ArticlePDF Available

Abstract and Figures

Polyunsaturated omega-3 fatty acids (n-3 PUFA) are a family of essential fatty acids with many biological activities. These fatty acids are incorporated into cell membranes, changing their structural and functional characteristics. N-3 PUFA can act by modulating inflammatory responses at different levels. Omega-3 PUFA can be converted in the body to longer-chain n-3 PUFA at a limited rate and are differently converted in body systems. It appears that when specific longer-chain n-3 PUFA are desired these need to be supplemented directly in the diet. In different species some evidence indicates a potential effect on improving insulin sensitivity. Recently, a novel class of n-3 PUFA-derived anti-inflammatory mediators have been recognized, termed E-series and D-series resolvins, formed from EPA and DHA, respectively. N-3 PUFA derived resolvins and protectins are heavily involved in the resolution of inflammation. Supplementation with n-3 fatty acids in horses may help manage chronic inflammatory conditions such as osteoarthritis, equine metabolic syndrome, laminitis, and thereby help to improve longevity of sport horse.
Content may be subject to copyright.
Invited Review
Omega-3 fatty acid supplementation in horses
Tanja Hess1, Trinette Ross-Jones2
1 Colorado State University, Department of Animal Science, Fort Collins, CO, USA.
2 Department of Animal Science and Wildlife Management, Tarleton State University, Stephenville, TX, USA.
ABSTRACT - Polyunsaturated omega-3 fatty acids (n-3 PUFA) are a family of essential fatty acids with many biological
activities. These fatty acids are incorporated into cell membranes, changing their structural and functional characteristics.
N-3 PUFA can act by modulating inflammatory responses at different levels. Omega-3 PUFA can be converted in the body to
longer-chain n-3 PUFA at a limited rate and are differently converted in body systems. It appears that when specific longer-
chain n-3 PUFA are desired these need to be supplemented directly in the diet. In different species some evidence indicates
a potential effect on improving insulin sensitivity. Recently, a novel class of n-3 PUFA-derived anti-inflammatory mediators
have been recognized, termed E-series and D-series resolvins, formed from EPA and DHA, respectively. N-3 PUFA derived
resolvins and protectins are heavily involved in the resolution of inflammation. Supplementation with n-3 fatty acids in horses
may help manage chronic inflammatory conditions such as osteoarthritis, equine metabolic syndrome, laminitis, and thereby
help to improve longevity of sport horse.
Key Words: alpha linolenic acid, arachidonic acid inflammation, docosahexaenoic acid, eicosapentaenoic acid, linoleic acid
Revista Brasileira de Zootecnia
© 2014 Sociedade Brasileira de Zootecnia
ISSN 1806-9290
R. Bras. Zootec., 43(12):677-683, 2014
Received May 22, 2014 and accepted October 1, 2014.
Corresponding author:
Copyright © 2014 Sociedade Brasileira de Zootecnia. This is an Open Access article
distributed under the terms of the Creative Commons Attribution Non-Commercial
License, which permits unrestricted non-commercial use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Dietary n-3 and n-6 long-chain polyunsaturated
fatty acids (PUFA)
Dietary fats are required to support absorption of
fat-soluble vitamins and provide the essential fatty acids
(NRC, 2007), linoleic acid (LA) and alpha-linolenic acid
(ALA). The long-chain fatty acid family of omega-6
(n-6) and omega-3 polyunsaturated fatty acids (PUFA) are
essential components of the diet and are necessary in daily
physiological functions as well as for fetal development and
neonatal growth. The ‘parent’ fatty acids are linoleic acid
(LA) for the n-6 family and alpha-linolenic acid (ALA) for
the n-3 family. These ‘parent’ fatty acids are considered
essential in mammalian diets; the lack of proper enzymes
prevents their endogenous synthesis. The derivatives of these
‘parents’ are likely of even greater importance; LA can be
elongated and converted to arachidonic acid (ARA), whose
primary role is to produce 20 carbon-signaling molecules
known as eicosanoids. Eicosanoids have short half-lives
and are localized close to their production site, influencing
events within and around the cells that produce them.
Arachidonic acid and other eicosanoid- producing fatty
acids must be present in tissue in order for these signaling
molecules to be effective. Eicosanoids are important in that
they regulate a variety of cellular functions, during both
physiological (normal) and inflammatory events. The most
well-known classes of eicosanoids are prostaglandins (PG),
thromboxanes (TX), leukotrienes (LT) and lipoxins (LX);
with PG and TX being synthesized via the cyclooxygenase
(COX) pathway and LT and LX being converted from
ARA by lipoxgenases (Figure 1). While all classes are vital
physiological components, prostaglandins are important
as they are utilized by all major organ systems including
reproductive, gastrointestinal and neurological. Of these
active eicosanoids, prostaglandin E2 is the primary PG,
synthesized exclusively from ARA, playing an important
role in the inflammatory response. In terms of joint
health and the development of osteoarthritis, PGE2 has
been implicated as therapeutic target as it is elevated
in early stages of the disease and contributes to down-
stream production of degradative cartilage enzymes
(McIlwraith, 2005).
Long-chain derivatives of ALA, specifically
eicosapentaenoic acid (EPA), n-3 docosapentanoic acid
(DPA) and docosahexaenoic acid (DHA) (Figure 2), have
as equally important roles as ARA in cellular function and
physiologic homeostasis. While all ALA derivatives can be
converted to produce eicosanoids, EPA is the most widely
recognized n-3 PUFA that is a source for anti-inflammatory
678 Hess and Ross-Jones
R. Bras. Zootec., 43(12):677-683, 2014
PG, TX, LT and LX (Figure 1). However, research results
indicate that n-3 DPA and DHA also play vital roles in
mediating the inflammatory response in conjunction with
EPA (Kaur et al., 2011). Increased intake of EPA and DHA
in a dose-dependent manner has been shown to decrease
ARA amounts in cell membrane phospholipids involved in
inflammation (Calder, 2014). Furthermore, increased EPA
intake has been shown to inhibit ARA metabolism (Calder,
2014) and decrease the expression of the pro-inflammatory
gene COX-2 (Calder, 2014). One of the premier sources of
EPA and DHA is marine fish oil, also known as menhaden
oil. Eicosapentaenoic acid, though found in the largest
quantities in marine fish oil, originates from ALA (Figure 2),
which is encountered in high concentrations in plant fats.
Plant oils such as linseed, soybean and flaxseed oils are
all sources of ALA, therefore, when consumed, the animal
may be able to synthesize EPA, DPA and DHA from these
plant oils (Figure 2). Alpha-linolenic acid is converted
to EPA, DPA and DHA via a desaturation and elongation
pathway (Figure 2). The initial step, the addition of a
double bond to ALA by the ∆6-desaturase enzyme, is the
rate-limiting step in the pathway and contributes to the
reported low conversion efficiency of ALA to the longer-
chain PUFA (Calder, 2013). Both LA and ALA share a need
for ∆6-desaturase (Figure 2), and while the enzyme has a
higher affinity for ALA, in humans dietary fats contain a
higher percentage of LA, therefore competing for the same
enzyme ALA needs for conversion to its longer derivate
(Tu et al., 2010). In addition, ALA has been shown to have
the highest oxidation rate among all unsaturated fatty acids
in human tracer studies (Nettleton, 1991), contributing to
the low conversion of ALA to its longer derivate. A review
of studies investigating the efficiency of dietary ALA
conversion in humans reported the conversion of ALA to
EPA ranged from 8-10% with conversion efficiency being
as low at 4% for DHA (Williams and Burdge, 2006). Due to
evidence of a low conversion rate, it is recommended to supply
EPA and DHA directly in the diet (Arterburn et al., 2006).
