Spontaneous Physical Activity in Obese Condition Favours Antitumour Immunity Leading to Decreased Tumour Growth in a Syngeneic Mouse Model of Carcinogenesis

Our goal was to evaluate the effect of spontaneous physical activity on tumour immunity during aging. Elderly (n = 10/group, 33 weeks) ovariectomized C57BL/6J mice fed a hyperlipidic diet were housed in standard (SE) or enriched (EE) environments. After 4 weeks, orthotopic implantation of syngeneic mammary cancer EO771 cells was performed to explore the immune phenotyping in the immune organs and the tumours, as well as the cytokines in the tumour and the plasma. EE lowered circulating myostatin, IL-6 and slowed down tumour growth. Spleen and inguinal lymph node weights reduced in relation to SE. Within the tumours, EE induced a lower content of lymphoid cells with a decrease in Th2, Treg and MDCS; and, conversely, a greater quantity of Tc and TAMs. While no change in tumour NKs cells occurred, granzyme A and B expression increased as did that of perforin 1. Spontaneous physical activity in obese conditions slowed tumour growth by decreasing low-grade inflammation, modulating immune recruitment and efficacy within the tumour.

Metabolic effects of 3,5-Diiodo-L-Thyronine

Thyroid hormones have been proposed as anti obesity drugs due to their effects on basal metabolism and the ability to increase energy expenditure. However, their clinical use has been strongly curbed by the concomitant onset of thyrotoxicosis. In this setting, several studies have been undertaken to assess the role of 3,5 diiodo- L-thyronine (T2), an endogenous metabolite of thyroid hormone derived from the enzymatic deiodination of triodothyronine T3. The metabolic effects of T2 are similar to those induced by T3. However, these effects appear to involve different and not welldefined mechanisms that make this molecule clinically useful as potential drug in the treatment of pathological conditions such as obesity and hepatic steatosis. The main pharmacological target of T2 appears to be the mitochondria. Therefore, the administration of T2 to obese subjects might improve the mitochondrial performance, which is generally recognized to be reduced in these subjects who must oxidize greater quantities of substrates. In this context, it can be hypothesized that T2, by acting mainly on mitochondrial function and oxidative stress, might be able to prevent and revert the tissue damages and hepatic steatosis induced by a hyperlipidic diet and a concomitant reduction in the circulating levels LDL and triglycerides as well. This review the discuss the mechanisms of action of T2 and the possible, future clinical uses of T2 analogs for the treatment lipid dysmetabolism related to obesity and overweight.

Hyperlipidic Diet-induced Obesity Increased Proliferative Signals- AR, ERK1/2- on Mice Prostate, Which can be Restored through Physical Training

Aims: To evaluate the effects of hyperlipidic diet on the mouse prostate and also investigate if physical exercise is able to restore such effects. Methodology: Adult male Swiss mice were fed with a balanced (ND) or hyperlipidic diet (45% saturated fat, HD) for 16 weeks. Half were submitted to a sedentary (NDS and HDS) or exercise routine (swimming- NDE and HDE) for 8 weeks. Then, the prostate was analyzed by immunoreactions (proliferating cell nuclear antigen- PCNA, androgen receptor- AR, and estrogen receptor-ERβ), western blotting (ERK 1/2), and caspase-3 activity. Results: We found that saturated fat uptake promoted 16% weight gain, increased fat-mass and hyperglycaemia, as well as reduced testosterone levels. In addition, HD atrophied prostate secretory epithelium and stimulated cell proliferation through higher expression of AR and activation of ERK signaling. Additionally, saturated fat reduced prostatic ERβ content. Physical exercise per se promoted an anabolic effect by increasing testosterone and stimulating cell proliferation in the prostate of sedentary animals. Finally, exercise was able to restore the proliferative signals caused by the hyperlipidic diet on prostate. Conclusion: We suggest that the combination of hyperlipidic diet and sedentary lifestyle could negatively affected some prostate stimulating pathways that could trigger proliferative diseases in mice and physical exercise may be an interesting strategy to reverse such effects.

Cactus young cladodes improves unbalanced glycemic control, dyslipidemia, prooxidant/antioxidant stress biomarkers and stimulate lecithin-cholesterol acyltransferase and paraoxonase activities in young rats after cafeteria diet exposure

Purpose This paper aims to evaluate the protective potential of prickly pear cactus fresh cladodes (opuntia ficus indica (OFI)) on glycemic disorders, dyslipidemia, prooxidant/antioxidant stress biomarkers and reverse cholesterol transport (by evaluating the activity of lecithin-cholesterol acyltransferase (LCAT)) and paraoxonase (PON1) in rats prematurely exposed to cafeteria diet (CD). Design/methodology/approach Sixteen young rats were divided into two groups fed CD containing 50 per cent of hyperlipidic diet (HLD) and 50 per cent of junk food mix supplemented or not with 50 g of fresh young cladodes of OFI to 100 g of CD, during 30 days. Findings OFI cladodes supplementation decreased significantly body weight (p < 0.001), food intake (p < 0.05), adipose tissue weight (p < 0.01), fasting glycemia and glycosylated hemoglobin (p < 0.01), homeostasis model assessment (HOMA-IR) and insulinemia (p < 0.001), levels of cholesterol (C) (p < 0.05) and triacylglycerols (TG) (p < 0.01) in serum and in very low-density lipoproteins (VLDL-C p < 0.05 and VLDL-TG p < 0.01) and improves reverse cholesterol transport by increasing high-density lipoprotein cholesteryl-esters concentrations (p < 0.001) and by stimulating LCAT activity. Moreover, they attenuated lipid peroxidation in VLDL and low-density lipoproteins by increasing atheroprotective activity of PON-1 and in liver and adipose tissue by enhancing enzymatic antioxidant defence. Social implications The young cladodes of OFI because of their antiobesity benefits could constitute a novel functional ingredient in pharmaceutical and nutraceutical applications. Originality/value Young cladodes of OFI in rat precociously submitted to a hyperlipidic diet/junk food (cafeteria model) seem to prevent metabolic disorders associated with obesity.

Alterations in the biochemical parameters and the spermatic function generated by obesity in rats

The aim of the present study was to assess the effects of a hyperlipidic diet set before puberty in male Wistar rats’ gonadal weights and testicular func-tions. Males rats were used for the study, they were randomly distributed into 2 groups: Control Group (CG: standard diet (normolipidemic) and the second: Intervention Group (IG: hyperlipidemic diet), after 7 days of experi-mentation, 3 rats were sacrificed per week, blood samples were collected and level of HDL, LDL and triglyceride were analyzed. A significant reduction (p<0.05) in testicular weight in the control group was observed compared with the hyperlipidic diet group, triglyceride levels showed a consistent change over the weeks of the study, HDL levels showed a consistent change during the 5 weeks of the study, Photomicraphie of the testicles of Wistar rats in the hyperlipid diet group for the first week showed Sertoli cell hyper-plasia ,during the second week microscopic examination showed significant testicular hypertrophy the microscopic examination during the fifth week showed hyperplasia of the seminal vesicle characterized by an increase in the number of glandular epithelial cells. The proliferating epithelium may form papillary structures with supporting stroma and with extension into the glandular lumen and total absence of sperm cells. Obesity is associated with many metabolic abnormalities. It has been found that these metabolic ab-normalities induce disorders of spermatogenesis. Our results show that the hyperlipidic diet affects the gonads significantly with hypertrophic testes, the presence of hyperplastic seminiferous tubes, as well as a fine basement membrane.