Effect of Low-Dose Progesterone on Glycemic Metabolism, Morphology and Function of Adipose Tissue and Pancreatic Islets in Diet-Induced Obese Female Mice.

Background: Obesity is a worldwide concern due to its global rapid expansion and remarkable impact on individual's health by predisposing to several other diseases. About twice as many women as men suffer from severe obesity and, in fact, there are stages in a woman's life when weight gain and adiposity can result in greater damage to health. For example, obesity triples the chance of a woman developing gestational diabetes.

Aerobic Physical Exercise Improves Exercise Tolerance and Fasting Glycemia Independent of Body Weight Change in Obese Females.

Obesity is associated with increased risk of several chronic diseases and the loss of disease-free years, which has increased the focus of much research for the discovery of therapy to combat it. Under healthy conditions, women tend to store more fat in subcutaneous deposits. However, this sexual dimorphism tends to be lost in the presence of comorbidities, such as type 2 diabetes mellitus (T2DM).

Effects of a moderate iron overload and its interaction with yacon flour, and/or phytate, in the diet on liver antioxidant enzymes and hepatocyte apoptosis in rats.

The effect of moderate Fe overload in the diet and its interaction with phytate, and/or yacon flour (YF), recognized as an inhibitor, and facilitator, of Fe absorption, respectively, was evaluated in healthy rats. For this purpose the following parameters were analyzed: (1) apparent iron (Fe), copper (Cu) and zinc (Zn) absorption; (2) blood Fe; (3) blood lipids (cholesterol, tryacylglicerol); (4) blood AST and ALT; (5) liver histology (histopathology, hemosiderin depots, apoptosis index; (6) liver fatty acid incorporation; (7) liver antioxidant enzyme activity. Moderate Fe overload may cause change in some liver markers (hemosiderin depots, apoptosis index and GPx) and blood lipids (total cholesterol and VLDL) and the interaction with yacon flour, and phytate, in the Fe overloaded diets may exert a protective effect on these alterations.

Comparative effects of DHA and EPA on cell function.

Fish oil supplementation has been reported to be generally beneficial in autoimmune, inflammatory and cardiovascular disorders. Most researchers have attributed these beneficial effects to the high content of omega-3 fatty acids in fish oil (FO). The effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are not differentiated in most studies.

Persistent activation of Akt or ERK prevents the toxicity induced by saturated and polyunsaturated fatty acids in RINm5F β-cells.

The aim of this study was to investigate whether the toxicity of saturated and polyunsaturated fatty acids (PUFA) on RINm5F cells is related to the phosphorylation state of Akt, ERK and PKC delta. The regulation of these kinases was compared in three experimental designs: (a) 4h-exposure, (b) 4h-exposure and a subsequent withdrawn of the FA for a 20 h period and (c) 24h-exposure. Saturated and PUFA were toxic to RINm5F cells even at low concentrations.

Fatty acid-induced toxicity and neutral lipid accumulation in insulin-producing RINm5F cells.

Fatty acids have been shown to cause death of rat and human primary pancreatic beta cells and of insulin-producing cell lines. These studies focused mainly on saturated and monounsaturated FA such as palmitic, stearic and oleic acids. In this study, we have performed a comparison of the toxicity of a wider range of FA.

Chewing over physiology integration.

An important challenge for both students and teachers of physiology is to integrate the different areas in which physiological knowledge is didactically divided. In developing countries, such an issue is even more demanding, because budget restrictions often affect the physiology program with laboratory classes being the first on the list when it comes to cuts in expenses. With the aim of addressing this kind of problem, the graduate students of our department organized a physiology summer course offered to undergraduate students.

Improvement of the mitochondrial antioxidant defense status prevents cytokine-induced nuclear factor-kappaB activation in insulin-producing cells.

Proinflammatory cytokines (interleukin-1beta [IL-1beta], tumor necrosis factor-alpha [TNF-alpha], and gamma-interferon [IFN-gamma]) initiate a variety of signal cascades in pancreatic beta-cells that affect the expression level of genes involved in both the destruction and the protection of the beta-cell. The generation of nitric oxide (NO) via the inducible NO synthase (iNOS) and oxygen free radicals play a key role in cytokine-mediated beta-cell destruction. Within these signal cascades, the activation of the transcription factor nuclear factor-kappaB (NF-kappaB) is crucial, and many cytokine-sensitive genes contain binding sites for this transcription factor in their promoter regions.