In avian species, lipids and especially triglycerides may be stored in adipocytes, hepatocytes and growing oocysts.

Intestinal digestion of dietary lipids, which consist essentially of triglycerides, involves their partial hydrolysis, absorption and reassembly in the intestinal mucosal cells into very large lipoprotein particles. Because the intestinal lymphatic system is poorly developed in birds, lipoproteins are secreted directly into the portal system. Lipoproteins pass through the liver before they reach the rest of the circulation.

Lipoprotein synthesis and secretion in the liver
The liver plays a key role in providing lipids destined to be used by all tissues, including the liver itself. Fatty acid synthesis in birds takes place mainly in the liver; adipose tissue growth and subsequent fattening depend on the availability of plasma triglycerides, which are transported as components of lipoproteins.

Hepatic lipogenesis in birds. Fatty acid synthesis in birds depends on several factors :insulin stimulates the activity of the main enzymes involved in lipogenesis namely fatty acid synthase (FAS). In laying hens, hepatic lipogenesis is dramatically enhanced by estrogens. Although the main products of hepatic lipogenesis are triglycerides, the liver is also the major site of cholesterol and phospholipidsynthesis. These lipids, along with protein, are the main components of lipoproteins.

Lipoprotein synthesis. Very low density lipoprotein VLDL and High density Lipoproteins HDL are the two main classes of lipoprotein particles that are synthesized and secreted bythe liver.

Regulation of lipoprotein secretion. Very little is known about the regulation of lipoprotein synthesis and secretion in avian liver, at least in growing birds. Insulin enhances both lipogenesis and VLDL synthesis, whereas thyroxine and glucagon have opposite effects.

Ttriglyceride storage in the body depends on the availability of a plasma lipid originating from either the diet or lipogenesis in the liver. In young broiler chickens approaching market weight, about 80-85% of the fatty acids that accumulate in the adipose tissue are derived from plasma lipids. The transfer of triglycerides from VLDL into the adipose tissue involves their catabolism by lipoproteinlipase (LPL). Lipoprotein lipase catalyses the hydrolysis of triglycerides to fatty acids and glycerol. The fatty acids then enter the surroundingtissues. Thus, adipose tissue growth in birds depends mainly on the availability of triglycerides transported by VLDL

Fatty liver occurs in birds when the increase in lipogenesis exceeds the capacity of synthesis and secretion of lipoproteins. This is the case in laying females, in which the dramatic enhancement of lipogenesis by estrogen is responsible for an increase in VLDL secretion. In fed chickens, considerable amounts of triglycerides are temporarily stored by the liver but need a further hydrolysis and reesterification before they can enter the secretion pathway. If lipogenesis exceeds the capacity of VLDL secretion, triglycerides accumulate in the liver. In other cases, and more specificallyin growing birds, the limitation of fattening relies on the controlof VLDL production. Nutritional attempts, such as a partial replacement of dietary energy by protein, are very effective in reducing lipogenesis and subsequent fattening, but the cost is prohibitive. Hormonal treatments are not allowed.