Journal of Feline Medicine and Surgery
The online version of this article can be found at:
2013 15: 74 originally published online 21 September 2012 Journal of Feline Medicine and Surgery
Lisa M Freeman, John E Rush, Kathryn M Meurs, Barret J Bulmer and Suzanne M Cunningham
Body size and metabolic differences in Maine Coon cats with and without hypertrophic cardiomyopathy
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Journal of Feline Medicine and Surgery
15(2) 74 –80
© ISFM and AAFP 2012
Reprints and permission:
In humans, hypertrophic cardiomyopathy (HCM) is
considered ‘… a disease entity caused by autosomal
dominant mutations in genes encoding protein compo-
nents of the sarcomere …’ and over 1400 mutations have
been identified.1 Mutations in myosin binding protein C
(MYBPC) have been described in Maine Coon and
Ragdoll cats with HCM,2–4 but genetic mutations have
not been found for most cats with HCM. Nonetheless,
the phenotypic expression of the disease is highly vari-
able in both Maine Coon cats and other cats with
HCM.5,6 This phenotypic variation is also seen in
humans with HCM in which there can be a wide varia-
tion in the clinical appearance of the disease in family
members with the same genetic mutation: some have
mild myocardial hypertrophy and others have severe
hypertrophy and advanced clinical signs.7 The cause of
this phenotypic disparity is unknown, but may be the
result of modifier genes or environmental factors.8,9
Nutrition is one factor that may have significant effects
on cardiovascular phenotype.
Nutrient deficiencies and excesses can play an impor-
tant role in cardiovascular diseases during the in utero
and early postnatal period. Human studies have shown
that low birth weight is associated with an increased inci-
dence of coronary heart disease and hypertension in later
Body size and metabolic differences
in Maine Coon cats with and without
Lisa M Freeman1, John E Rush1, Kathryn M Meurs2,*,
Barret J Bulmer1,† and Suzanne M Cunningham1
An interplay between growth, glucose regulation and hypertrophic cardiomyopathy (HCM) may exist, but has not
been studied in detail. The purpose of this study was to characterize morphometric features, insulin-like growth
factor-1 (IGF-1) and glucose metabolism in Maine Coon cats with HCM. Body weight, body condition score
(BCS), head length and width, and abdominal circumference were measured in Maine Coon cats >2 years of
age. Echocardiography and thoracic radiography (for measurement of humerus length, and fourth and twelfth
vertebrae length) were also performed. Blood was collected for biochemistry profile, DNA testing, insulin and
IGF-1. Sixteen of 63 cats had HCM [myosin binding protein C (MYBPC)+, n = 3 and MYBPC–, n = 13] and 47/63
were echocardiographically normal (MYBPC+, n = 17 and MYBPC–, n = 30). There were no significant differences in
any measured parameter between MYBPC+ and MYBPC– cats. Cats with HCM were significantly older (P <0.001),
heavier (P = 0.006), more obese (P = 0.008), and had longer humeri (P = 0.02) compared with the HCM– group.
Cats with HCM also had higher serum glucose (P = 0.01), homeostasis model assessment (HOMA) and IGF-1
(P = 0.01) concentrations, were from smaller litters (P = 0.04), and were larger at 6 months (P = 0.02) and at 1
year of age (P = 0.03). Multivariate analysis revealed that age (P <0.001), BCS (P = 0.03) and HOMA (P = 0.047)
remained significantly associated with HCM. These results support the hypothesis that early growth and nutrition,
larger body size and obesity may be environmental modifiers of genetic predisposition to HCM. Further studies are
warranted to evaluate the effects of early nutrition on the phenotypic expression of HCM.
Accepted: 20 August 2012
1 Department of Clinical Sciences, Tufts Cummings School of
Veterinary Medicine, North Grafton, MA, USA
2 Department of Veterinary Clinical Sciences, Washington State
University College of Veterinary Medicine, Pullman, WA, USA
* Dr Meurs is now at North Carolina State University College of
Veterinary Medicine, Raleigh, NC, USA
† Dr Bulmer is now at Tufts Veterinary Emergency Treatment and
Specialties, Walpole, MA, USA
This study was presented, in part, at the 2011 ACVIM Forum,
Denver, CO, USA
Lisa Freeman DVM, PhD, DACVN, Department of Clinical
Sciences, Tufts Cummings School of Veterinary Medicine,
200 Westboro Road, North Grafton, MA 01536, USA.
60847 JFM15210.1177/1098612X12460847Journal of Feline Medicine and SurgeryFreeman et al
Freeman et al
life.10–12 Of particular concern is when there is nutrient
restriction in utero, resulting in a low birth weight, fol-
lowed by rapid early growth (ie, catch-up growth).10–12
Restricted fetal growth is adaptive when nutrient availa-
bility is suboptimal, but when nutrients are sufficient or
excessive, these adaptations become detrimental.
Therefore, the environment in which a fetus develops
and subsequent growth rate influences long-term health,
particularly in the cardiovascular system. This idea of
‘fetal programming’ suggests that the phenotype of HCM
may be modifiable depending upon early nutrition or
other environmental factors.