A source of ALA in the equine diet is forage (hay or
pasture), which is the largest portion of equine diets. Many
horses are fed forage alone; however, performance horses
require additional energy-dense feeds such as grains or
oils due to their higher energy demands. Vegetable oils
are also a source of ALA, such as flaxseed and linseed
oil, which can be top-dressed onto feed. Linoleic acid is
very abundant in cereal grains such as corn and barley, and
makes up the majority of the fat in corn oil as well. Algae
produce the n-3 PUFA, EPA and DHA; therefore they are
present in fish because algae is an ordinary diet of fish. For
that reason, marine foods and fish oil are a good source of
EPA and DHA and may be consumed by humans and other
carnivores or omnivores. Additionally, they have been used
as supplements in equine diets. Horse studies indicated that
supplementation with ALA would not lead to increases in
circulating DHA (Hansen et al., 2002; Vineyard et al., 2010),
only increases in circulating EPA.
Inflammation and PUFA
Cellular activities involved in inflammatory responses
are designed to be harmful to pathogens; however, they
can cause damage to the host tissues (Calder, 2014).
Inflammation usually is self-limiting, and resolves rapidly
due to the activation of negative feed-back mechanisms like
secretion of anti-inflammatory cytokines or pro-resolving
lipid mediators, shedding of receptors for inflammation,
and activation of regulatory cells (Calder, 2014). Loss of
this regulatory process can result in excessive, inappropriate
or chronic inflammation that can cause damage to the
host organism (Calder, 2014). As part of these anti-
inflammatory and pro-resolving mediators, a novel class
Figure 1 - Eicosanoid formation from arachidonic acid (ARA) and
eicosapentaenoic acid (EPA).
ALA - α-linolenic acid; ARA - arachidonic acid; DGLA - dihomo-γ-linolenic acid;
DHA - docosahexaenoic acid; DPA - docosapentaenoic acid; EPA - eicosapentaenoic
acid; GLA - γ-linolenic acid; LA - linoleic acid.
Figure 2 - Biochemical pathway for the incorporation of n-3 and
n-6 fatty acids.
Source: Reprinted from Arterburn et al. (2006), with permission.
Omega-3 fatty acid supplementation in horses
R. Bras. Zootec., 43(12):677-683, 2014
of n-3 PUFA-derived anti-inflammatory mediators have
been recognized, termed E-series and D-series resolvins,
formed from EPA and DHA, respectively (Calder, 2009).
Protectins are another class of mediators produced from
DHA (Calder, 2014). While information is limited, it
appears n-3 PUFA-derived resolvins and protectins are
heavily involved in the resolution of inflammation (Kohli
and Levy, 2009). Protectins D1 are produced from DHA, and
known as protectins D1, owing to their protecting activity
in inflammatory and neural systems. Biological effects of
resolvins and protectins have been studied in cell culture
and animal models of inflammation and have been shown to
stimulate resolution and reduce magnitude of inflammatory
response in vivo (Serhan et al., 2008). Resolvin E1 reduces
inflammation in vivo and blocks human transendothelial
migration (Serhan et al., 2004). Resolvin E2 reduces
zymosan initiated neutrophil infiltration (Tjonahem et al.,
2006). Resolvin D1 has been shown to be a potent regulator
of mouse and human neutrophils (Serhan et al., 2004;
Sun et al., 2007). Resolvin E1 also has been shown to
initiate resolution of inflammation causing a decrease
in the number of neutrophils in exsudates sooner than
during spontaneous resolution. Resolvin E1 and resolvin
D1 prevented the infiltration of neutrophils into sites of
inflammation, and inhibited IL-1β production (Calder,
2014). Protectin D1 also blocked T cell migration in vivo,
reducing TNF-α (tumor necrosis factor alpha), IL-1β,
interferon-γ (IF-γ) secretion, and promoting T cell apoptosis
(Ariel et al., 2006). Protectin D1 shifted the onset of
resolution to an earlier time point in addition to shortening
the time to reduce the number of maximum neutrophils by
half (Serhan et al., 2008).
Other anti-inflammatory effects of n-3 PUFA from plant
and animal sources include a reduced cytokine production
in vitro (De Caterina et al., 1994) and in vivo (Meydani
et al., 1993; Grimm et al., 1994; McCann et al., 2000).
Sources of fatty acids in the diet
In humans, supplementation with long-chain n-3 PUFA
has been shown to improve inflammatory status, prevent
cardiovascular diseases (Calder, 2001), and reduce pain
and inflammation in patients with rheumatoid arthritis
(MacLean et al., 2004). In arthritic horses, supplementation
with EPA and DHA increased stride length (Woodward et al.,
2005) and reduced inflammatory markers (Manhart et al.,
2009). In horses, feeding Menhaden fish oil modulated
leucotriene synthesis influencing inflammatory conditions
(Hall et al., 2004).
Proposed mechanisms of EPA and DHA on
Several mechanisms have been proposed regarding the
processes by which EPA and DHA act on the inflammatory
response in tissues. It is well established that these lipids act
on both a direct (by alteration of eicosanoid production via
cyclooxygenase and lipoxygenase pathways) and indirect
(modification of gene transcription) mechanism (Calder,
2006). Direct modification of prostaglandin and leukotriene
synthesis was outlined previously. Supplementation of n-3
PUFA in feeds will also exert an effect on the expression of
inflammatory genes (Renier et al., 1993; Curtis et al., 2000;
Wallace et al., 2001).
It is hypothesized that particular fatty acids, such as
EPA and/or DHA, may modify transcription factors in
the nucleus and thus influence cytokine and eicosanoid
production at the level of gene expression (Figure 3).
Another theory is that n-6 (i.e., ARA) and n-3 (i.e., EPA and
DHA) fatty acids modify protein synthesis of inflammatory
mediators via modification of cell surface receptors on lipid
rafts or within the cell by suppression of nuclear receptor
activation (Chapkin et al., 2009). Additional regulation
comes in the form of peroxisome proliferator-activated
receptors, which are key nuclear receptors that regulate
transcription of genes through ligand binding with a variety
Figure 3 - Summary of the anti-inflammatory actions of n-3
polyunsaturated fatty acids; modified from Calder (2013).
EPA - eicosapentaenoic acid; DHA - docosahexaenoic acid; ARA - arachidonic
acid; COX - cyclooxigenase; NFkB - nuclear factor kappa B; PPAR - peroxisome
proliferator activated receptor.
Solid red lines indicate inhibition.
Solid blue lines indicate sources of n-3 PUFA.
Solid green lines indicate inflammatory activation.
680 Hess and Ross-Jones
R. Bras. Zootec., 43(12):677-683, 2014
of lipophilic metabolites, having a high affinity for PUFA,
in particular DHA (Stulnig, 2003). Peroxisome proliferator-
activated receptors usually have three isoforms; α, β, γ and
are believed to be potent regulators of adipocyte function
as well as immune molecules such as lymphocytes and
macrophages (Marx et al., 2002) influencing downstream
transcription of inflammatory cytokines (Figure 3).
