Modulation of Hepatic Insulin and Glucagon Signaling by Nutritional Factors in Broiler Chicken

Abstract

Influencing the endocrine metabolic regulation of chickens by nutritional factors might provide novel possibilities for improving animal health and productivity. This study was designed to evaluate the impact of dietary cereal type (wheat-based (WB) vs. maize-based (MB) diets), crude protein level (normal (NP) vs. lowered (LP)), and sodium (n-)butyrate (1.5 g/kg diet) supplementation (vs. no butyrate) on the responsiveness of hepatic glucagon receptor (GCGR), insulin receptor beta (IRβ) and mammalian target of rapamycin (mTOR) in the phase of intensive growth of chickens. Liver samples of Ross 308 broiler chickens (Gallus gallus domesticus) were collected on day 21 for quantitative real-time polymerase chain reaction and Western blot analyses. Hepatic GCGR and mTOR gene expressions were up-regulated by WB and LP diet. GCGR and IRβ protein level decreased in groups with butyrate supplementation; however, the quantity of IRβ and mTOR protein increased in WB groups. Based on these data, the applied dietary strategies may be useful tools to modulate hepatic insulin and glucagon signaling of chickens in the period of intensive growth. The obtained results might contribute to the better understanding of glycemic control of birds and increase the opportunity of ameliorating insulin sensitivity, hence, improving the production parameters and the welfare of broilers.

Keywords: butyrate; chicken; glucagon; hepatic glucagon receptor; insulin; insulin receptor beta; mammalian target of rapamycin; non-starch polysaccharides.

Figure 1

Relative gene expression (A) and protein abundance (B) of hepatic glucagon receptor. MB: maize-based diet; WB: wheat-based diet supplemented with NSP-degrading xylanase and glucanase enzymes; NP: “Normal protein” group reared on a diet with crude protein content adequate to the dietary phase; LP: “Low protein” group reared on a diet with crude protein content reduced by 15%, supplemented with limiting amino acids; But: sodium butyrate supplementation of the diet in the dose of 1.5 g/kg diet; Ctr: control group without sodium butyrate supplementation. Letters indicate groups that were significantly different with pairwise comparison. If two groups have different letters, p-values were <0.05.

Figure 1

Relative gene expression (A) and protein abundance (B) of hepatic glucagon receptor. MB: maize-based diet; WB: wheat-based diet supplemented with NSP-degrading xylanase and glucanase enzymes; NP: “Normal protein” group reared on a diet with crude protein content adequate to the dietary phase; LP: “Low protein” group reared on a diet with crude protein content reduced by 15%, supplemented with limiting amino acids; But: sodium butyrate supplementation of the diet in the dose of 1.5 g/kg diet; Ctr: control group without sodium butyrate supplementation. Letters indicate groups that were significantly different with pairwise comparison. If two groups have different letters, p-values were <0.05.

Figure 2

Relative gene expression (A) and protein abundance (B) of hepatic insulin receptor β. MB: maize based diet; WB: wheat based diet supplemented with NSP-degrading xylanase and glucanase enzymes; NP: “Normal protein” group reared on a diet with crude protein content adequate to the dietary phase; LP: “Low protein” group reared on a diet with crude protein content reduced by 15%, supplemented with limiting amino acids; But: sodium butyrate supplementation of the diet in the dose of 1.5 g/kg diet; Ctr: control group without sodium butyrate supplementation. Letters indicate groups that were significantly different with pairwise comparison. If two groups have different letters, p-values were <0.05.

Figure 3

Relative gene expression (A) and protein abundance (B) of hepatic mammalian target of rapamycin. MB: maize-based diet; WB: wheat-based diet supplemented with NSP-degrading xylanase and glucanase enzymes; NP: “Normal protein” group reared on a diet with crude protein content adequate to the dietary phase; LP: “Low protein” group reared on a diet with crude protein content reduced by 15%, supplemented with limiting amino acids; But: sodium butyrate supplementation of the diet in the dose of 1.5 g/kg diet; Ctr: control group without sodium butyrate supplementation. Letters indicate groups that were significantly different with pairwise comparison. If two groups have different letters, p-values were <0.05.

Figure 4

Overview of the insulin and glucagon signaling pathways and the observed main effects of the investigated nutritional factors. IRα: insulin receptor α subunit; IRβ: insulin receptor β subunit; IRS-1: insulin receptor substrate 1 (“a” lowercase subscript when activated); PI3K: phosphatidylinositol-3-kinase (“a” lowercase subscript when activated); PIP₂: phosphatidylinositol diphosphate; PIP₃: phosphatidylinositol triphosphate; PKB: protein kinase B; mTOR: mammalian target of rapamycin; Ca²⁺: calcium ion; cAMP: cyclic adenosine monophosphate; PKC: protein kinase C; PKA: protein kinase A; P: phosphate group; MB: maize-based diet; WB: wheat-based diet supplemented with NSP-degrading xylanase and glucanase enzymes; NP: “Normal protein” group reared on a diet with crude protein content adequate to the dietary phase; LP: “Low protein” group reared on a diet with crude protein content reduced by 15%, supplemented with limiting amino acids; But: sodium butyrate supplementation of the diet in the dose of 1.5 g/kg diet. ↓ and ↑ arrows indicate the lowering or increasing effect of the given nutritional factor on the investigated parameter.