The ingestion of excessive amounts of saturated fatty acids (SFAs) and transfatty acids (TFAs) is considered to be a risk factor for cardiovascular diseases, insulin resistance, dyslipidemia, and obesity. The focus of this paper was to elucidate the influence of dietary SFA and TFA intake on the promotion of lipotoxicity to the liver and cardiovascular, endothelial, and gut microbiota systems, as well as on insulin resistance and endoplasmic reticulum stress. The saturated and transfatty acids favor a proinflammatory state leading to insulin resistance. These fatty acids can be involved in several inflammatory pathways, contributing to disease progression in chronic inflammation, autoimmunity, allergy, cancer, atherosclerosis, hypertension, and heart hypertrophy as well as other metabolic and degenerative diseases. As a consequence, lipotoxicity may occur in several target organs by direct effects, represented by inflammation pathways, and through indirect effects, including an important alteration in the gut microbiota associated with endotoxemia. Interactions between these pathways may perpetuate a feedback process that exacerbates an inflammatory state. The importance of lifestyle modification, including an improved diet, is recommended as a strategy for treatment of these diseases.

Oral cancer accounts for 10% of head and neck tumors. Despite the recent advancements in surgical techniques, as well as in chemo- and radiotherapy therapeutic protocols, survival rates for oral cancer patients have not improved significantly in the last decades. Recently, toll like receptors (TLRs) have been described as promoters of cell proliferation, invasiveness, and angiogenesis in a variety of cancers. The aim of this review is to identify how TLRs participate in oral carcinogenesis in order to evaluate their biological relevance. Data revealed that some TLRs participate in oral carcinogenesis since TLR5 and TLR9 promote tumor growh, whereas TLR3 is closely involved to anti-cancer properties. They represent a promising alternative for oral cancer therapy. However, TLR2, TLR4 and TLR7 need further investigation, since current data are not sufficient to conclude about their role. Certainly, such data will contribute to new scientific knowledge, which will be incorporated to the preventive actions and therapeutic protocols for oral cancer patients suffering from this devasting disease.