Increased lipogenesis in isolated hepatocytes from cold-acclimated ducklings

Abstract

Thermogenic endurance and development of metabolic cold adaptation in birds may critically depend on their ability to synthesize and use fatty acids (FA) as fuel substrates. Hepatic lipogenesis and the capacity to oxidize FA in thermogenic tissues were measured in cold-acclimated (CA) ducklings (Cairina moschata) showing original mechanisms of metabolic cold adaptation in the absence of brown adipose tissue, the specialized thermogenic tissue of rodents. The rate of FA synthesis from [U-(14)C]glucose and from [1-(14)C]acetate, measured in incubated hepatocytes isolated from 5-wk-old thermoneutral (TN; 25 degrees C) or CA (4 degrees C) fed ducklings, was higher than in other species. Hepatic de novo lipogenesis was further increased by cold acclimation with both glucose (+194%) and acetate (+111%) as precursor. Insulin slightly increased (+11-14%) hepatic lipogenesis from both precursors in CA ducklings, whereas glucagon was clearly inhibitory (-29 to -51%). Enhanced de novo lipogenesis was associated with higher (+171%) hepatocyte activity of glucose oxidation and larger capacity (+50 to +100%) of key lipogenic enzymes. The potential for FA oxidation was higher in liver (+61%) and skeletal muscle (+29 to +81%) homogenates from CA than from TN ducklings, suggesting that the higher hepatic lipogenesis may fuel oxidation in thermogenic tissues. Present data underline the high capacity to synthesize lipids from glucose in species like muscovy ducks susceptible to hepatic steatosis. Lipogenic capacity can be further increased in the cold and may represent an important step in the metabolic adaptation to cold of growing ducklings.

Manipulation of Incubation Temperatures to Increase Cold Resistance of Broilers:Influence on Embryo Development, Organ Weights, Hormones and Body Composition

“…Here, lower body lipid content was observed only for T2 embryos from younger breeders at EA 14 suggesting that breeder age influences the response of embryos to cooler incubation temperatures. On DOH, higher body lipid content of T2 chicks could explain their resistance to cooler temperatures because lipids have an important role in avian temperature acclimation (Bedu et al, 2002). On the other hand, at DOH slightly higher protein but lower lipid contents of chicks from younger than older breeders were consistent with previous reports (Peebles et al, 2001 andYalçın et al, 2008 b).…”

“…Chick and heart weights interacted with breeder age providing further evidence that breeder age is a major factor determining sensitivity to environmental temperatures (Yalçın et al, 2005(Yalçın et al, , 2008a(Yalçın et al, , 2008c. Moreover, higher body lipid contents may play a specific role in cold acclimated avian muscle nonshivering thermogenesis both as activators and as energetic substrates (Bedu et al, 2002). As such they may contribute to resistance to cold stress during the growing period.…”

Lack of stearoyl-CoA desaturase 1 upregulates basal thermogenesis but causes hypothermia in a cold environment

“…An increase in the use of lipids allows the maintenance of heat production for a longer period and therefore improves chances of survival in the cold (40). Actually, cold induces a large increase of de novo lipogenesis in thermogenic tissue such as BAT and liver after cold exposure, suggesting that lipogenesis is an essential step of cold acclimation (38,39). We found a decrease in hepatic TG content and an increase in plasma FFA level in SCD1 Ϫ/Ϫ mice after cold exposure.…”

“…These results suggest that the depletion of glycogen and glucose may contribute to the hypothermia in SCD1 Ϫ/Ϫ mice exposed to 4ЊC. In a cold environment, de novo lipogenesis enhances cold acclimation by increasing lipid utilization and heat production (38,39). To determine whether cold exposure changes fat stores in plasma, BAT, and liver, the amount of TG was analyzed.…”

Cold-acclimation-induced non-shivering thermogenesis in birds is associated with upregulation of avian UCP but not with innate uncoupling or altered ATP efficiency

“…Hence, skeletal muscle NST would rather be sustained either by increasing ATP breakdown through the futile cycling of calcium across the sarcoplasmic reticulum membrane, for example (Dumonteil et al, 1995), or by decreasing mitochondrial ATP efficiency through the oxidation of FADH 2 -linked substrates such as fatty acyl-carnitine (Clerc et al, 2007). The latter hypothesis would link avUCP gene expression with the mobilization of fat reserves and the increased potential of skeletal muscle to oxidize fatty acid when birds are exposed to low temperatures (Barré et al, 1986;Benistant et al, 1998;Bedu et al, 2002). Further insight, avUCP can also have a role in the control of radical oxidative species production ( al., 2010b) when skeletal muscle mitochondria oxidize fatty acids Seifert et al, 2008).…”