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L-Carnitine is an amino acid derivative required for the β-oxidation of long-chain fatty acids, a process necessary for deriving energy from fat. Carnitine deficiency has been shown to cause dilated cardiomyopathy in a small population of dogs, and effects of carnitine deficiency on other tissue are being explored. Preliminary evidence reveals that feline hepatic lipidosis may result from a relative carnitine deficiency and may respond to supplementation. Carnitine supplementation also has been shown to alter body composition in swine by increasing lean body mass and decreasing fat mass, an important characteristic that may be applicable to the treatment and prevention of obesity in dogs and cats. Historically, the use of carnitine in veterinary medicine has been limited to cardiology, in which carnitine deficiency has been demonstrated to cause dilated cardiomyopathy (DCM) in some dogs. Recent research is helping identify noncardiac conditions that may respond to carnitine therapy, including feline hepatic lipidosis (HL) and obesity. Although the current body of knowledge regarding carnitine is rapidly expanding, well-controlled therapeutic trials, especially in the areas of HL and obesity, are lacking to date. This article outlines the role of carnitine and fatty acid (FA) metabolism in cellular physiology, discusses the conditions potentially associated with carnitine deficiency, and reviews important information on carnitine supplementation. FUNCTIONS OF CARNITINE Fat Metabolism Carnitine plays a central role in many cellular processes, most of which are related to fat metabolism and energy production. The primary function of carnitine is mitochondrial transport and subsequent β-oxidation of long-chain fatty acids (LCFAs), which results in ATP production. When fat is mobilized from peripheral body stores to be used for energy production (lipolysis), hormone-sensitive lipase catalyzes the breakdown of stored triglycerides into glycerol and free fatty acids (FFAs). FFAs are bound to albumin in the circulation and are a major energy source for many tissues. FAs taken up by the liver are either (1) esterified with glycerol to form triglyceride, which is transported to extrahepatic tissue via very-low-density lipoprotein (VLDL), or (2) “activated” to fatty acyl coenzyme A (CoA), which then undergoes β-oxidation in the mitochondria. β-Oxidation results in the production of acetyl CoA, which can be converted to ketone bodies or enter the Krebs cycle for the production of ATP; the latter process is essential for the fundamental metabolic reaction of converting fat to energy. Shortand medium-chain FAs CE V n Carnitine deficiency adversely affects energy production and fat metabolism, p. 46. n The highest concentrations of carnitine are found in skeletal and cardiac muscles, p. 47. n Carnitine is considered a “conditionally essential” nutrient because, in certain conditions, endogenous synthesis is insufficient to meet physiologic