Dietary patterns and type 2 diabetes—relationship to metabolic syndrome and inflammation

Noncommunicable chronic diseases have been on the rise for decades. Almost 10% of the world adult population lives with type 2 diabetes mellitus (T2DM)—a leading cause of severe complications associated with disability and premature mortality. Worldwide, nearly 500 million adults are living with T2DM and 4.2 million deaths were caused directly by the disease. Dietary quality is a major component influencing the development of T2DM, due to diet-related inflammatory processes, linked to metabolically unhealthy obesity (MUO) and metabolic syndrome (MetS). In addition to systemic and tissue-specific low-grade chronic inflammation, characterized by mediators such as various cytokines, T2DM is characterized by a disturbed homeostasis of oxidative stress, as well as a dysregulated glucose and lipid metabolism. Poor inflammatory and antioxidant status have been related to an enhanced risk of developing MUO, MetS, and T2DM. However, diet also is an important source of antioxidants, which are antiinflammatory and may reduce disease risk and improve symptomology. This includes dietary patterns rich in fruits/vegetables, which are good sources of fiber, vitamins, minerals, and phytochemicals such as polyphenols, and low in animal products, ultraprocessed foods, sugar, saturated fats, total calories, and salt. Mechanistic studies have highlighted that antiinflammatory and antioxidant diets might positively influence several cellular processes. These include direct effects on the homeostasis of reactive oxygen species (ROS) such as quenching effects by antioxidants, but also the interaction of dietary constituents with transcription factors, especially with nuclear factor kappa-B (NF-κB) and nuclear factor erythroid 2-related factor 2 (Nrf-2), important for regulating inflammation and oxidative stress, respectively. In this chapter, we evaluate the association between dietary patterns and T2DM, as well as the role played by MUO and oxidative stress in influencing inflammation and increasing the risk of MetS and, eventually, T2DM.