Fat content

Fat content refers to the total accumulation of lipids, primarily triacylglycerols, stored within specialized adipose tissue or ectopically in organs such as the liver and skeletal muscle [11, 16]. It is not a discrete molecular target like a receptor or enzyme, but rather a complex physiological phenotype and a key clinical endpoint for metabolic health [1, 9]. The regulation of fat content involves an intricate network of pathways including adipogenesis, lipogenesis, and lipolysis, which are governed by various hormones and signaling molecules [2, 5]. In the context of drug discovery, reducing fat content is the primary therapeutic goal for conditions such as obesity, metabolic syndrome, and non-alcoholic fatty liver disease (NAFLD) [6, 9]. Pharmacological intervention to lower fat content typically involves targeting specific proteins like fatty acid synthase (FASN), peroxisome proliferator-activated receptors (PPARs), or incretin receptors such as GLP-1R [1, 12]. For example, lipase inhibitors like orlistat prevent fat absorption, while GLP-1 receptor agonists like semaglutide reduce body fat through appetite suppression and metabolic modulation [1, 5]. Excessive fat content, particularly in visceral depots, is a significant driver of insulin resistance, chronic inflammation, and cardiovascular disease [5, 6].

Other names

Body fatAdiposityAdipose massLipid contentFat massIntramuscular fat

Reduction of fat content is achieved through various mechanisms depending on the drug class: Orlistat inhibits gastric and pancreatic lipases to reduce dietary fat absorption; GLP-1 and GIP receptor agonists (e.g., Semaglutide, Tirzepatide) reduce body fat by suppressing appetite and improving insulin sensitivity; sympathomimetic agents like Phentermine reduce food intake via central nervous system pathways.