## 1 Introduction  
According to the WHO (2021), obesity is a global epidemic that constitutes an acquired disease. In 2016, about 650 million adults (13% of the world population) were obese, and 1.9 billion were overweight [1; 2]. According to the WHO European Region (2022), almost 60% of adults and nearly one in three children are overweight or obese (29% of boys and 27% of girls) [3]. Obesity is a risk factor for several diseases, including cancer [4; 5]. Recent findings indicate that over 40% of individuals diagnosed with gastrointestinal cancer, such as colorectal cancer, are overweight, with obesity being the primary external risk factor for the development of this cancer [4; 5]. This risk factor is linked to the growth of intra-abdominal tumors, which thrive in the momentum majus environment. This region is rich in white adipocytes that function as an energy reservoir, where lipolysis and \(\beta\)-oxidation in tumor cells facilitate rapid proliferation through energy metabolism [6]. One of the four emerging markers proposed by [PERSON] and [PERSON] is unregulated energy metabolism. Thus, generalized obesity and increased energy supply in the momentum majus potentiate important risk factors produced by excess white adipose tissue (WAT) [6; 7]. Currently, the intestinal microbiota has been associated with vital physiological functions and could have a beneficial or detrimental impact on the metabolism of adipose tissue and cancer [8]. White adipose tissue (WAT), an endocrine organ that may store energy in the form of triglycerides for the maintenance of local and systemic energetic homeostasis, is the source of changes that lead to obesity, modulating different biological processes and consequently influencing the metabolism of various organs, such as the liver, muscle, pancreas, and brain, via endocrine mechanisms [2; 9]. Under normal conditions, WAT is deposited in subcutaneous locations, where it carries out thermoregulatory functions and facilitates the easy mobilization of triglycerides in response to need [10]. However, in the context of obesity, WAT exceeds its capacity for energy storage in subcutaneous regions, leading to a compensatory response characterized by hyperplasia (an increase in the number of adipocytes) and hypertrophy (an increase in adipocyte size). This excess adipose tissue is deposited in other areas of the body, such as the visceral region [2; 10]. The growth of WAT involves tissue remodeling characterized by increased extracellular matrix production, higher immune cells infiltration, and a stronger pro-inflammatory response [2; 11]. This condition defines meta-inflammation, supported by WAT, as a medical issue associated with obesity. Excess fat, especially visceral fat, being metabolically active and continuously releasing free fatty acids (FFAs) into portal circulation, can lead to insulin resistance and several other health problems, including systemic inflammation, dyslipidemia, atherosclerosis, and metabolic syndrome [2; 11]. Insulin resistance stands as the primary mechanism derived from the remodeled white adipose tissue deposited in the visceral region. This resistance is closely associated with various metabolic dysfunctions, including type 2 diabetes mellitus (T2 DM), cancer, and cardiometabolic risk. Traditional treatment for diabetic patients involves antidiabetic drugs or insulin therapy, such as Piogltazone (PGZ). PGZ is an insulin-sensitizing drug involved in the mediation of nuclear peroxisome proliferator-activated gamma receptor (PPARy), a transcriptional regulator of adipocyte differentiation and lipid storage that is abundant in adipose tissue [12]. Paradoxically, treatment with PGZ can result in weight gain by the formation of new adipocytes, despite promoting improvement of lipid profile, insulin sensitivity, and glycemic control [12].