Insulin sensitivity and n-3 PUFA
Insulin resistance (decreased insulin sensitivity) in
horses has been linked to the development of laminitis,
osteochondrosis, and metabolic syndrome (Coffman and
Coles, 1983; Ralston, 1996; Treiber et al., 2006; Frank et al.,
2010) and is therefore considered a problem in the equine
industry. These diseases can result in a loss of function and
performance of the horse. Several factors may predispose
a horse to developing insulin resistance, such as diet, age,
breed/genetics and obesity (Jeffcot et al., 1986; Treiber et al.,
2006; Vick et al., 2007). Supplementation with certain
dietary components could increase insulin sensitivity in
animals that have insulin resistance, reducing the risk for
the development of diseases such as metabolic syndrome
and laminitis.
Dietary supplementation with n-3 PUFA has been shown
to increase insulin sensitivity in pigs and rats (Behme,
1996; Luo et al., 1996). Dietary EPA and DHA incorporate
into cell membranes increasing membrane fluidity due to
greater unsaturation of the membrane improving glucose
transport function (Lardinois et al., 1987; Zhao et al., 2008).
Incorporation of EPA and DHA in muscle cell membrane
has been shown to increase binding of insulin (Storlein et al.,
1991) and m-RNA expression of GLUT-4 transporters in
rats (Figueiras et al., 2010). Supplementation with EPA
and DHA has shown to improve insulin sensitivity in rats
(Storlein et al., 1991), pigs (Behme, 1996), and in humans
(Rasic-Milutinovic et al., 2007).
n-3 PUFA supplementation and exercise
Supplementation with EPA and DHA in horses has
also been shown to lower heart rate, plasma glycerol, free
fatty acids and cholesterol during an exercise test compared
to horses supplemented with corn oil (O’Connor et al.,
2004). In human trained athletes supplemented with fish
oil, heart rate and oxygen consumption was lower than
in subjects supplemented with olive oil (Peoples et al.,
2008). Incorporation of n-3 PUFA to muscle membranes
increased insulin sensitivity (Pan et al., 1995) and resulted
in increased ability of skeletal muscle to take up glucose.
Furthermore, studies have shown that lower proportions of
long-chain PUFA and higher proportions of saturated fatty
acids in skeletal muscle phospholipids are associated with
insulin resistance. Skeletal muscle characteristics (i.e., fatty
acid profile) have some genetic influence (Baur et al., 1999)
but diet and physical activity also influence skeletal muscle
fatty acid profile in rats, humans, and horses (Ayre et al.,
1996; Andersson et al., 2000; Hess et al., 2012).
Specific horse studies
Effects of two different dietary sources of n-3 PUFA on
incorporation into the plasma, red blood cell, and skeletal
muscle in horses (Hess et al., 2012)
In humans, the PUFA DHA and EPA need to be
supplemented in order for them to be incorporated into
tissues. There is limited conversion of ALA to DHA in
humans (Burdge et al., 2001; Arterburn et al., 2006). As
stated before, in horses, supplementation with ALA did not
lead to increases in circulating DHA (Hansen et al., 2002;
Vineyard et al., 2010), only EPA. Feeding of n-3 PUFA
to horses may increase circulating levels and increase
incorporation into muscle tissue. This could potentially
improve chronic inflammatoryconditions in horses; however,
the optimal type of fatty acid to be supplemented needed to
be investigated.
In a related study in our laboratory (Hess et al., 2012)
in order to compare different sources of dietary omega-3
fatty acid supplementations on plasma, red blood cell and
skeletal muscle fatty acid compositions in horses, three
(alfalfa/bromegrass) hay and barley diets were fed: one
was supplemented with an algae and fish oil containing
DHA and EPA (MARINE; Magnitude; JBS United,
Sheridan, IN); another group was supplemented with the
same amount of ALA in flaxseed (FLAX) as FLAX, and a
third group (control; CON) was fed hay and barley to make
all diets have the same calorie amount. Treatments were
supplemented for 90 d. Blood samples and muscle middle
gluteal biopsies were collected on d 0, 30, 60, and 90 of
Direct supplementation of EPA and DHA through a
marine source increased PUFA concentrations in the plasma,
red blood cell and muscle tissue of equines (Hess et al.,
2012). Although present in muscle tissue at baseline, EPA
and DHA increased in horses supplemented with a marine
source containing these specific fatty acids. In plasma and
red blood cells, EPA and DHA were below detection levels
in all groups and increased only in MARINE-supplemented
horses. Supplementation with dietary sources containing
Omega-3 fatty acid supplementation in horses
R. Bras. Zootec., 43(12):677-683, 2014
EPA and DHA may be indicated when increased
incorporation of these n-3 fatty acids to muscle and red
blood cells is desired. Conversion of ALA from flaxseed
and forages to EPA and DHA occurs in the skeletal
muscle, as seen in this study (Hess et al., 2012) by
the detection of these fatty acids in equine muscles at
baseline. Supplementation with ALA through flaxseed
lead to higher incorporation of muscle n-3 DPA, a derivate
of EPA, compared to MARINE supplementation. Some
positive effects of n-3 DPA on inflammation have been
reported; however, the effects of such increases should
be evaluated in further studies addressing inflammatory
responses and compared to EPA and DHA in horses
(Hess et al., 2012). In this study, conversion of ALA to
EPA and DHA did not occur after supplementation with
extra ALA (above the control dietary n-3 PUFA level) from
Effects of n-3 PUFA supplementation on insulin sensitivity
in horses (Hess et al., 2013)
Dietary supplementation with n-3 PUFA has been
shown to increase insulin sensitivity as described above.
In order to test the hypothesis that supplementation with
n-3 PUFA would improve insulin sensitivity, the same
diets described for the previous study were fed to a group
of 21 adult mares to test glucose and insulin dynamics.
Specific tests to determine insulin sensitivity (frequent
sampling intravenous glucose tolerance tests) were
performed on days 0, 30, 60, and 90 of supplementation
(Hess at al., 2013).
No overall treatment effect was observed when
all mares within each treatment were compared among
themselves. However, when treatments were compared
among mares with the lowest quintile in insulin sensitivity
(Treiber et al., 2005) (11 mares) there was a trend (P = 0.08)
for a treatment effect, where MARINE (n = 5 and
FLAX (n = 3) horses had higher insulin sensitivity (SI =
1.18±0.16 in FLAX, and 1.05± 0.16 in MARINE compared
to 0.59±0.16 in CON, n = 3). Although a small number
of insulin resistant mares were compared, further studies
should be performed in a larger group of insulin resistant
horses. If proven effective, supplementation with omega-3
fatty acids could help to reduce problems associated with
insulin resistance in horses (Hess et al., 2013).
Evaluation of synovial fluid in horses fed two different sources
n-3 PUFA: a pilot study (Ross-Jones et al., 2014)
Elevating n-3 PUFA in mammalian diets may
downregulate inflammatory processes in the joint
(Proudman et al., 2008) and has been shown to have
symptom-modifying effects in inflammatory diseases
(Lau et al., 1993). One hypothesized mechanism is the
potential of long-chain n-3 PUFA to reduce the production
of potent inflammatory eicosanoids (Chapkin et al., 2009),
primarily PGE2. In order to test the effects of different
sources of n-3 PUFA on synovial fluid composition, the
diets described on the first study (Hess et al., 2012) were
supplemented for 90 days (Ross-Jones et al., 2014).
