![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
INRA, Station de Recherches Avicoles, 37380 Nouzilly, France
ABSTRACT
INTRODUCTION
INTESTINAL LIPOPROTEINS
LIPOPROTEIN SYNTHESIS AND SECRETION
IN THE LIVER
LIPOPROTEIN CATABOLISM AND TRIGLYCERIDE STORAGE
CONTROL OF EXTRAHEPATIC FATTENING IN GROWING BIRDS VIA LIPOPROTEIN METABOLISM
LIVER STEATOSIS
CONCLUSION
FOOTNOTES
LITERATURE CITED
ABSTRACT 
Because de novo 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. In growing birds, VLDL is the major transporter of triglycerides, and attempts to reduce excessive fatness in poultry have involved the control of VLDL metabolism. Lean and fat lines of chickens have been selected on the basis of either their abdominal fat content or plasma VLDL concentration. In both cases, hepatic lipogenesis or LPL activity in adipose tissue did not differ between lean and fat lines, and therefore they did not appear to be limiting factors of susceptibility to fattening. In contrast, hepatic secretion and plasma concentration of VLDL were always higher in fat chickens than in lean chickens. Thus, current methods of selection of broilers against excessive fatness are based on this direct relationship between plasma VLDL and adiposity. When hepatic lipogenesis exceeds the capacity of VLDL secretion, triglycerides accumulate in the liver, causing steatosis. Although fatty liver is associated with reduced egg production and increased mortality in laying hens, hepatic steatosis in overfed ducks and geese is of positive economic value, serving as the basis for "foie-gras" production. The balance between synthesis and secretion of VLDL is therefore the key point that regulates hepatic and extrahepatic fattening in poultry.
KEY WORDS: chicken · geese · fattening · liver steatosis · VLDLINTRODUCTION
In avian species, lipids and especially triglycerides may be stored in adipocytes, hepatocytes and growing oocytes. Lipid storage in the latter is associated with vitellogenesis and further development of the embryo and will not be discussed in the present review. Excessive accumulation of lipids in the adipose tissue of modern lines of broilers is a major concern for producers, because most fat depots are lost during evisceration of the carcass or processing of the meat, which results in lower meat yields. Finally, hepatic steatosis must be avoided in laying hens but is of economic value in the overfed Palmipedes (web-footed birds). Any attempt to modify these metabolic processes must take into consideration the specific features of lipid metabolism in birds.
First of all, de novo lipogenesis, i.e., synthesis of fatty acids, is very limited in adipose tissue and does not occur in the ovary (Saadoun and Leclercq 1987
). Thus, triglyceride storage in these compartments depends on the availability of a plasma lipid substrate 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 (Griffin et al. 1992). Because commercial avian breeds are usually fed lipid-poor diets (less than 10%), the liver plays a key role in providing lipids destined to be used by all tissues, including the liver itself.
Intestinal and hepatic lipids are assembled and secreted as lipoprotein particles. Extrahepatic fattening in poultry depends therefore on two successive steps of lipoprotein metabolism: 1) the level of their synthesis and secretion, and 2) their intravascular catabolism, leading to lipid uptake and storage by adipose tissue.
INTESTINAL LIPOPROTEINS
). Their size (mean diameter of about 150 nm) and composition (about 90% triglycerides) are very similar to those of mammalian chylomicrons (Griffin et al. 1982).
). They are absent from the plasma of unfed birds and are in very low concentration in fed immature birds. This situation reflects not only the relatively low amounts of fat in most poultry diets but also the very rapid catabolism of portomicrons in extrahepatic tissues (see below).
LIPOPROTEIN SYNTHESIS AND SECRETION
IN THE LIVER
. In laying hens, hepatic lipogenesis is dramatically enhanced by estrogens in order to meet the demand for vitellogenesis. Although the main products of de novo hepatic lipogenesis are triglycerides, the liver is also the major site of cholesterol and phospholipid synthesis. These lipids, along with protein, are the main components of lipoproteins.
Lipoprotein synthesis.
Very low density lipoprotein and HDL are the two main classes of lipoprotein particles that are synthesized and secreted by the liver. The specific protein moieties [apolipoproteins (apo)] of these lipoprotein particles are also synthesized in the liver. Apolipoprotein B-100 (Siuta-Mangano et al. 1982) and apo A-I (Banarjee and Redman 1984) are the major apolipoproteins of chicken VLDL and HDL, respectively. With regard to VLDL, the assembly of triglycerides, phospholipids, cholesterol and apo B (together with apo VLDL-II in laying females) is a sequential process that begins in the endoplasmic reticulum and ends in the Golgi apparatus, from which nascent particles are packaged in vesicles and secreted. The entire sequence lasts less than 40 min after the initiation of apo B translation. Synthesis and secretion pathways of chicken HDL are believed to be similar to those of VLDL.
on chicken hepatocytes demonstrated that insulin enhances both de novo lipogenesis and VLDL synthesis, whereas thyroxine and glucagon have opposite effects. In this context, the hormonal background may be very important in generating differences in rates of hepatic lipogenesis produced by genetic selection (see below). However, lipid secretion as lipoproteins may be not tightly coordinated with lipid synthesis. Indeed, in vitro studies clearly indicate that high concentrations of insulin, similar to those found in fed animals, enhance lipogenesis while inhibiting apo B synthesis. Therefore VLDL assembly and secretion is inhibited, and some triglycerides are channeled toward temporary storage into cytoplasmic vesicles (Mooney and Lane 1981).
