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Modulation of the carotid body activity to treat obesity / Miguel Carvalho Ravasco Milhano Correia ; orient. Sílvia Conde

Main Author Correia, Miguel Carvalho Ravasco Milhano Secondary Author Conde, Sílvia Vilares Language Inglês. Country Portugal. Publication Lisboa : NOVA Medical School, Faculdade de Ciências Médicas, 2017 Description 71 p. : fig. ; 30 cm Dissertation Note or Thesis: Dissertação de Mestrado, Bioquímica para a Saúde, Universidade Nova de Lisboa
Topical name Obesity
Insulin resistance
Rats, Zucker
Carotid Body
Carotid sinus nerve resection
Academic Dissertation
CDU 616 Classification Bioquímica para a Saúd Online Resources Click here to access the eletronic resource List(s) this item appears in: Teses NL
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COR9 TeseM-2017 Presencial/Restrito 20180071NL

Dissertação de Mestrado, Bioquímica para a Saúde, Universidade Nova de Lisboa

Nowadays the prevalence of obesity is rapidly increasing to levels higher than several decades ago. Associated to obesity are cardiovascular diseases, type II diabetes mellitus and cancer. Recently, it has been proposed that the carotid body (CB), a classic mediator of hypoxic responses, plays a role in energy and glucose homeostasis regulation and that its activity could be modulated to treat metabolic pathologies such as obesity and type II diabetes. In this thesis, we have used a genetic animal model of obesity and diabetes, by the lack of functional leptin receptors, the Zucker diabetic fatty (ZDF) rats, to investigate the role of the CB in the development of obesity and to evaluate the impact of carotid sinus nerve (CSN) denervation on obesity and on metabolic dysfunction. Male ZDF rats with fasting glycemia over 120 mg/dl at 10 weeks old and lean controls were submitted to CSN resection or sham procedure (early stage group). Another group of animals was left until the 18th week and submitted to CSN resection or sham procedure (late stage group). Weight gain, insulin sensitivity and glucose tolerance have been evaluated. Assessment of basal ventilation, as well as hypoxic and hypercapnic ventilatory responses, blood pressure, heart rate, and paO2 was performed. After the sacrifice, the major fat depots’ mass and liver lipid content was assessed. In early and late stage animals, we found that CSN resection did not modify weight gain, glucose tolerance, fat mass deposition and insulin secretion. However, produced a small decrease in fasting glycemia, totally reversed insulin resistance and decreased lipid deposition in the liver. We can conclude that modulation of the CB in this genetic model appears to play an important role in counteracting insulin resistance, however it does not seem to be a good method for the treatment of obesity per se.

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