On day 90 of supplementation, approximately 3 mL
of synovial fluid were extracted from the right carpus of
each horse. Fluid was analyzed for fatty acid concentration
and PGE2 concentration. Synovial fluid samples from
the MARINE group exhibited EPA and DHA, whereas
the FLAX and CON groups did not express detectable
concentrations. Synovial prostaglandin E2 concentration in
the MARINE group tended to be lower compared to CON
horses (P<0.10).
Synovial fluid fatty acid levels for EPA and DHA
were significantly higher in the MARINE group
compared to either CON or FLAX groups, indicating
that direct supplementation of EPA and DHA is required
if higher fluid concentrations of those fatty acids are
desired (Ross-Jones et al., 2014). A small difference between
treatment and control in synovial fluid PGE2 concentration
in the current study may be due to all horses being healthy
and free of existing joint inflammation or disease. Inducing
experimental inflammation in healthy animals receiving
a dietary n-3 PUFA supplement may cause measurable
differences in eicosanoid levels.
Results indicated a possible inhibition of inflammatory
eicosanoid prostaglandin E2 production in equine synovial
fluid by oral supplementation of the polyunsaturated
fatty acids EPA and DHA. Further research is needed
to determine if oral n-3 PUFA supplementation can be
therapeutically advantageous in horses experiencing joint
Based on results from several studies, supplementation
with n-3 polyunsaturated fatty acids has the potential to
benefit humans and horses in diverse ways. Future studies
should address the effects of n-3 polyunsaturated fatty
acid supplementation on inflammation and specifically
in horses with chronic inflammatory diseases such as
laminitis, metabolic syndrome, pituitary pars intermedia
disease and osteoarthritis improving the horses’ health
and wellbeing.
682 Hess and Ross-Jones
R. Bras. Zootec., 43(12):677-683, 2014
Andersson, A.; Sjodin, A.; Hedman, A.; Olsson, R. and Vessby, B.
2000. Fatty acid profile of skeletal muscle phospholipids in trained
and untrained young men. American Journal of Physiology:
Endocrinology and Metabolism 279:E744-E751.
Ariel, A.; Li, P. L.; Wang, W.; Tang, W. X.; Fredman, G.; Hong,
S.; Gotlinger, K. H. and Serhan, C. N. 2006. The docosatriene
protectin D1 is produced by TH2 skewing and promotes human T cell
apoptosis via lipid raft clustering. Journal of Biological Chemistry
Arterburn, L. M.; Hall, E. B. and Oken, H. 2006. Distrubution,
interconversion and dose response of n-3 fatty acids in hum ans .
American Journal of Clinical Nutrition 83:S1467-1476.
Ayre, K. J. and Hulbert, A. J. 1996. Dietary fatty acid profile influences
the composition of skeletal muscle phospholipids in rats. Journal
of Nutrition 126:653-662.
Baur, L. A.; O’Connor, J.; Pan, D. A. and Storlein, L. H. 1999.
Relationships between maternal risk of insulin resistance and
the child’s muscle membrane fatty acid composition. Diabetes
Behme, M. T. 1996. Dietary fish oil enhances insulin sensitivity in
miniature pigs. Journal of Nutrition 126:1549-1553.
Burdge, G. C.; Jones, A. E. and Wootton, S. A. 2002. Eicosapentaenoic
and docosapentaenoic acids are the principal products of α-linolenic
acid metabolism in young men. British Journal of Nutrition
Calder, P. C. 2001. Omega 3 polyunsaturated fatty acids, inflammation
and immunity. World Review on Nutrition and Dietetics 88:109-116.
Calder, P. C. 2006. n-3 polyunsaturated fatty acids, inflammation, and
inflammatory diseases. American Journal of Clinical Nutrition
Calder, P. C. 2009. Polyunsaturated fatty acids and inflammatory
processes: New twists in an old tale. Biochimie 91:791-795.
Calder, P. C. 2013. Omega-3 polyunsaturated fatty acids and
inflammatory processes: nutrition or pharmacology? British
Journal of Clinical Pharmacology 75:645-662. doi: 10.1111/j.1365-
Calder, P. C. 2014. Marine omega-3 fatty acids and inflammatory
processes: Effects, mechanisms and clinical relevance. Biochinica
et Byophysica Acta, doi: 10.1016/j.bbalip.2014.08.010 (in press).
Chapkin, R. S.; Kim W.; Lupton J. R. and McMurray, D. N. 2009.
Dietary docoahexaenoic and eicosapentaenoic acid: emerging
mediators of inflammation. Prostaglandins, Leukotrienes and
Essential Fatty Acids 81:187-191.
Coffman, J. R. and Colles, C. M. 1983. Insulin tolerance in laminitic
ponies. Canadian Journal of Comparative Medicine 47:347-351.
Curtis, C.; Hughes C. E.; Flannery C. R.; Little C. B.; Harnson B. and
Carterson, B. 2000. n-3 fatty acids specifically modulate catabolic
factors involved in articular cartilage degradation. Journal of
Biological Chemistry 275:721-724.
De Caterina, R.; Cybulsky M. I.; Clinton S. K.; Gimbrone, M. A.
and Libby, P. 1994. The omega-3 fatty acid docosahexaenoate
reduces cytokine-induced expression of proatherogenic
and proinflammatory proteins in human endothelial cells.
Artheriosclerosis and Thrombosis 14:1829-1836.
Figueiras, M.; Olivan, M.; Busquets, S.; Lopez-Soriano, F. J. and
Argiles, J. M. 2010. Effects of eicosapentaenoic acid (EPA)
treatment on insulin sensitivity in an animal model of diabetes:
improvement of the inflammatory status. Obesity 19:362-369.
Frank, N.; Geor, R. J.; Durham, A. E. and Johnson, P. J. 2010. Equine
metabolic syndrome. Journal of Veterinary Internal Medicine
Grimm, H.; Tibell, A.; Norrlind, B.; Blecher, C.; Wilker, S. and
Schwemmle, K. 1994. Immunoregulation by parenteral lipids:
impact of the n-3 to n-6 fatty acid ratio. Journal of Parenteral and
Enteral Nutrition 18:417-421.
Hall, J.; Van Saun, R. and Wander, R. C. 2004. Dietary (n-3) fatty
acids from Menhaden fish oil alter plasma fatty acid and leukotriene
B synthesis in healthy horses. Journal of Veterinary Internal
Medicine 18:871-879.
Hansen, R. A.; Savage, C. J.; Reidlinger, K.; Traub-Dargatz, J. L.;
Ogilvie, G. K.; Mitchell D. and Fettman, M. J. 2002. Effects of
dietary flaxseed oil supplementation on equine plasma fatty acid
concentrations and whole blood platelet aggregation. Journal of
Veterinary Internal Medicine 16:457-463.
Hess, T. M.; Rexford, J.; Hansen, D. K.; Ahrens, N. S.; Harris, M.;
Engle, T.; Ross, T. and Allen, K. G. 2013. Effects of omega-3 (n-3)
fatty acid supplementation on insulin sensitivity in horses. Journal
of Equine Veterinary Science 33:446-453.
Hess, T. M.; Rexford, J. K.; Hansen, D. K.; Harris, M.; Schauermann,
N.; Ross, T.; Engle, T. E.; Allen, K. G. D. and Mulligan, C. M.
