Evolution of intestinal microbiota and body compartments during spontaneous hyperphagia in the Greylag goose.

The aim of this work was to study the effects of spontaneous hyperphagia on the evolution of intestinal microbiota and body compartments in old goose. From October 25th to November 26th, 5-yr-old breeding Greylag Landaise geese (106 males and 106 females) were fed with grass during 1 mo (G period). From November 26th (0 d) the birds had ad libitum access to pellets (AMEn: 10.5 MJ/kg, CP: 18.9 g/kg; spontaneous fattening (SF) period). Some birds were killed at -31 d (n = 24; 50/50 sex ratio), 0 d (n = 48), 14 (n = 46), 22 d (n = 46), and 70 d (n = 48) after the start of G period to measure body traits. For microbial analysis, 10 of the samples per sex at 0 d, 14 d, and 70 d were selected to be representative of body traits. Between 0 and 22 d, liver weight increased from 98 g to 194 g in males and from 89 g to 199 g in females (P < 0.001). Liver weight decreased between 22 and 70 d from 194 to 174 g in males and from 199 to 163 g in females (P < 0.001). Irrespective of the diet (G or SF period) and the sex of the bird, the two major phyla were Proteobacteria (49%) and Firmicutes (48%). Bacteroidetes represented around 3.0% of the sequences. At order level, Firmicutes were dominated by Clostridiales (33% of total sequences) and Lactobacillales (13% of total sequences) and Proteobacteria were dominated by Campylobacteriales (34% of total sequences). Finally, Bacteroidetes were dominated by Bacteroidales. SF and sex did not change the microbial diversity but sparse partial least squares discriminant analysis allowed us to highlight discriminant operational taxonomic unit between experimental groups. In conclusion, our result showed that changes in the body compartments of old geese during spontaneous hyperphagia depend on the sex of the birds, but not so much in gut microbial composition. Further investigations are necessary to understand the functional microbiota and highlight the role of gut microbiota in hepatic steatosis induced with hyperphagia in geese.

Liver gene expression in relation to hepatic steatosis and lipid secretion in two duck species.

The susceptibility to development of hepatic steatosis is known to differ between Muscovy and Pekin ducks. Although some experiments were conducted to decipher these differences, few data have been produced to analyse the role of specific genes in this process. For this purpose, expression levels of genes involved in lipid (ATP citrate lyase, malic enzyme 1, fatty acid synthase, stearoyl-CoA desaturase 1, diacylglycerol O-acyl transferase 2, microsomal triglyceride transfer protein, apolipoprotein A1, apolipoprotein B, sterol regulatory element binding factor 1, hepatocyte nuclear factor 4, choline/ethanolamine phosphotransferase 1, carnitine palmitoyl transferase 1A, peroxisome proliferator-activated receptor alpha and sterol O-acyltransferase) and carbohydrate (activating transcription factor 4 or cAMP-response element binding protein, mitochondrial malate dehydrogenase 2 and carbohydrate responsive element binding protein) metabolism and in other functions were analysed in the liver of Pekin and Muscovy ducks fed ad libitum or overfed. A specific positive effect of feeding was observed on the expression of genes involved mainly in fatty acids and TG synthesis and glycolysis, and negative effect on genes involved in beta-oxidation. Interestingly, a strong species effect was also observed on stearoyl-CoA desaturase 1 and to a lesser extent on diacylglycerol O-acyl transferase 2 expression, leading to large differences in expression levels between Pekin and Muscovy overfed ducks, which could explain the difference in lipid metabolism and steatosis ability observed between the two duck species. These results should shed light on gene expression that might underlie susceptibility to hepatic steatosis in humans.

Effects of dietary fructose on liver steatosis in overfed mule ducks.

Overfeeding of some waterfowl species results in obesity, which is mainly characterized by a dramatic hepatic steatosis induced by strong accumulation of lipids synthesized from dietary glucose in the liver. In mammals, fructose is known to be able to raise plasma triacylglycerol concentrations significantly; consequently, this may induce obesity. The aim of this study was to assess the effect of partial replacement of dietary glucose provided by corn starch with fructose on metabolism and fatty liver production in the Mule ducks. On the basis of 9.5 kg maize (132,920 kJ) given twice a day for 14 days, a supplementation of 9,800 kJ was provided in form of glucose, sucrose or high fructose corn syrup (HFCS: 50 % glucose, 42 % fructose and 8 % other saccharides). Fatty liver weight in ducks fed with glucose supplementation was 499 +/- 21 g. Sucrose or HFCS supplementation brought about a significant increase in liver weight (+ 18.7 % and + 16.3 % vs. glucose supplementation respectively, p < 0.05). These results suggest that the dietary fructose favors the liver steatosis by increasing hepatic lipogenesis. Postprandial plasma insulin concentrations were similar in ducks fed diets with or without fructose, suggesting that the effect of fructose on liver steatosis is not mediated by insulin.

Pancreatic hormonal and metabolic responses in overfed ducks.

When overfed at their maximum (intensive overfeeding) or at only 80% (moderate overfeeding) of food intake capacity, Mule ducks developed strong liver steatosis, whereas Pekin ducks showed very marked extrahepatic fattening. During overfeeding, evolution of plasma glucose and triacylglycerol concentrations suggested a very strong increase in the hepatic lipogenesis as well as genotype- and diet-independent lipoprotein secretion. In contrast, lipoprotein-lipase activity was dependent on alimentary status (the intensive overfeeding induces the highest activities), and Pekin ducks showed higher lipoprotein-lipase activity than Mule ducks, which could favor extrahepatic fattening to the detriment of hepatic steatosis. In Pekin ducks, plasma pancreatic hormone concentrations are related to diet levels and blood sugar. With similar food intake, Mule ducks (moderately overfed) showed global blood insulin lower than that of Pekin ducks (intensively overfed) despite similar blood sugar levels, suggesting a trend towards reduced pancreas response to glucose in Mule ducks. This may result from their lower lipoprotein-lipase activity as previously shown in these two ducks overfed at only 60% of their maximal food intake capacity (unpublished results). These results suggest that high plasma insulin concentrations may be necessary to induce an optimum lipoprotein-lipase activity in overfed ducks.