Lipid metabolism is a fundamental process responsible for the synthesis, breakdown, and storage of lipids, which are essential components of all cell membranes and play vital roles in energy storage and cell signalling. Lipid metabolism encompasses several interconnected processes, including lipid synthesis (lipogenesis), breakdown (lipolysis), and lipid oxidation. Lipogenesis primarily involves the synthesis of triglycerides from acetyl-CoA and malonyl-CoA and occurs in the liver, adipose tissue, and lactating mammary gland. Lipolysis, on the other hand, is the breakdown of triglycerides into glycerol and free fatty acids, which can be utilized as an energy source during fasting or increased energy demand. Adipose tissue is the primary site of lipolysis. Finally, lipid oxidation refers to the degradation of fatty acids within mitochondria to produce energy in the form of ATP. Lipids, particularly phospholipids, sphingolipids, and sterols, play crucial roles in cell signalling as signalling molecules and as components of cellular membranes. One prominent example of lipid-mediated signalling is the phosphoinositide signalling pathway. Phosphoinositides, derived from phosphatidylinositol, serve as key regulators of various cellular processes, including cell growth, differentiation, and intracellular trafficking. Phosphoinositides are modified by specific kinases and phosphatases, resulting in the generation of different lipid species that act as second messengers and bind to specific proteins, such as kinases or ion channels, to initiate signalling cascades. Another vital lipid signalling pathway is the production of lipid-derived signalling molecules known as eicosanoids. Eicosanoids are synthesized from polyunsaturated fatty acids, such as arachidonic acid, and include prostaglandins, leukotrienes, and thromboxanes. These lipid mediators are involved in various physiological processes, such as inflammation, blood clotting, and smooth muscle contraction. Prostaglandins, for example, regulate inflammation and pain perception by activating specific G-protein coupled receptors. Lipid metabolism also influences the activation of nuclear receptors, a class of transcription factors that regulate gene expression in response to specific lipid ligands. For example, peroxisome proliferator-activated receptors (PPARs) are activated by fatty acids and their derivatives. Upon activation, PPARs heterodimerize with retinoid X receptors (RXRs) and bind to specific DNA sequences, known as peroxisome proliferator response elements (PPREs), to modulate the expression of target genes involved in lipid metabolism, glucose homeostasis, and inflammation. Finally, lipid metabolism is intimately linked to insulin signalling and glucose metabolism. Lipid accumulation in non-adipose tissues, such as the liver and skeletal muscle, can lead to insulin resistance, a hallmark of type 2 diabetes. Increased lipid availability can activate protein kinases, such as PKCθ and IKK-β, which phosphorylate insulin receptor substrate (IRS) proteins, inhibiting insulin signal transduction and promoting insulin resistance. We provide a wide product catalogue of research tools for investigating lipid metabolism, including Albumin antibodies, Adiponectin antibodies, Clusterin antibodies, IGF1 ELISA Kits, and Adiponectin ELISA Kits. Explore our full lipid metabolism product range below and discover more, for less.