Abstract
BackgroundBecause the cost of cereals is unstable and represents a large part of production charges for meat-type chicken, there is an urge to formulate alternative diets from more cost-effective feedstuff. We have recently shown that meat-type chicken source is prone to adapt to dietary starch substitution with fat and fiber. The aim of this study was to better understand the molecular mechanisms of this adaptation to changes in dietary energy sources through the fine characterization of transcriptomic changes occurring in three major metabolic tissues – liver, adipose tissue and muscle – as well as in circulating blood cells.ResultsWe revealed the fine-tuned regulation of many hepatic genes encoding key enzymes driving glycogenesis and de novo fatty acid synthesis pathways and of some genes participating in oxidation. Among the genes expressed upon consumption of a high-fat, high-fiber diet, we highlighted CPT1A, which encodes a key enzyme in the regulation of fatty acid oxidation. Conversely, the repression of lipogenic genes by the high-fat diet was clearly associated with the down-regulation of SREBF1 transcripts but was not associated with the transcript regulation of MLXIPL and NR1H3, which are both transcription factors. This result suggests a pivotal role for SREBF1 in lipogenesis regulation in response to a decrease in dietary starch and an increase in dietary PUFA. Other prospective regulators of de novo hepatic lipogenesis were suggested, such as PPARD, JUN, TADA2A and KAT2B, the last two genes belonging to the lysine acetyl transferase (KAT) complex family regulating histone and non-histone protein acetylation. Hepatic glycogenic genes were also down-regulated in chickens fed a high-fat, high-fiber diet compared to those in chickens fed a starch-based diet. No significant dietary-associated variations in gene expression profiles was observed in the other studied tissues, suggesting that the liver mainly contributed to the adaptation of birds to changes in energy source and nutrients in their diets, at least at the transcriptional level. Moreover, we showed that PUFA deposition observed in the different tissues may not rely on transcriptional changes.ConclusionWe showed the major role of the liver, at the gene expression level, in the adaptive response of chicken to dietary starch substitution with fat and fiber.
Highlights
Because the cost of cereals is unstable and represents a large part of production charges for meattype chicken, there is an urge to formulate alternative diets from more cost-effective feedstuff
We showed that the main metabolism impacted by changes in dietary energy sources was fatty acid (FA) metabolism, FA synthesis and polyunsaturated FA (PUFA) deposition in the liver
These observations, suggesting a direct deposition of FA for chicken fed an HF diet, are further supported by the higher amount of n-3 and n-6 PUFA vs. MUFA+SFA observed in liver, adipose tissue and muscle, since C18:2 and C18:3 cannot be synthesized by animals
Summary
Because the cost of cereals is unstable and represents a large part of production charges for meattype chicken, there is an urge to formulate alternative diets from more cost-effective feedstuff. To sustain production traits such as growth or breast muscle weight, dietary energy primarily derived from starch in cereal-based diets must be maintained by adding fat sources such as vegetable oils to fiber-rich diets. This results in changing both energy sources and nutrients in diets. Cellulose – a compound resistant to digestion in the small intestine – was used as an insoluble fiber source in the HF diet, as it was considered a simple diluent of energy In these three studies, no effect of diets was observed on production performance (i.e., weight gain, feed efficiency or body composition), showing that chicken is prone to adapt to variations in dietary energy sources. We highlighted known and potential regulator genes for this metabolism by combining differential expression, co-expression and genomics co-localization analyses
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