2012. Effects of two different dietary sources of long chain
omega-3, highly unsaturated fatty acids on incorporation into the
plasma, red blood cell, and skeletal muscle in horses. Journal of
Animal Science 90:3023-3031.
Jeffcott, L. B.; Field, J. R.; McLean, J. G. and O’Dea, K. 1986. Glucose
tolerance and insulin sensitivity in ponies and standardbred horses.
Equine Veterinary Journal 18:97-101.
Kaur, G.; Cameron-Smith, D.; Garg, M. and Sinlcair, A. J. 2011.
Docosapentaenoic acid (22:5n-3): a review of it biological effects.
Progress in Lipid Research 50:28-34.
Kohli, P. and Levy, B. D. 2009. Resolvins and protectins: mediating
solutions to inflammation. British Journal of Pharmacology
Lardinois, C. K. 1987. The role of omega 3 fatty acids on insulin
secretion and insulin sensitivity. Medical Hypotheses 24:243-248.
Lau, C. S.; Morley, K. D. and Belch, J. J. 1993. Effects of fish
oil supplementation on non-steroidal anti-inflammatory drug
requirement in patients with mild rheumatoid arthritis-A double-
blind placebo controlled study. British Journal of Rheumatology
Luo, J.; Rizkalla, S. W.; Boillot, J.; Alamowitch, C.; Chaib, H.; Bruzzo,
F.; Desplanque, N.; Dalix, A. M.; Durand, G. and Slama, G. 1996.
Dietary (n-3) polyunsaturated fatty acids improve adipocyte insulin
action and glucose metabolism in insulin-resistant rats: Relation to
membrane fatty acids. Journal of Nutrition 126:1951-1958.
MacLean, C. H.; Mojica, W. A.; Morton, S. C.; Pencharz, J.;
Hasenfeld, R.; Garland, T. W.; Newberry, S. J.; Jungvig, L. K.;
Grossman, J.; Khanna, P.; Rhodes, S. and Shekelle, P. 2004.
Effects of omega-3 fatty acids on lipids and glycemic control in
type II diabetes and the metabolic syndrome and on inflammatory
bowel disease, rheumatoid arthritis, renal disease, systemic lupus
erythematosus, and osteoporosis. Evidence Report/Technology
Assessment No. 89 (Prepared by Southern California/RAND
Evidence-based Practice Center, under Contract No. 290-02-0003).
AHRQ Publication No. 04-E012-2. Agency for Healthcare Research
and Quality, Rockville, MD.
Manhart, D. R.; Scott, B. D.; Gibbs, P. G.; Honnas, C. M.;
Hoo d, D. M. and Coverdale, J. A. 2009. Markers of inflammation
in arthritic horses fed omega-3 fatty acids. Professional Animal
Scientist 25:155-160.
Marx, N.; Kehrle, B.; Kohlhammer, K.; Grub, M.; Koenig, W.;
Homback, V.; Libby, P. and Plutzky, J. 2002. PPAR activators as
anti-inflammatory mediators in human T lymphocytes: Implications
for atherosclerosis and transplantation-associated arterosclerosis.
Circulation Research 90:703-710.
Omega-3 fatty acid supplementation in horses
R. Bras. Zootec., 43(12):677-683, 2014
McIlwraith, C. W. 2005. Frank Milne Lecture: From arthroscopy to
gene therapy-30 years of looking in joints. Proceedings of the
American Association of Equine Practitioners 51:65-113.
McCann, M.; Moore, J. N.; Carrik, J. B. and Barton, M. H. 2000. Effect
of intravenous infusion of omega-3 and omega-6 lipid emulsions
on equine monocyte fatty acid composition and inflammatory
mediator production in vitro. Shock 14:222-228.
Meydani, S.; Lichtenstein, A. H.; Cornwall, S.; Meydani, M.; Goldin,
B. R.; Rasmussen, H.; Dinarello, C. A. and Schaefer, E. J. 1993.
Immunologic effects of national cholesterol education panel step-2
diets with and without fish-derived N-3 fatty acid enrichment.
Journal of Clinical Investigation 92:105-113.
National Research Council - NRC. 2007. Nutrient requirements of
horses. 6th rev ed. National Academic Press, Washington, DC.
Nettleton, J. A. 1991. Omega-3 fatty acids: comparison of plant and
seafood sources in human nutrition. Journal of the American Dietetic
Association 91:331-337.
O’Connor, C. I.; Lawrence, L. M.; St Lawrence, A. C.; Janicki, K. M.;
Warren, L. K. and Hayes, S. 2004. The effect of dietary fish oil
supplementation on exercising horses. Journal of Animal Science
Pan, D. A.; Lillioja, S.; Milner, M. R.; Kritetos, A. D.; Baur, L. A.;
Borgadus, C. and Storlein, L. H. 1995. Skeletal muscle membrane
lipid composition is related to adiposity and insulin action. Journal
of Clinical Investigation 96:2802-2808.
Peoples, G. E.; McLennan, L. P.; Howe, P. R. C. and Groeller, H.
2008. Fish oil reduces heart rate and oxygen consumption during
exercise. Journal of Cardiovascular Pharmacology 52:540-547.
Proudman, S. M.; Cleland, L. G. and James, M. J. 2008. Dietary
omega-3 fats for treatment of inflammatory joint disease: efficacy
and utility. Rheumatic Disease Clinic of North America 34:469-479.
Ralston, S. L. 1996. Hyperglycemia/hyperinsulinemia after feeding
a meal of grain to young horses with osteochondritis dissecans
(OCD) lesions. Pferdeheilkunde 12:320-322.
Rasic-Milutinovic, Z.; Perunicic, G.; Pljesa, S.; Gluvic, Z.; Sobajic, S.;
Djuric, I. and Ristic, D. 2007. Effects of n-3 PUFA supplementation
on insulin resistance and inflammatorybiomarkers in hemodialysis
patients. Renal Failure 29:321-329.
Renier, G.; Skamene, E.; de Sanctis, J. and Radzioch, D. 1993.
Dietary n-3 polyunsaturated fatty acids prevent the development
of artherosclerotic lesions in mice: modulation of macrophage
secretory activities. Journal of Artherosclerosis and Thrombosis
Ross-Jones, T.; Hess, T. M.; Rexford, J.; Ahrens, N.; Engle, T. and
Hansen, K. 2014. Effects of omega-3 long chain polyunsaturated
fatty acid supplementation on equine synovial fluid fatty acid
composition and prostaglandin E2. Journal of Equine Veterinary
Science 34:779-783.
Serhan, C.; Gotlinger, K.; Hong S. and Arita, M. 2004. Resolvins,
docosatrienes, and neuroprotectins, novel omega-3-derived
mediators, and their aspirin-triggered endogenous epimers: an
overview of their protective roles in catabasis. Prostaglandins and
other Lipid Mediators 73:155-172.
Serhan, C.; Chiang, N. and Van Dyke, T. 2008. Resolving inflammation:
dual anti-inflammatory and pro-resolution lipid mediators. Nature
Reviews Immunology 8:349-361.
Storlien, L. H.; Jenkins, A. B.; Chisholm, D. J.; Pascoe, W. S.; Khouri,
S. and Kraegen, E. W. 1991. Influence of dietary fat composition on
development of insulin resistance in rats. Relationship to muscle
triglyceride and omega-3 fatty acids in muscle phospholipid.
