**Background**
Metabolic diseases, including obesity and diabetes, are characterized by systemic imbalances in energy homeostasis and nutrient metabolism. A critical factor in the development of these conditions is the dietary intake of sugars and the subsequent behavioral preference for sweet tastes. Understanding how different genetic predispositions, such as obesity-prone versus obesity-resistant phenotypes, influence the consumption of carbohydrates is essential for developing therapeutic strategies to manage metabolic syndrome. In this context, researchers often utilize specific sugars to study diet-induced obesity and preference shifts. Therefore, we will introduce a human endogenous metabolite – Sucrose.
**Definition**
Sucrose (D-(+)-Saccharose) is a disaccharide composed of the monosaccharides glucose and fructose, with a molecular weight of 342.30 and a Sucrose formula of C12H22O11.
**In Vitro and In Vivo Studies**
The Sucrose biological activity has been evaluated across various cellular and animal models. In vitro studies focusing on cytotoxicity and inflammatory responses demonstrated that Sucrose (Compound 8) exhibited minimal toxicity. Specifically, the IC50 values for cell growth inhibition after 48 hours were > 30 μM in human A549, HCT-15, SK-MEL-2, and SK-OV-3 cell lines. Additionally, in mouse BV2 cells, Sucrose showed an IC50 > 200 μM for the inhibition of LPS-induced nitric oxide production when treated for 30 minutes prior to a 24-hour LPS stimulation.
Regarding Sucrose in vivo applications, the compound is frequently used in animal models of metabolic disease and diet preference. Research indicates that high-energy (HE)-feeding leads to an overall decreased preference for sucrose solutions compared to chow-feeding in both obesity-prone (OP) and obesity-resistant (OR) rats. Specifically, OP rats showed a decreased preference for 0.3 M and 1.0 M sucrose solutions during HE-feeding (P=0.046 and P=0.012, respectively). OR rats exhibited decreased preferences for 0.01 M, 0.03 M, and 1.0 M sucrose solutions when HE-fed (P<0.0001, P=0.043, and P=0.013, respectively). Furthermore, chow-fed OP rats consumed significantly less 0.03 M and 0.1 M sucrose solutions compared to OR animals (P<0.0001). In conclusion, Sucrose is a vital endogenous metabolite used to investigate the complex relationship between diet, genetic predisposition, and metabolic dysfunction. Keywords Sucrose, 57-50-1, D-(+)-Saccharose, Endogenous Metabolite, metabolic disease, obesity, diet on preference, diabete, disaccharide, monosaccharide, glucose, fructose, Inhibitor, inhibitor, inhibit References [1] Duca FA, et al. Effect of diet on preference and intake of sucrose in obese prone and resistant rats. PLoS One. 2014 Oct 20;9(10):e111232.