Kinetic study of the expression of genes related to hepatic steatosis, glucose and lipid metabolism, and cellular stress during overfeeding in mule ducks

Author:

Pioche Tracy1,Skiba Fabien2,Bernadet Marie-Dominique3,Seiliez Iban1,Massimino William1,Houssier Marianne1,Tavernier Annabelle1,Ricaud Karine1,Davail Stéphane1,Skiba-Cassy Sandrine1,Gontier Karine1

Affiliation:

1. Institut National de la Recherche Agronomique, Univ Pau & Pays Adour, Energy and Environment Solutions initiative, Nutrition, Métabolisme, Aquaculture, Saint-Pée-sur-Nivelle, France

2. Nutricia, Route de Saint-Sever, Haut-Mauco, France

3. Unité Expérimentale Palmipèdes à Foie Gras, Institut National de la Recherche Agronomique Bordeaux-Aquitaine, Domaine d’Artiguères, Benquet, France

Abstract

Induced by overfeeding, hepatic steatosis is a process exploited for the “foie gras” production in mule ducks. To better understand the mechanisms underlying its development, the physiological responses of mule ducks overfed with corn for a duration of 11 days were analyzed. A kinetic analysis of glucose and lipid metabolism and cell protection mechanisms was performed on 96 male mule ducks during overfeeding with three sampling times (after the 4th, the 12th, and the 22nd meal). Gene expression and protein analysis realized on the liver, muscle, and abdominal fat showed an activation of a cholesterol biosynthetic pathway during the complete overfeeding period mainly in livers with significant correlations between its weight and its cholesterolemia ( r = 0.88; P < 0.0001) and between the liver weight and the hmgcr and soat1 expression ( r = 0.4, P < 0.0001 and r = 0.67; P < 0.0001, respectively). Results also revealed an activation of insulin and amino acid cells signaling a pathway suggesting that ducks boost insulin sensitivity to raise glucose uptake and use via glycolysis and lipogenesis. Cellular stress analysis revealed an upregulation of key autophagy-related gene expression atg8 and sqstm1( P < 0.0001) during the complete overfeeding period, mainly in the liver, in contrast to an induction of cyp2e1( P < 0.0001), suggesting that autophagy could be suppressed during steatosis development. This study has highlighted different mechanisms enabling mule ducks to efficiently handle the starch overload by keeping its liver in a nonpathological state. Moreover, it has revealed potential biomarker candidates of hepatic steatosis as plasma cholesterol for the liver weight.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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