Diabetes 40:280-289.
Stulnig, T. M. 2003. Immunomodulation by polyunsaturated fatty
acids: Mechanisms and effects. International Archives of Allergy
and Immunology 132:310-321.
Sun, Y.; Oh, S.; Uddin, J.; Yang, R.; Gotlinger, K.; Campbell, E.;
Colgan, S. P.; Petasis, N. A. and Serhan, C. N. 2007. Resolvin D1
and its aspirin-triggered 17R Epimer stereochemical assignments,
anti-inflammatory properties, and enzymatic inactivation. Journal
of Biological Chemistry 282:9323-9334.
Tjonahen, E.; Oh, S. F.; Siegelman, J.; Elangovan, S.; Percapio, K.
B.; Hong, S.; Arita, M. and Serhan, C. N. 2006. Resolvin E2:
identification and anti-inflammatory actions: pivotal role of human
5-lipoxygenase in resolvin E series biosynthesis. Chemistry and
Biology 13:1121-1122.
Treiber, K. H.; Kronfeld, D. S.; Hess, T. M.; Boston, R. C. and Harris,
P. A. 2005. Insulin sensitivity and pancreatic β-cell response in
the horse: screening proxies and reference quintiles assessed by
the minimal model. American Journal of Veterinary Research
Treiber, K. H.; Kronfeld, D. S.; Hess, T. M.; Byrd, B. M.; Splan, R.
K. and Staniar, W. B. 2006. Evaluation of genetic and metabolic
predispositions and nutritional risk factors for pasture-associated
laminitis in ponies. Journal of American Veterinary Medical
Association 228:1538-1545.
Tu, W. C.; Cook-Johnson, R. J.; James, M. J.; Muhlausler, B. S. and
Gibson, R. A. 2010. Omega-3 long chain fatty acid synthesis
is regulated more by substrate levels than gene expression.
Prostaglandins, Leukotrienes and Essential Fatty Acids 83:61-68.
Vick, M. M.; Adams, A. A.; Murphy, B. A.; Sessions, D. R.; Horohov,
D. W.; Cook, R. F.; Shelton, B. J. and Fitzgerald, B. P. 2007.
Relationships among inflammatory cytokines, obesity, and insulin
sensitivity in the horse. Journal of Animal Science 85:1144-1155.
Vineyard, K. R.; Warren, L. K. and Kivipelto, J. 2010. Effect of
dietary omega-3 fatty acid source on plasma and red blood cell
membrane composition and immune function in yearling horses.
Journal of Animal Science 88:248-257.
Wallace, F.; Miles, E. A.; Evans, C.; Stock, T. E.; Yaqoob, P. and
Calder, P. C. 2001. Dietary fatty acids influence the production of
Th1-but not TH-2 type cytokines. Journal of Leukocyte Biology
Williams, C. M. and Burdge, G. 2006. Long chain n-3 PUFA: plant v.
marine sources. Proceedings of the Nutrition Society 65:42-50.
Woodward, A. D.; Nielsen, B. D.; O’Conner, C. I.; Webel, S. K. and Orth,
M. W. 2005. Supplementation of dietary long-chain polyunsaturated
fatty acids high in docosahexaenoic acid (DHA) increases plasma
DHA concentrations and may increase trot stride lengths in horses.
Equine and Comparative Exercise Physiology 4:71-78.
Zhao, S. M.; Jia, L.W.; Gao, P.; Li, Q. R.; Lu, X.; Li, J. S. and Xu,
G. W. 2008. Study on the effect of eicosapentaenoic acid on
phospholipids composition in membrane microdomains of tight
junctions of epithelial cells by liquid chromatography/electrospray
mass spectrometry. Journal of Pharmaceutical and Biomedical
Analysis 47:343-350.
... O óleo de peixe, por conter alto nível de ácidos graxos polinsaturados, pode tornar-se instável à deterioração oxidativa a uma velocidade variável, dependendo fortemente das condições de extração e das quantidades detectadas no perfil de ácidos graxos (Hess & Ross-Jones, 2014). Em geral, o óleo de peixe está ligado à matriz proteica. ...
Full-text available
A extração do óleo de subprodutos do processamento de tilápia tem sido uma forma bastante interessante de aproveitamento de resíduos sólidos, devido aos seus potenciais benefícios à saúde humana. Neste sentido, o objetivo deste estudo foi extrair e refinar o óleo de tilápias nilóticas (Oreochromis niloticus) obtido dos resíduos (cabeças) empregando três temperaturas diferentes (40ºC, 50ºC e 60ºC). Os óleos (bruto e refinado) foram caracterizados quimicamente, por meio dos índices de peróxido, saponificação, acidez e iodo, e perfil de ácidos graxos, bem como foi calculado o rendimento de cada tratamento. Os resultados mostraram que as temperaturas avaliadas pouco influenciaram na qualidade de óleo e que os maiores índices de significância foram encontrados quando comparados os óleos bruto e refinado. No entanto, o emprego de diferentes temperaturas para a extração do óleo de cabeças de tilápias nilóticas pode ser considerado efetivo, em que a temperatura de 60ºC propiciou um óleo de melhor qualidade, principalmente pelo índice de acidez apresentado e pelas quantidades de ácidos graxos.
... Fat (e.g., obtained as a by-product of the rendering industry) and vegetable oil, a subgroup of lipids, production has increased as these substances are directly supplemented into livestock and poultry feed and pet foods (Kerr et al., 2015). Fatty acid addition has demonstrated beneficial effects in several species such as horses (Hess and Ross-Jones, 2014), pigs (Rostagno et al., 2017;Liu et al., 2018), dairy cows (NRC, 2001;Harvatine and Allen, 2006), poultry (Poorghasemi et al., 2013;Rostagno et al., 2017) and, especially, management of several diseases and clinical problems in pets (Lenox and Bauer, 2013;Wąsik et al., 2016). Of particular interest are, for example, linoleic (9c12c-C 18:2 ), eicosapentaenoic acid (5c8c11c14c17c-C 20:5 ), and docosahexaenoic acid (4c7c10c13c16c19c-C 22:6 ), (C 20:5 ) in puppy and dog food (Ahlstrøm et al., 2004); relevant for cardiovascular health and nervous system development (Biagi et al., 2004;Fraeye et al., 2012). ...
Full-text available
Fatty acid determination is used for the characterization of the lipid fraction in foods, providing essential information regarding feed and food quality. Most edible fats and oils are composed primarily of linear saturated fatty acids, branched, mono-unsaturated, di-unsaturated, and higher unsaturated fatty acids. To attain this information we developed a gas chromatography (GC) method that can separate fatty acids from C4 to C24 using mass spectrometry identification. A simplified sample preparation procedure was applied so it is not time-consuming and short enough to avoid fat degradation. Additionally, one-step derivatization was applied to obtained fatty acid methyl esters in situ in the gas chromatograph injection port, using tetramethylammonium hydroxide and a high polarity polyethylene glycol-based cross-linked microbore chromatographic column was coupled to achieve the separation of 60 compounds in under 15 minutes with extreme sensibility. The versatility of the method allows fatty acid profile (including saturated [SFA], monounsaturated [MUFA], and polyunsaturated fatty acids [PUFA]) information to be gathered in different products of primary production i. raw materials commonly used in the production of animal feed, ii. profiles for balanced feed for laying hens, beef cattle and dairy cattle and iii. products of animal origin intended for human consumption, such as meat, eggs, and milk. Our data (performance parameters and fatty acid profiles) support the validity of the results; the method can be used for quality assurance both in productive species feed and feed ingredients, pet food, and related food matrices. The technique presented herein can be used as a high-throughput routine screening tool to assess fat quality as this data is paramount to improve animal nutrition and health and animal-derived products of human consumption.