LIPOPROTEIN CATABOLISM AND TRIGLYCERIDE STORAGE
). In laying hens, the plasma catabolism of VLDL is very limited (Griffin et al. 1982), which allows the transport of lipids to oocytes, where VLDL are endocytosed, rather than to other tissues. Indeed, laying hen apo VLDL contain large amounts of apo VLDL-II, an apolipoprotein that is synthesized only under the influence of estrogen and which has been shown to be a specific inhibitor of LPL (Schneider et al. 1990).
Regulation of lipoprotein lipase activity.
In fed mammals, LPL activity is enhanced in adipose tissue but is low in muscle, which results in fat storage. The opposite is seen in unfed animals. In birds, LPL regulation in the adipose tissue seems to be less sensitive to the nutritional state (Hermier et al. 1984). There is a paucity of information on the hormonal regulation of LPL in birds. Very high concentrations of insulin stimulate LPL activity in chicken adipose tissue (Borron et al. 1979), whereas dibutyryl cAMP can decrease both the synthesis and the activity of the enzyme in chicken adipocytes (Bensadoun and Martin 1986).
CONTROL OF EXTRAHEPATIC FATTENING IN GROWING BIRDS VIA LIPOPROTEIN METABOLISM
]. This hypothesis has been tested on chickens selected for leanness and fatness on either abdominal fat content at 9 wk (lean and fat lines; Leclercq et al. 1980) or plasma VLDL concentration at 7 wk (H-VLDL and L-VLDL lines; Whitehead and Griffin 1984) (Table 1, and see below). Hepatic lipogenesis was estimated via the incorporation of tritiated water and was found to be higher in the fat line rather than in the lean line (Saadoun and Leclercq 1987), whereas H-VLDL and L-VLDL chickens exhibited no consistent differences (Asante and Griffin 1988). In the latter lines, Bannister et al. (1984) found that the activities of enzymes involved in fatty acid synthesis in birds, such as FAS, MD and ATP citrate lyase, were significantly higher in the liver of fat H-VLDL chickens. In contrast, the differences in the activity of MD were not significant between fat and lean chickens (Asante and Bulfield 1988). However, as compared with lean birds, fat chickens exhibited a significantly higher hepatic 
9 desaturase activity, which is thought to facilitate the incorporation of fatty acids into VLDL and their subsequent secretion towards extrahepatic tissues (Legrand et al. 1987). Very low density lipoprotein secretion was also determined directly after inhibition of LPL in H-VLDL and L-VLDL chickens (Griffin et al. 1989) as well as in lean and fat chickens (Leclercq et al. 1990). In both studies, plasma VLDL accumulation was considerably higher in the fat line.
|
Table 1. Anatomic and metabolic changes in fat chickens compared with their lean counterparts |
), which indicated that VLDL concentration reflected the availability of plasma triglycerides and therefore the susceptibility to fattening, in accordance with previous studies (Whitehead and Griffin 1982). As a consequence, divergent selection for plasma VLDL level resulted in two lines with a sixfold difference in plasma VLDL and a threefold difference in the relative abdominal fat pad weight (Whitehead and Griffin 1984).
and 1984). Thus, this variable has been included in selection programs against excessive fattening of broilers in Great Britain.
). This is also in accordance with the results of Kouba et al. (1995), who showed that at the same age and similar body weight, the 80% lower proportion of the abdominal adipose tissue in turkeys compared with chickens was associated with a 85% lower plasma VLDL concentration.
), but this does not prove that fatness results from higher LPL activity. More likely, LPL activity increases with the number of adipocytes and thus reflects the degree of hyperplasia, rather than an increase in the fat-storing ability of individual cells per se. Indeed, fat chickens selected on the basis of their abdominal fat content exhibited a dramatic adipocyte hyperplasia. Consequently, in these birds compared with lean chickens, abdominal fat pad and LPL activity/pad were fourfold higher, whereas LPL activity per cell did not differ between lean and fat lines (Hermier et al. 1989).
). This is in accordance with the preferential use of VLDL-triglyceride for oxidation in the muscle rather than for adipose storage (Griffin et al. 1992).
LIVER STEATOSIS
). The disease generally results in reduced egg production and increased mortality.
). Liver steatosis is due to a specific accumulation of triglyceride within the parenchymal cells, the mechanism of which remains poorly understood. In geese, overfeeding leads to a dramatic increase in VLDL and HDL concentrations. However, these VLDL contain less triglycerides (29-35% vs. 43% in control geese), indicating that a defect in the incorporation of triglycerides into nascent VLDL particles may be responsible for the hepatic fat accumulation in this species (Hermier et al. 1994). The reason why neosynthezised triglycerides are channeled towards intracytoplasmic storage rather than secretion remains unclear. 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 (Mooney and Lane 1981). It is possible that, because the overfed geese are never deprived of food, hormonal regulation does not allow the liver to secrete the excess of triglycerides, which continue to accumulate.
CONCLUSION
). This would increase glucose uptake by the liver cells, activity of lipogenic enzymes, VLDL production, preadipocyte multiplication, and LPL activity (Table 1).
FOOTNOTES
LITERATURE CITED
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
