Pet Wellness and Vitamin A: A Narrative Overview

Abstract

The health of companion animals, particularly dogs and cats, is significantly influenced by nutrition, with vitamins playing a crucial role. Vitamin A, in particular, is indispensable, with diverse roles ranging from vision to immune modulation and reproduction. Despite its importance, the metabolism and dietary requirements of vitamin A in companion animals remain complex and not fully understood. This review provides a comprehensive overview of the historical perspective, the digestion, the metabolism, the physiological roles, the deficiency, the excess, and the interactions with other micronutrients of vitamin A in companion animals. Additionally, it highlights future research directions and gaps in our understanding. Insights into the metabolism of vitamin A in companion animals, personalized nutrition strategies based on genetic variability, longitudinal studies tracking the status of vitamin A, and investigations into its immunomodulatory effects are crucial for optimizing pet health and wellness. Furthermore, understanding the stability and bioavailability of vitamin A in pet food formulations is essential for ensuring the provision of adequate micronutrients. Overall, this review underscores the importance of vitamin A in companion animal nutrition and the need for further research to enhance our understanding and to optimize dietary recommendations for pet health and well-being.

Keywords: cat; dog; health; pets; vitamin A; well-being.

Figure 1

Structural formula for all-trans-retinol.

Figure 2

Diagram of the current model of vitamin A absorption, transport, and storage. Retinoid metabolism can be classified into three major processes—intestinal uptake, hepatic storage, and tissue-specific metabolism that are interconnected via lymphatic and blood vitamin A transport [47]. “Although each of these steps is characterized by a set of specialized proteins, lecithin:retinol acyltransferase (LRAT) plays a pivotal role in each of them. The abbreviations used are the following: 11c-RAL, 11-cis-retinal; ADHs, alcohol dehydrogenases; ALDHs, aldehyde dehydrogenases; βC, β,β-carotene; BCO1, β,β-carotene-15,15-dioxygenase; CRABPs, cellular retinoic acid-binding proteins; CRALBP, cellular retinaldehyde-binding protein; CRBP1, cellular retinol-binding protein 1; CRBP2, cellular retinol-binding protein 2; ER, endoplasmic reticulum; LRAT, lecithin:retinol acyltransferase; RA, all-trans-retinoic acid; RAL, all-trans-retinaldehyde; REHs, retinyl ester hydrolases; REs, retinyl esters; RESs, retinyl esterases; RPE65, retinoid isomerase; ROL, all-trans-retinol; RBP, serum retinol-binding protein; SCARB1, scavenger receptor class B, type I; SDRs, short-chain dehydrogenases/reductases; STRA6, stimulated by retinoic acid 6; TTR, transthyretin”.

Figure 3

Schematic showing the proposed sites of RA (all-trans-retinoic acid; ATRA) function during eye morphogenesis (left) and differentiation (right) [102]. At the early stages of the eye development, the RA generated by RALDH1 and RALDH3 acts as a paracrine signal binding to the RARs located in the perioptic mesenchyme to support the anterior eye segment development and the closure of the optic fissure. Pitx2 is a RA/RAR-regulated transcription factor that is required both for anterior eye segment morphogenesis, as well as the closure of the optic fissure. At the later stages of development, the RA promotes the differentiation of the neural retina. The mechanism is unclear but could involve either a paracrine effect of the RA outside of the neural retina or a direct effect on the cells within the retina itself. https://creativecommons.org/licenses/by/3.0/ (accessed on 3 January 2024).

Figure 4

ATRA (all-trans-retinoic acid) as a modulator of T cell immunity [120].

Figure 5

Oxygen consumption in adipocytes exposed to 2 µM of ATRA (all-trans-retinoic acid) was measured using Clarke’s electrode (adapted from Tourniaire et al. [157]). Control refers to control cells, which received the vehicle (dimethyl sulfoxide). Data are the mean  ±  SEM of three independent cultures per treatment condition. The assessment compared ATRA-treated cells to untreated cells and measured their oxygen consumption rates to determine if ATRA-induced gene expression changes altered cellular metabolism. ATRA increased oxygen consumption by 15% (* p  <  0.05).

Figure 6

Immunomodulatory capacity of vitamin A and D [186]. Th = T helper cells: Th1 (they primarily produce cytokines such as interferon-gamma (IFN-γ) and interleukin-2 (IL-2) and are involved in cell-mediated immunity), Th17 (they produce cytokines such as interleukin-17 (IL-17) and interleukin-22 (IL-22) and are involved in the defense against extracellular pathogens), and Th2 (they produce cytokines such as interleukin-4 (IL-4), interleukin-5 (IL-5), and interleukin-13 (IL-13) and are involved in humoral immunity and allergic responses); and Treg = regulatory T cells (they express the transcription factor Foxp3 and play a crucial role in immune tolerance and regulation).