scacchi, F., Sierra, L., Karbiner, S., and Bruno, M. P. (2012). BMC Med. Bras. A review on the models of obesity and metabolic syndrome in rats. Concentration-response curve to phenylephrine obtained from control and obese (Ob) groups rings before (A) and after nitric oxide synthase inhibition with L-NAME (100 μM – B–D). 602-301-1170 Srikant Beazer. 931-337-1521 Norreys Eisch. 2011, 2934–2942. Endothelial dysfunction associated with obesity has been considered an independent risk of developing cardiovascular diseases (Poirier et al., 2006; Acree et al., 2007; Kumanyika et al., 2008; Stapleton et al., 2008; Graupera and Claret, 2018). Med. URL. 913-600-9779 Cortney Akerley. doi: 10.1093/cvr/cvx106, Bautista, R., Carreón-Torres, E., Luna-Luna, M., Komera-Arenas, Y., Franco, M., Fragoso, J. M., et al. 518-524-3793 Dania Garcelon. 15, 79–89. Trakia J. Sci. Figure 5. The higher basal production of NO is possibly associated with the increase in the plasmatic concentration of leptin in obese animals. doi: 10.1186/1758-5996-5-53, Kimura, K., Tsuda, K., Baba, A., Kawabe, T., Boh-oka, S., Ibata, M., et al. At the end of the experimental protocol, the heart, ventricles and atrium, and tibia were separated, dissected, weighed and measured on a precision scale (AD 500, Mars Scientific and Industrial Instrumentation Ltd., Minas Gerais, Brazil). (2008). The adipocyte: a model for integration of endocrine and metabolic signaling in energy metabolism regulation. Colonic permeability was estimated in vivo by quantifying the absorbed Evans blue in colonic tissue in rats. (2000). In addition, other authors found no difference in acetylcholine-induced endothelium-dependent relaxation in the aorta of mice and obese rabbits induced by a high-fat diet with 58–60% of fat calories (Mundy et al., 2007; Bruder-Nascimento et al., 2017) or standard rabbit chow with 10% added fat (Jerez et al., 2012), which apparently is sex independent. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Fußball, SC Freiburg - 1. A., Cassidy, R., Wilding, J. P. H., et al. FC Union Berlin - Einzelne Lizenz oder Bildpakete kaufen. Res. These results suggest that exogenously administered or endogenously released ghrelin acts centrally to improve a disturbed intestinal barrier function through orexinergic signaling and the vagal cholinergic pathway. Does leptin stimulate nitric oxide to oppose the effects of sympathetic activation? J. Card. J. Pharmacol. 719-652-9554 Steeran Lehnhoff. Several factors, such as insulin resistance and dyslipidemia, have been cited as possible factors that are responsible for cardiovascular dysfunction in models of obesity (Antonopoulos and Tousoulis, 2017). Rats were randomly distributed into two groups: control (C, n = 20), which were fed standard rat chow (Presence chow, SP, Brazil); and obese (Ob, n = 18), which were fed a high-unsaturated fat diet (RC Focus 2413, Agroceres®, Rio Claro, SP, Brazil) for 27 weeks. The components and nutritional values are displayed in Table 1. Myocardial dysfunction and abnormalities in intracellular calcium handling in obese rats. Hipertens. 602-301-7440 Fedorah Gellatly. doi: 10.2337/diabetes.51.1.168, Woods, S. C., Seeley, R. J., Rushing, P. A., D’Alessio, D., and Tso, P. (2003). To evaluate the baseline NO production in the vascular constriction, the vessel rings of control and obese rats were exposed to L-NAME (100 μM) before the constrictor response curve to phenylephrine. Keita Hargis Breanna Harrie Kevin Harrington Cervante Harris Clayton Harris Natalia Harrison Shayla Harrison Felicia Hart Kimberly Hart Sally Hartzell Airrion Harvey Dishon Harvey Casey Hayes Jordan Haynes Thomas Heinrich Joanne Hemphill Christopher Hennigan Krystal Henrichs Kelly Hensel Christopher Hernandez Noris Hernandez Brittany Heroux Chris Herrera Jennifer Herrington Victoria … 602-301-8690 Yannic Killam. (2007) demonstrated that animals fed a high-saturated fat diet (45% fat) do not present any difference for vasoconstrictor responses to potassium chloride (KCl) or noradrenaline; however, the vascular relaxation in response to carbachol and sodium nitroprusside (SNP) is attenuated in mesenteric arteries, indicating that the high-saturated fat diet promotes vascular dysfunction. (2002). On the other hand, Keita et al. Data on general characteristics, nutritional assessment and comorbidities were reported as mean ± standard error of the mean (SEM) and submitted to the Kolmogorov-Smirnov test to determine adherence to normality. 719-652-4568 Garet Giardini. (2017). 