Severe pantothenic acid deficiency induces alterations in the intestinal mucosal proteome of starter Pekin ducks

Jing Tang,Yongbao Wu,Ming Xie,Shuisheng Hou,Suyun Liang,Bo Zhang,Yulong Feng,Zhanbao Guo,Zhengkui Zhou

doi:10.1186/s12864-021-07820-x

Abstract

BackgroundPantothenic acid deficiency (PAD) results in growth depression and intestinal hypofunction of animals. However, the underlying molecular mechanisms remain to be elucidated. Mucosal proteome might reflect dietary influences on physiological processes.ResultsA total of 128 white Pekin ducks of one-day-old were randomly assigned to two groups, fed either a PAD or a pantothenic acid adequate (control, CON) diet. After a 16-day feeding period, two ducks from each replicate were sampled to measure plasma parameters, intestinal morphology, and mucosal proteome. Compared to the CON group, high mortality, growth retardation, fasting hypoglycemia, reduced plasma insulin, and oxidative stress were observed in the PAD group. Furthermore, PAD induced morphological alterations of the small intestine indicated by reduced villus height and villus surface area of duodenum, jejunum, and ileum. The duodenum mucosal proteome of ducks showed that 198 proteins were up-regulated and 223 proteins were down-regulated (> 1.5-fold change) in the PAD group compared to those in the CON group. Selected proteins were confirmed by Western blotting. Pathway analysis of these proteins exhibited the suppression of glycolysis and gluconeogenesis, fatty acid beta oxidation, tricarboxylic acid cycle, oxidative phosphorylation, oxidative stress, and intestinal absorption in the PAD group, indicating impaired energy generation and abnormal intestinal absorption. We also show that nine out of eleven proteins involved in regulation of actin cytoskeleton were up-regulated by PAD, probably indicates reduced intestinal integrity.ConclusionPAD leads to growth depression and intestinal hypofunction of ducks, which are associated with impaired energy generation, abnormal intestinal absorption, and regulation of actin cytoskeleton processes. These findings provide insights into the mechanisms of intestinal hypofunction induced by PAD.

Highlights

Pantothenic acid deficiency (PAD) results in growth depression and intestinal hypofunction of animals
The coenzymes of this vitamin participate in various metabolic reactions, such as glucose, fatty acids and amino acids entering into energy-yielding tricarboxylic acid (TCA) cycle, fatty acid oxidation and synthesis, cholesterol synthesis, acetylcholine synthesis, and heme synthesis etc. [1, 2]
Plasma parameters Plasma pantothenic acid concentration decreased by 85%, while plasma alkaline phosphatase (ALP) activity decreased by approximately 70% as a result of PAD when compared to the CON group (P < 0.001; Table 2)

Summary

Introduction

Pantothenic acid deficiency (PAD) results in growth depression and intestinal hypofunction of animals. Pantothenic acid is a precursor of two coenzymes, coenzyme A (CoA) and acyl-carrier-protein. Its importance is highlighted by the adverse effects of pantothenic acid deficiency (PAD) in mammals such as rats, cats, and pigs, including growth depression, skin lesions, diarrhea, loss of hair [2,3,4,5,6]. Intestinal hypofunction was shown to be a major consequence of PAD in rats, dogs, cats, chicks, and fish, such as intestinal ulceration, diarrhea, and colitis [4, 5, 17,18,19,20,21]. Previous studies in fish showed that PAD decreased intestinal digestive and absorptive capacities by reducing the activities of both intestinal brush border enzymes and digestive enzymes [14, 21]

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