Control of fatty acid storage and release in adipose tissue is fundamental in energy homeostasis and the development of obesity and type 2 diabetes. We here take the whole signalling network into account to identify how insulin and β-adrenergic stimulation in concert controls lipolysis in mature subcutaneous adipocytes obtained from non-diabetic and, in parallel, type 2 diabetic women. We report that, and show how, the anti-lipolytic effect of insulin can be fully explained by protein kinase B (PKB/Akt)-dependent activation of the phosphodiesterase PDE3B. Through the same PKB-dependent pathway β-adrenergic receptor signalling, via cAMP and PI3Kα, is anti-lipolytic and inhibits its own stimulation of lipolysis by 50%. Through this pathway both insulin and β-adrenergic signalling control phosphorylation of FOXO1. The dose–response of lipolysis is bell-shaped, such that insulin is anti-lipolytic at low concentrations, but at higher concentrations of insulin lipolysis was increasingly restored due to inhibition of PDE3B. The control of lipolysis was not altered in adipocytes from diabetic individuals. However, the release of fatty acids was increased by 50% in diabetes due to reduced reesterification of lipolytically liberated fatty acids. In conclusion, our results reveal mechanisms of control by insulin and β-adrenergic stimulation — in human adipocytes — that define a network of checks and balances ensuring robust control to secure uninterrupted supply of fatty acids without reaching concentrations that put cellular integrity at risk. Moreover, our results define how selective insulin resistance leave lipolytic control by insulin unaltered in diabetes, while the fatty acid release is substantially increased.

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The present research had the purpose to analyze morphologically the sites of endometrial implants on the external area of the musculature of the anterior abdominal wall of female rats, treated with dexamethasone. For so, these 15 albino female rats were used (Rattus norvegicus albinus), of the lineage Wistar with 90 days of age, that were submitted to the induction of the endometriosis, and divided in the following groups: Group I-induced female rats to endometriosis and evaluated after 21 days (control); Group IIinduced female rats to endometriosis and after 21 days, treated with dexamethasone for 10 days; Group III-induced female rats to endometriosis, and after 21 days, treated with dexamethasone for 15 days. The dexamethasone was administered in the dosage of 0,8 mg/ day/animal. Our results showed that the chronic inflammatory process in the endometriosis doesn't decrease after treatment with dexamethasone for 10 days, while the treatment with dexamethasone for 15 days reverted the chronic inflammatory process in the endometriosis, besides stimulating the proliferation of glands in endometrial implants.

Introdução: A literatura relata que os implantes endometriais possuem receptores para hormônios esteroides, sendo estimulados principalmente pelo estrógeno, e que algumas estratégicas de tratamento têm sido propostas em modelos experimentais, tais como a utilização de glicocorticoides sintéticos, como a dexametasona. Objetivo: analisar histoquímica e morfometricamente lesões endometrióticas induzidas em ratas e tratadas com 0,8 mg/kg/dia de dexametasona. Material e métodos: Quarenta ratas albinas (linhagem Wistar) com 90 dias de vida, pesando aproximadamente 150 g, foram induzidas à endometriose e divididas em grupos: 1. ratas com endometriose e avaliadas após 34 dias (G1); 2. ratas com endometriose e avaliadas após 47 dias (G2); 3. ratas com endometriose e, após 21 dias do pós-operatório, tratadas com dexametasona por 13 dias (G3) e 4. ratas com endometriose e, após 21 dias do pós-operatório, tratadas com dexametasona por 13 dias e eutanasiadas após um período de 13 dias, contados a partir do término do tratamento com dexametasona (G4). Os fragmentos dos implantes endometriais foram fixados em Bouin, incluídos em paraplast e corados por hematoxilina-eosina e tricrômico de Mallory. As médias do número de glândulas foram submetidas ao teste não-paramétrico de Tukey-Kramer (p ≤ 0,05 05). Results: Dexamethasone reduced inflammation in the endometrial implants, the collagen content in the stroma and decreased significantly the area occupied by glands