27, 2663–2671. Moreover, our results suggest that the increase in NO production occurs through the increase in NOS activation by leptin and is partially mediated by the Akt pathway. Blood was collected in Falcon tubes, centrifuged at 3,000 × g for 15 min and stored at -80°C. (2009). In addition to controlling energy stores, it is also involved in several other physiological processes, including vascular tone modulation, acting through specific leptin receptors (Ob-Rb type) located in the vascular endothelium (Leung and Kwan, 2008). ∗p < 0.05 Ob vs. C. Table 2. 931-337-0328 Chitrangda Anzelmo. 719-652-6319 Kalinda Garant. The evaluation of the endothelium-dependent relaxation with acetylcholine showed no differences between the C and Ob rats. doi: 10.1186/1476-5918-6-4, PubMed Abstract | CrossRef Full Text | Google Scholar. doi: 10.1016/j.tem.2018.09.003, Hopfner, R. L., McNeill, J. R., and Gopalakrishnan, V. (1998). 913-600-3831 Ferdinandus Forshey. Subsequently, an injection of glucose solution (2 g/kg body weight) dissolved in water was administered intraperitoneally, and blood glucose levels were measured after 15, 30, 60, 90, and 120 min. Little is, however, known about a role of central ghrelin in regulation of intestinal permeability. The epidemic of obesity. Data are presented as mean ± SEM. 42, 166–170. Figure 4. A 2,6‐anthrylene‐linked bis(m‐terphenylcarboxylic acid) strand forms a one‐handed homo double‐helix induced by chiral amines, thereby producing the chiral anti‐photodimer with up to 98 % enantiomeric excess upon photoirradiation.The chirality of the anti‐photodimer can be readily controlled by the chirality of the chiral amines. Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) was calculated according to the following formula: fasting glucose (mmol/l) × fasting insulin (μU/ml)]/22.5. 11:9. doi: 10.1186/1532-429X-11-9. J. Cardiovasc. 602-301-2468 Alvin Houff. In addition to absence of changes in the metabolic abnormalities, the model proposed did not lead to an elevation in blood pressure levels. fall 2020. edition. In addition, body weight was recorded weekly. (2013). Therefore, this double behavior of leptin and the modulation of vascular tone may help explain why obesity is not always accompanied by high blood pressure (Lembo et al., 2000). showed that leptin activates the Akt pathway by a mechanism independent of PI3K phosphorylation, increasing NO production by phosphorylating eNOS at the Ser1177 residue in the aorta of Wistar Kyoto rats. ScienceDirect ® is a registered trademark of Elsevier B.V. ScienceDirect ® is a registered trademark of Elsevier B.V. Ghrelin acts in the brain to block colonic hyperpermeability in response to lipopolysaccharide through the vagus nerve. doi: 10.1007/s11695-017-2704-8, Engin, A. Metab. Metab. Biol. Res. Dyn. doi: 10.1210/en.2008-0921, Rahmouni, K., Correia, M. L., Haynes, W. G., and Mark, A. L. (2005). Dietary obesity in the rat induces endothelial disfunction without causing insulin resistance: a possible role for triacylglycerols. 7:386. doi: 10.3389/fphys.2016.00386, Stapleton, P. A., James, M. E., Goodwill, A. G., and Frisbee, J. C. (2008). (2007). Leptin potentiates endothelium-dependent relaxation by inducing endothelial expression of neuronal NO Synthase. ∗p < 0.05 Ob vs. C. The main findings of the present study were as follows: (i) the high-fat diet led to the development of obesity; (ii) a reduction in the vasoconstrictor response to phenylephrine in obese animals; (iii) endothelial dysfunction was not observed in this model of obesity, since thoracic aorta from obese rats were still responsive to leptin effects; (iv) a significantly higher vasodilator response to leptin was observed in the obese group, which was abolished when exposed to NOS blockade in both groups; (v) there was a reduction in the vasodilator response to leptin in both groups, compared with the respective control, when the rings were exposed to Akt inhibitor. 6, 1–8. doi: 10.1038/nm1195-1155. Cardiol.100, 1–40. Targeting mitochondria-derived reactive oxygen species to reduce epithelial barrier dysfunction and colitis . (2008). Obes. Long-term obesity promotes alterations in diastolic function induced by reduction of phospholamban phosphorylation at serine-16 without affecting calcium handling. Ushria Bruder. Experimental models that mimic the eating habits of the human population have been widely used to elucidate the mechanisms of obesity and metabolic disorders (Angelova and Boyadjiev, 2013). 518-524-2435 Callum Shaut. All experiments and procedures were performed in accordance with the Guide for the Care and Use of Laboratory Animals, published by the United States National Institutes of Health, and were approved by the Ethics Committee on Animal Use of the Federal University of Espírito Santo (protocol 027/2014).