Dietary Soy Isoflavones Prevent Metabolic Disturbs Associated with a Deleterious Combination of Obesity and Menopause.

This study aimed to evaluate the effects of soy isoflavone supplementation (25 mg/kg) on insulin resistance and inflammation in adipose tissue in an experimental model of menopause-obesity. Twenty-four female Wistar rats were ovariectomized (O) and distributed among the groups: OSD-ovariectomized rats submitted to normocaloric standard diet (n = 6); OHF-ovariectomized rats submitted to high-fat diet (n = 9); and OHFI-ovariectomized rats submitted to high-fat diet with isoflavones (n = 9). Weight gain, body adiposity, food and caloric intake, blood pressure, and glucose tolerance were assessed. After 24 weeks, the rats were euthanized; the thoracic blood collected for serum insulin determination and the homeostatic model assessment-insulin resistance) (HOMA-IR) and homeostatic model assessment-ß cell (HOMA-ß) indices were calculated. Abdominal adipose tissues were removed, weighed, and fixed for immunohistochemical and morphometric studies. Isoflavones decreased weight gain and blood pressure without changing the food and caloric intake (P < .05). Isoflavones did not affect the weight of the abdominal adipose tissue depots (P < .05). Although they did not alter glucose tolerance, the isoflavones reduced HOMA-IR and HOMA-ß, serum insulin levels, in addition to reducing adipocytes' size (P < .05). The number of macrophages, lymphocytes, and crown-like structures in adipose tissue was lower in the group treated with isoflavones (P < .05). In conclusion, our data show that dietary soy isoflavones' supplementation prevents many of well-known deleterious combination of obesity and menopause on metabolism, such as body overweight, adipocyte hypertrophy, and hypertension, as well as insulin resistance and adipose tissue inflammation.

Time-Course of Redox Status, Redox-Related, and Mitochondrial-Dynamics-Related Gene Expression after an Acute Bout of Different Physical Exercise Protocols.

We investigated the magnitude of exercise-induced changes in muscular bioenergetics, redox balance, mitochondrial function, and gene expression within 24 h after the exercise bouts performed with different intensities, durations, and execution modes (continuous or with intervals). Sixty-five male Swiss mice were divided into four groups: one control (n = 5) and three experimental groups (20 animals/group), submitted to a forced swimming bout with an additional load (% of animal weight): low-intensity continuous (LIC), high-intensity continuous (HIC), and high-intensity interval (HII). Five animals from each group were euthanized at 0 h, 6 h, 12 h, and 24 h postexercise. Gastrocnemius muscle was removed to analyze the expression of genes involved in mitochondrial biogenesis (Ppargc1a), fusion (Mfn2), fission (Dnm1L), and mitophagy (Park2), as well as inflammation (Nos2) and antioxidant defense (Nfe2l2, GPx1). Lipid peroxidation (TBARS), total peroxidase, glutathione peroxidase (GPx), and citrate synthase (CS) activity were also measured. Lactacidemia was measured from a blood sample obtained immediately postexercise. Lactacidemia was higher the higher the exercise intensity (LIC < HIC < HII), while the inverse was observed for TBARS levels. The CS activity was higher in the HII group than the other groups. The antioxidant activity was higher 24 h postexercise in all groups compared to the control and greater in the HII group than the LIC and HIC groups. The gene expression profile exhibited a particular profile for each exercise protocol, but with some similarities between the LIC and HII groups. Taken together, these results suggest that the intervals applied to high-intensity exercise seem to minimize the signs of oxidative damage and drive the mitochondrial dynamics to maintain the mitochondrial network, similar to low-intensity continuous exercise.

Interaction between cigarette smoke exposure and physical training on inflammatory and oxidative profile in mice muscle.

Regular physical training and cigarette smoke exposure (CSE) have opposite effects on physical performance, antioxidant, and inflammatory profile. However, the interaction between these events is not well studied. We aimed to investigate how regular physical training and CSE interact, and in what is the outcome of this interaction on the physical performance, skeletal muscle antioxidant defense and molecular profile response of pro and anti-inflammatory cytokines. Male C57BL/6 mice were randomly divided into 4 groups (n = 8/group): 1) Sedentary group (SED); 2) 4 weeks of control, followed by 4 weeks of CSE (SED + CSEG); 3) Physically active (PA) along 8 weeks (forced swim training, 5 times a week); 4) Physically active and exposed to the cigarette smoke (PA + CSEG), group submitted to forced swim training for 4 weeks, followed by 4 weeks of concomitant training and CSE. Physical performance was evaluated before and after the experimental period (8 weeks), total peroxidase and glutathione peroxidase (GPx) activities, expression of genes encoding TNF-α, MCP-1, IL1ß, IL-6, IL-10, TGF-ß, HO-1 and the TNF-α/IL-10 ratio were determined from gastrocnemius muscle at the end of experimental period. The CSE attenuated the aerobic capacity adaptation (time to exhaustion in swimming forced test) promoted by physical training and inhibit the improvement in local muscle resistance (inverted screen test). The regular physical training enhanced the antioxidant defense, but the CSE abrogated this benefit. The CSE induced a harmful pro-inflammatory profile in skeletal muscle from sedentary animals whereas the regular physical training induced an opposite adaptation. Likewise, the CSE abolished the protective effect of physical training. Together, these results suggest a negative effect of CSE including, at least in part, the inhibition/attenuation of beneficial adaptations from regular physical training.

Relationship between Th17 immune response and cancer.

Cancer is the second leading cause of death worldwide and epidemiological projections predict growing cancer mortality rates in the next decades. Cancer has a close relationship with the immune system and, although Th17 cells are known to play roles in the immune response against microorganisms and in autoimmunity, studies have emphasized their roles in cancer pathogenesis. The Th17 immune response profile is involved in several types of cancer including urogenital, respiratory, gastrointestinal, and skin cancers. This type of immune response exerts pro and antitumor functions through several mechanisms, depending on the context of each tumor, including the protumor angiogenesis and exhaustion of T cells and the antitumor recruitment of T cells and neutrophils to the tumor microenvironment. Among other factors, the paradoxical behavior of Th17 cells in this setting has been attributed to its plasticity potential, which makes possible their conversion into other types of T cells such as Th17/Treg and Th17/Th1 cells. Interleukin (IL)-17 stands out among Th17-related cytokines since it modulates pathways and interacts with other cell profiles in the tumor microenvironment, which allow Th17 cells to prevail in tumors. Moreover, the IL-17 is able to mediate pro and antitumor processes that influence the development and progression of various cancers, being associated with variable clinical outcomes. The understanding of the relationship between the Th17 immune response and cancer as well as the singularities of carcinogenic processes in each type of tumor is crucial for the identification of new therapeutic targets.