Browsing by Author "Coelho, Marisa"
Now showing 1 - 2 of 2
Results Per Page
Sort Options
- Biochemistry of adipose tissue: an endocrine organPublication . Coelho, Marisa; Oliveira, Teresa; Fernandes, RúbenAdipose tissue is no longer considered to be an inert tissue that stores fat. This tissue is capable of expanding to accommodate increased lipids through hypertrophy of existing adipocytes and by initiating differentiation of pre-adipocytes. Adipose tissue metabolism exerts an impact on whole-body metabolism. As an endocrine organ, adipose tissue is responsible for the synthesis and secretion of several hormones. These are active in a range of processes, such as control of nutritional intake (leptin, angiotensin), control of sensitivity to insulin and inflammatory process mediators (tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), resistin, visfatin, adiponectin, among others) and pathways (plasminogen activator inhibitor 1 (PAI-1) and acylation stimulating protein (ASP) for example). This paper reviews some of the biochemical and metabolic aspects of adipose tissue and its relationship to inflammatory disease and insulin resistance.
- Expanding our therapeutic options: β-blockers for colon cancer?Publication . Coelho, Marisa; Ribeiro, Laura; Fernandes, RúbenColon cancer is the fourth and third most common cancer, respectively in men and women worldwide and its incidence is increasing. Stress response has been associated to the incidence and development of cancer. The catecholamines (CA), adrenaline (AD) and noradrenaline (NA), are crucial mediators of stress response, exerting their effects through interaction with α- and β- adrenergic receptors (AR). Colon cancer cells express β-AR and their activation has been implicated in carcinogenesis and tumor progression. Recently, interest in the efficacy of β-AR blockers as possible additions to cancer treatment paradigms has been gaining strength. The aim of this work was to investigate the effect of several AR agonists and β-blockers, upon cellular proliferation and viability of HT-29 cells, a human colon adenocarcinoma cell line. For this purpose, in the first phase of this work, we determined the EC50 and IC50 values for proliferative and antiproliferative effects, respectively of AR agonists and antagonists. Afterwards, HT-29 cells were incubated in the absence (control) or in the presence of the AR-agonists, AD, NA and isoprenaline (ISO) (0.1-100 μM) for 12 hours or 24 hours. All tested AR agonists revealed proliferative effects upon HT-29 cells. In order to study the effect of several β-blockers upon both proliferation and viability induced by AR activation, cells were treated with propranolol (PRO; 50 μM), carvedilol (CAR; 5μM), atenolol (ATE; 50 μM), or ICI 118,551 (ICI; 5 μM) for 45 minutes prior, and simultaneously, to the incubation with each of the AR agonists, AD and ISO, both at 1 and 10 μM. Our results suggest that adrenergic activation play an important role in colon cancer cells proliferation most probably through β-AR. All the β-blockers under study were able to revert the proliferation induced by AD and ISO, and some of them, per se, significantly decreased the proliferation of HT-29 cells. The elucidation of the intracellular pathways involved in CA-induced proliferation of colon cancer cells, and also in the reversion of this effect by β-blockers, might contribute to reveal promising strategies in cancer treatment.