Full-text available
IntroductionHorses with asthma or osteoarthritis frequently receive ω-3 fatty acid supplements. Docosahexaenoic (DHA; 22:6) and eicosapentaenoic (EPA; 20:5) acids are essential ω-3 fatty acid precursors of anti-inflammatory mediators and components of structural glycerophospholipids (GPL) that act as reservoirs of these fatty acids. Analysis of the incorporation of dietary DHA + EPA into GPL pools in different body compartments has not been undertaken in horses.Objectives We undertook a detailed study of dietary supplementation with DHA + EPA in horses and monitored incorporation into DHA- and EPA-containing glycerophosphocholines (GPC) 38:5, 38:6, 40:5, and 40:6 in plasma, synovial fluid (SF), and surfactant.Methods Horses (n = 20) were randomly assigned to the supplement or control group and evaluated on days 0, 30, 60, and 90. GPC in plasma, SF, and surfactant were measured by high-resolution mass spectrometry with less than 3 ppm mass error. Validation of DHA and EPA incorporation into these GPC was conducted utilizing MS2 of the [M + Cl]− adducts of GPC.ResultsDietary supplementation resulted in augmented levels of GPC 38:5, 38:6, 40:5, and 40:6 in all compartments. Maximum incorporation into GPCs was delayed until 60 days. Significant increases in the levels of GPC 38:5, 40:5, and 40:6, containing docosapentaenoic acid (DPA; 22:5), also was noted.ConclusionsDHA and EPA supplementation results in augmented storage pools of ω-3 essential fatty acids in SF and surfactant GPC. This has the potential to improve the ability of anti-inflammatory mechanisms to resolve inflammatory pathways in these critical compartments involved in arthritis and asthma.
Full-text available
Twelve adult Slovak warmblood sport horses were used to study the effect of dried grape pomace (DGP) on health through blood serum biochemical indicators, and on apparent total tract digestibility of dry matter (DM), organic matter (OM), crude protein (CP), acid detergent fibre (ADF) and neutral detergent fibre (NDF). The digestibility analysis was carried out by two in vivo methods, total faeces collection (TFC) and using lignin as a marker (ADL). Animals were divided into 3 groups: control group (C, without supplementation), experimental group 1 (E1, feed rations + 200 g of DGP) and experimental group 2 (E2, feed rations + 400 g of DGP). In animals, no health problems were detected during the trial. Of the blood serum indicators, only the concentrations of potassium (increase in E2 group compared to C group) and alanine aminotransferase (decrease in E2 group in comparison with E1 and C group) were affected (P < 0.05). The ADL method resulted in underestimated digestibility coefficients due to low recovery rates of lignin (less than 90%) in C group and E1 group. According to TFC, in E1 group higher digestibility coefficients were detected for DM, OM and CP (P > 0.05) compared to C group. However, in E2 group lower digestibility of all the studied nutrients was found (P > 0.05) in comparison with C group and E1 group. These results suggest that DGP could be used in horse diets up to 200 g without negative effect on their health and for a possible digestibility improvement of some nutrients.
Exercise stimulates the release of inflammatory cytokines and supplementation with n-3 fatty acids reduces inflammation. The effects of different doses of docosahexaenoic acid (DHA) on inflammation in polo horses submitted to field lactate threshold tests (LT) were analyzed. We hypothesized that higher doses of DHA would reduce postexercise inflammation. Twenty polo horses were assigned to different treatments: control group fed (n = 5) grain and hay, 3 treatment groups (n = 5) fed 10, 20, or 50 g/day of DHA with grain and free choice hay during 60 days. Horses underwent LT tests before start, 30, and 60 days of supplementation. Blood samples were taken at rest for blood cytokine expression (CEx), plasma cytokine enzyme-linked immunosorbent assay (CEL), fatty acid, vitamin E, and creatine kinase (CK) analysis, after LT for CEx analysis (interferon gamma, tumor necrosis factor alpha [TNF-α], interleukin-1 [IL-1], interleukin-6 [IL-6], interleukin-10 [IL-10]), CEL, and CK analysis. Effects of treatment, time, and exercise were analyzed by analysis of variance, significant results compared by least square means analysis, and significance set at P <.05. There was a dose-dependent increase in plasma DHA, and highest arachidonic acid was found in 20 and 50 g. Vitamin E was lowest in 20 and 50 g. LT did not change IL-6, downregulated IL-1 and TNF-α upregulated IL-10, and interferon gamma. The 10 g led to postexercise downregulation of interferon gamma and IL-10 CEx compared to other treatments. A lack of antioxidants in the supplements may have led to the absence of treatment effects in the 20 and 50 g. 10 g DHA helped moderate postexercise inflammation.
The fatty acid composition of inflammatory and immune cells is sensitive to change according to the fatty acid composition of the diet. In particular, the proportion of different types of polyunsaturated fatty acids (PUFA) in these cells is readily changed, and this provides a link between dietary PUFA intake, inflammation, and immunity. The n-6 PUFA arachidonic acid (AA) is the precursor of prostaglandins, leukotrienes, and related compounds, which have important roles in inflammation and in the regulation of immunity. Fish oil contains the n-3 PUFA eicosapentaenoic acid (EPA). Feeding fish oil results in partial replacement of AA in cell membranes by EPA. This leads to decreased production of AA-derived mediators. In addition, EPA is a substrate for cyclooxygenase and lipoxygenase and gives rise to mediators that often have different biological actions or potencies than those formed from AA. Animal studies have shown that dietary fish oil results in altered lymphocyte function and in suppressed production of proinflammatory cytokines by macrophages. Supplementation of the diet of healthy human volunteers with fish oil-derived n-3 PUFA results in decreased monocyte and neutrophil chemotaxis and decreased production of proinflammatory cytokines. Fish oil feeding has been shown to ameliorate the symptoms of some animal models of autoimmune disease. Clinical studies have reported that fish oil supplementation has beneficial effects in rheumatoid arthritis, inflammatory bowel disease, and among some asthmatics, supporting the idea that the n-3 PUFA in fish oil are anti-inflammatory and immunomodulatory.
Sixteen mature horses with arthritis in the knee, fetlock, hock, or stifle joints were blocked by severity of arthritis, affected joints, and age, and randomly divided into 2 groups. The control group (n = 8) received a commercial 12% CP feed at 1% BW per day. Treated horses (n = 8) received the same mixed feed with the addition of 2 n-3 fatty acid supplements to supply an additional 15 g/d of eicosapentaenoic acid and 19.8 g/d of docosahexaenoic acid. Both groups had access to coastal bermudagrass hay at approximately 1.3% of BW. Horses received respective dietary treatments for 90 d. Synovial fluid was collected from at least one affected joint of each horse on d 0, 30, 60, and 90. Blood samples were collected every 15 d beginning on d 0. Compared with control horses, treatment horses experienced a greater decrease (P< 0.05) in synovial fluid white blood cell concentration and plasma prostaglandin E2 A trend (P = 0.076) toward lower normalized plasma fibrinogen concentration was observed in treated horses compared with control horses throughout the entire trial. When data were analyzed from d 30 through 90, fibrinogen concentrations between groups were significantly different (P < 0.05). Force plate data from 7 horses were obtained to determine potential changes in weight distribution. No significant increase in weight placed on arthritic limbs (P = 0.12) was seen. These data provide further evidence that supplemental long-chain n-3 fatty acids in the equine diet could be advantageous for horses with existing arthritis.
