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There is increasing attention on the complex interactions occurring between schistosome parasites and their hosts. However, little is known about the occurrence, epidemiology, and mechanisms of schistosomiasis-associated infertility. In this article, we argue that an in-depth understanding of the interplay between parasites and the host endocrine system may significantly enhance current knowledge of infertility in infected individuals. We discuss the basic hormonal mechanisms that may lead to the discovery of entirely novel anthelmintic interventions against schistosomiasis. In spite of a plethora of epidemiological evidence supporting a key role for schistosome infection for infertility, little is known about the mechanisms of their association. To date, one of the few well characterized mechanisms by which schistosomes interact with their hosts is the estrogenic imbalance and downregulation of the estrogen receptor. Remarkably, our understanding of this mechanism has already been successfully studied in cancer-associated schistosomiasis. The relentless advancement in molecular studies, together with the discovery of novel biomarkers, provide unprecedented opportunities to investigate schistosomiasis and exploit parasite–host relationships for the development of novel strategies of disease control. [ABSTRACT FROM AUTHOR]

Abstract Aims Obesity is a complex health disorder and a trigger to many diseases like Diabetes mellitus (DM) and breast cancer (BrCa), both leading causes of morbidity and mortality worldwide. Also evidence demonstrates that abnormal glucose metabolism termed 'the Warburg effect' in cancer cell is closely associated with malignant phenotypes and promote the aggressiveness of several types of cancer, including BrCa. In this study, we evaluated the breast cancer cell metabolism in normoglycemia, hyperglycemia and in an obesity condition in order to clarify the potential underlined mechanisms that link these disorders. Materials and methods MCF-7 cells were exposed to low and high glucose levels, the latter either in the presence of 3T3-L1 adipocyte conditioned medium (CM), thus mimicking the adiposity observed in obese patients. Cell viability, migration, proliferation, cytotoxicity and cell death assays were performed under the different culture conditions. Hormonal and lipid profile were also characterized by biochemical assays and primary metabolism was determined by Nuclear Magnetic Resonance (NMR)-based metabolomics. Results Our results show an increased aggressiveness in the condition mimicking diabetogenic obesity with an altered energy/lipid metabolism. Interestingly in the experimental obesity-mimicking status, lipids and amino acids were expended while glucose was produced by tumor cells from lactate. These findings reveal a shift on tumor cells metabolism that is opposite to 'the Warburg effect'. Conclusions Overall, this experimentally obesity-mimicking condition not only revealed an increased tumor proliferation and aggressiveness but also disclosed a new mechanism of cancer metabolism, the 'Warburg Effect Inversion'. [ABSTRACT FROM AUTHOR]

Background and aims: Glucose homeostasis is a critical cornerstone in both health and disease. It is described to be regulated by the balance of insulin and glucagon secretion but, this bi-hormonal perspective is long overdue since glucose homeostasis is now known to be a multi-hormonal process. Metabolic syndrome (MetS) is a cluster of metabolic features that includes impaired glucose metabolism and obesity. Obesity promotes a low chronic inflammation state due to the release of bioactive molecules like cytokines, ultimately contributing to cardiovascular disease, diabetes, and cancer. The gastrointestinal tract (GIT), namely the stomach and intestine, has a vital role not only in the food uptake and absorption but also in the production of incretin hormones, such as GLP-1. We aim to evaluate the GLP-1 receptor (GLP-1R) in the GIT of a MetS animal model and to assess whether it correlates with inflammatory levels. Material and method: The expression of GLP-1R and interleukin-6 (IL-6) was evaluated in the stomach and intestine of mice subjected to normal diet (ND) and high fat diet (HFD) by immunohistochemistry. Results: We observed that HFD fed animals presented lower levels of GLP-1R in the stomach and intestine when compared with animals fed with ND. Concomitantly, these mice expressed increased levels of IL-6. Conclusions: GLP-1R expression is inversely correlated with the expression of the pro-inflammatory cytokine IL-6. [ABSTRACT FROM AUTHOR]