## 1 Introduction  
Intestinal mucosa is where dietary phytochemicals are absorbed and where intestinal resident macrophages coordinate immune tolerance to dietary antigens and microbiota, while also providing surveillance and protection against infection. Hepatocytes are the main target of phytochemicals entering the liver through portal veins and are responsible for metabolizing these compounds [1]. Some dietary phytochemicals reach the small intestine in the form of glycosides, which are cleaved by the enterocyte brush border enzymes, such as lactase phlorizin hydrolase (LPH) or cytoplasmic \(\beta\)-glucosidase. These enzymes release biologically active aglycons [2; 3; 4]. Such compounds diffuse into the mucus layer and are absorbed through paracellular or transcellular routes. Water, ions, sugars and solutes up to 600 Da in molecular weight are destined to follow the first route, but most phytochemicals undergo the latter, either through passive diffusion for nonpolar aglycones or carotenoids, or through facilitated transport by transmembrane carriers [5]. Usually, sodium-glucose-linked transporter 1 (SGLT-1) or mono-carboxyl transporter 1 (MCT-1) are engaged in polyphenol aglycone uptake [6; 7]. Once phenolic compounds enter the intestinal epithelial cells (IECs), they undergo a broad range of activities, including anti-inflammatory actions through modulation of the signal transduction pathways or through epigenetic regulation [8; 9]. After being absorbed in the intestine, phenolic compounds reach the liver through portal circulation. The liver is responsible for the metabolism of a majority of xenobiotics, including phytochemicals and polyphenols, and can also be their main target. For that reason, plant-derived compounds such as silymarin or berberine are used as hepatocyte energetics agents to promote liver regeneration and help in prophylaxis against chronic liver diseases, including non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) [10]. NAFLD manifests through the accumulation of lipid droplets in hepatocytes and results from an imbalance between de novo lipogenesis in liver, uptake of dietary fats and insufficient mitochondrial fatty acid catabolism and expenditure. Acute lipid accumulation in the liver leads to steatosis, hepatocyte cell death caused by lipotoxicity and inflammation [11]. Risk factors for NAFLD onset include obesity, insulin resistance, type II diabetes and high percentage of consumed calories coming from fats. Macrophages are the most abundant immune cell population in the gut [12]. Intestinal, lamina propria resident macrophages are also a target for dietary bioactive compounds absorbed in the small intestine. Kupffer cells constitute a special population of macrophages residing in the liver that support hepatocyte functions by taking part in iron recycling, clearing apoptotic cells and tolerance to innocuous dietary antigens [13]. During infection, they are the first line of innate immune defence against pathogens that enter through the gastrointestinal route. They also promote hepatocyte proliferation and liver regeneration after injury [14]. In NAFLD, Kupffer cells respond to hepatocyte damage with enhanced synthesis of proinflammatory cytokines, such as IL-1\(\beta\) and TNF\(\alpha\). The inflammatory environment further stimulates lipid accumulation in hepatocytes, which creates a vicious cycle of disease progression to NASH [15]. Currently, a \"multiple hits\" hypothesis is the prevailing explanation for the onset of NAFLD [16; 17]. Initial metabolic conditions, such as prolonged excessive energy intake leading to obesity, insulin resistance and a diet rich in fat and fructose, are considered \"the first hit\". These factors lead to gut dysbiosis and a prevalence of _Proteobacteria_ in the microbiota community, which impair the intestinal mucosa integrity and initiate so-called \"leaky gut\" problem.