To test the hypothesis that hyperinsulinemia/hyperglycemia may be correlated with OCD, plasma glucose and insulin responses to feeding high grain rations were evaluated in 15 young Standardbred horses. Four horses had osteochondritis dissecans (OCD), the other horses were normal (NL). Horses with OCD had higher (p<.01) postprandial glucose and insulin responses to feeding than did NL horses. Age differences in responses were also observed. Postprandial hyperglycemia and/or hyperinsulinemia may be correlated with the development of OCD lesions in young Standardbred horses.
Inflammation is a condition which contributes to a range of human diseases. It involves a multitude of cell types, chemical mediators, and interactions. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are omega-3 (n-3) fatty acids found in oily fish and fish oil supplements. These fatty acids are able to partly inhibit a number of aspects of inflammation including leukocyte chemotaxis, adhesion molecule expression and leukocyte-endothelial adhesive interactions, production of eicosanoids like prostaglandins and leukotrienes from the n-6 fatty acid arachidonic acid, production of inflammatory cytokines, and T-helper 1 lymphocyte reactivity. In addition, EPA gives rise to eicosanoids that often have lower biological potency than those produced from arachidonic acid and EPA and DHA give rise to anti-inflammatory and inflammation resolving mediators called resolvins, protectins and maresins. Mechanisms underlying the anti-inflammatory actions of marine n-3 fatty acids include altered cell membrane phospholipid fatty acid composition, disruption of lipid rafts, inhibition of activation of the pro-inflammatory transcription factor nuclear factor kappa B so reducing expression of inflammatory genes, activation of the anti-inflammatory transcription factor peroxisome proliferator activated receptor γ and binding to the G protein coupled receptor GPR120. These mechanisms are interlinked, although the full extent of this is not yet elucidated. Animal experiments demonstrate benefit from marine n-3 fatty acids in models of rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and asthma. Clinical trials of fish oil in RA demonstrate benefit, but clinical trials of fish oil in IBD and asthma are inconsistent with no overall clear evidence of efficacy. This article is part of a Special Issue entitled "Oxygenated metabolism of PUFA: analysis and biological relevance."
C57Bl6 mice were fed for 6 weeks on a low-fat diet or on high-fat diets containing coconut oil (rich in saturated fatty acids), safflower oil [rich in n-6 polyunsaturated fatty acids (PUFAs)], or fish oil (rich in n-3 PUFAs) as the main fat sources. The fatty acid composition of the spleen lymphocytes was influenced by that of the diet fed. Thymidine incorporation into concanavalin A-stimulated spleen lymphocytes and interleukin (IL)-2 production were highest after feeding the coconut oil diet. Interferon (IFN)-γ production was decreased by safflower oil or fish oil feeding. IL-4 production was not significantly affected by diet, although production was lowest by lymphocytes from fish oil-fed mice. The ratio of production of Th1- to Th2-type cytokines (determined as the IFN-γ/IL-4 ratio) was lower for lymphocytes from mice fed the safflower oil or fish oil diets. After 4 h of culture, IL-2 mRNA levels were higher in cells from mice fed coconut oil, and IFN-γ mRNA levels were higher in cells from mice fed coconut oil or safflower oil. After 8 h of culture, IL-2, IFN-γ, and IL-4 mRNA levels were lowest in cells from mice fed fish oil. The ratio of the relative levels of IFN-γ mRNA to IL-4 mRNA was highest in cells from mice fed coconut oil and was lowest in cells of mice fed fish oil. The influence of individual fatty acids on IL-2 production by murine spleen lymphocytes was examined in vitro. Although all fatty acids decreased IL-2 production in a concentration-dependent manner, saturated fatty acids were the least potent and n-3 PUFAs the most potent inhibitors, with n-6 PUFAs falling in between in terms of potency. It is concluded that saturated fatty acids have minimal effects on cytokine production. In contrast, PUFAs act to inhibit production of Th1-type cytokines with little effect on Th2-type cytokines; n-3 PUFAs are particularly potent. The effects of fatty acids on cytokine production appear to be exerted at the level of gene expression.
The objective of this study was to examine the effects of dietary ω-3 fatty acid supplementation on insulin sensitivity (SI) in horses. Twenty-one mares were blocked by age, body weight (BW), and body condition score (BCS) and randomly assigned to one of three dietary treatments. Treatments consisted of (1) 38 g of n-3 fatty acids via fish and algae supplement and diet (MARINE), (2) 38 g of n-3 fatty acids via a flaxseed meal from the supplement and diet (FLAX), and (3) control (CON) no supplemental fatty acid. Treatments were supplemented for 90 days. Frequent sampling intravenous glucose tolerance tests were performed on days 0, 30, 60, and 90. Blood samples were analyzed for glucose and insulin. The minimal model was applied for the glucose and insulin curves using MinMod Millennium. SI increased 39% (P < .007) across all treatment groups. Acute insulin response to glucose decreased 22% (P < .006) between days 30 and 60 and increased (P = .040) again at day 90. Disposition index (combined SI and β pancreatic response) increased (P = .03) by 53% in the MARINE- and 48% in the FLAX-supplemented horses and did not change with time in the CON group. In insulin-resistant mares, MARINE- and FLAX-treated horses had an increase in SI (P = .09). It would be interesting to test this supplement in a larger group of insulin-resistant horses. If proven effective, supplementation with ω-3 fatty acids would help to reduce problems associated with insulin resistance in horses.
The effect of intravenous administration of lipid emulsions enriched with omega-3 (n3) and omega-8 (n6) fatty acids on equine monocyte phospholipid fatty acid composition and the synthesis of inflammatory mediators in vitro was evaluated. In a randomized crossover design, horses were infused intravenously with 20% lipid emulsions containing n3 or n6 fatty acids. Monocytes were isolated from the horses before and 0 h, 8 h, 24 h, and 7 days after lipid infusion. Monocyte fatty acid analysis demonstrated incorporation of the parenteral n3 and n6 fatty acids in monocyte phospholipids immediately after infusion, with changes in the fatty acid composition persisting for up to 7 days after infusion. In vitro production of the inflammatory mediators thromboxane B-2 /thromboxane B-3 (TXB2/3) and tumor necrosis factor-alpha (TNF alpha) by peripheral blood monocytes was diminished by n3 lipid infusion and was unchanged or increased by n6 lipid infusion. The results of this study demonstrate that short-term infusions of n3 and n6 fatty acid-enriched lipid emulsions alter the fatty acid composition of equine monocyte phospholipids and modify the inflammatory response of these cells in vitro. These results also support further investigation into the use of parenteral n3 fatty acids as part of the supportive therapy of patients with multiple organ dysfunction (MODS) or systemic inflammatory response syndrome (SIRS).