Whilst most research on fetal programming and later
cardiovascular disease has focused on coronary heart
disease and hypertension, there is also evidence that in
utero and early postnatal nutrition can impact myocar-
dial hypertrophy. Studies in sheep have shown that
maternal nutrient restriction results in fetal left ventricu-
lar hypertrophy, insulin resistance, increased myocardial
insulin-like growth factor-1 (IGF-1) and upregulation of
myocardial genes whose mutations have been associ-
ated with HCM (eg, alpha-cardiac actin, caveolin-1 and
titin).13–15 Insulin resistance may play an important role
in the pathogenesis of myocardial hypertrophy that is
induced via in utero and early nutrient alterations affect-
ing growth. Insulin resistance can occur in humans with
heart failure because the heart reverts to fetal metabolic
pathways in which glucose becomes the major fuel for
myocytes, yet capacity for glucose utilization is lim-
ited.16,17 However, insulin resistance is also present in
humans with HCM, even without heart failure, as a
result of alterations in glucose transporters.18
In utero or postnatal modifications in nutrient supply
and growth patterns may also alter phenotype through
alterations in growth hormone or IGF-1 production.
Growth hormone, whose actions are mediated via IGF-1,
is related intimately to many aspects of growth, from
overall body growth (eg, stature) down to the cellular
level (eg, protein synthesis in myocytes). IGF-1 regulates
cardiomyocyte maturation in utero, as well as postnatal
hypertrophic responses, so is an important determinant
of ventricular growth responses. IGF-1 overproduction
increases myocardial protein synthesis and causes left
ventricular hypertrophy.19–21 IGF-1 is regulated by many
factors, including growth hormone, nutrients (eg, pro-
tein, certain amino acids), left ventricular pressure over-
load, angiotensin II and IGF binding proteins.19,22,23
Studies have shown that myocardial IGF-1 and circulat-
ing IGF-1 concentrations are elevated in humans with
One study showed that cats with HCM were signifi-
cantly larger (ie, body weight, head length and width,
and humeral and vertebral length), but not more obese
than healthy controls.26 However, it is not yet known if
these same morphometric alterations occur in Maine
Coon cats with HCM, or if there is a relationship between
body size and the MYBPC mutation found in some cats
of this breed. The larger size of cats with HCM may be
associated with increased growth hormone and IGF-1
production. One study found elevated growth hormone
concentrations in cats with HCM,27 but interpretation is
difficult as growth hormone concentrations fluctuate
dramatically throughout the day. In a previous study of
cats with HCM, IGF-1 concentrations were not signifi-
cantly different between cats with HCM and controls.26
However, IGF-1 concentrations were correlated signifi-
cantly with body weight, and vertebral and humeral
length.26 These data suggest a relationship between body
size and the growth hormone–IGF axis, but it is not yet
definitively known if IGF-1 is altered in cats with HCM.
Thus, a possible interplay between glucose dysregu-
lation, fast or excessive growth, and HCM may exist, but
has not been studied in detail. Therefore, the purpose of
this study was to characterize morphometric features,
IGF-1 and glucose metabolism in Maine Coon cats with
HCM. We hypothesized that morphometric features,
glucose metabolism and IGF-1 are abnormal in cats with
HCM and that these alterations may contribute to the
phenotypic expression of the disease.
Materials and methods
Maine Coon cats of at least 2 years of age and without
other major diseases were eligible for the study. Cats with
congestive heart failure were excluded. Historical infor-
mation, if available, was collected from the owner on litter
size, size at 6 and 12 months, and early feeding method.
For size at 1 year, owners were asked for the cat’s body
weight, but size at 6 months it was assessed using a sub-
jective assessment (ie, very small, somewhat small, aver-
age size, somewhat large or very large). Feeding method
was assessed by asking owners if the kittens were meal-
fed or fed free-choice. Cats were fasted for at least 8 h
prior to the evaluation. Body weight, body condition
score (BCS) (using a nine-point scale),28 head length and
width,26 and abdominal circumference26 were measured.
BCS was assigned in all cats by a single investigator (LF).
Echocardiography [two-dimensional (2D), M-mode,
and color flow, spectral and tissue Doppler (Vivid 7
Dimension, General Electric Healthcare)] and blood
pressure measurements (Doppler technique with >170
mmHg considered hypertensive) were performed on
all cats without sedation. For echocardiography, 2D
right parasternal long- and short-axis, 2D left paraster-
nal and M-mode right parasternal short axis views
were obtained. Left ventricular, left atrial and aortic
M-mode dimensions were measured in right parasternal
short axis views using 2D guidance in accordance with
the guidelines established by the American Society
of Echocardiography.29 The 2D left atrial and aortic
76 Journal of Feline Medicine and Surgery 15(2)
dimensions were obtained in the right parasternal short
axis view in diastole,30 and the 2D interventricular sep-
tum and left ventricular free wall measurements were
obtained in the right parasternal short or long axis view
of the left ventricle in end-diastole. Mitral inflow E and A
wave velocities were evaluated using pulsed wave
Doppler in the left apical view by placing a 2 mm sample
volume at the tips of the mitral valve leaflets and the
ratio of mitral E wave to A wave velocity (mitral E:A)
was calculated. Pulsed wave tissue Doppler E’ and A’
velocities were recorded from the lateral and septal
mitral annulus. The ratios of mitral E wave velocity to
lateral and septal E’ velocities (E/E’ LVW and E/E’ IVS)
were calculated. To be classified as normal, cats had to
have both an interventricular septal thickness in diastole
(IVSd) and left ventricular free wall thickness in diastole
(LVWd) <0.6 cm on M-mode, short axis and long axis 2D
measures; a subjectively normal left atrial size; no sys-
tolic anterior motion of the mitral valve; and an aortic
velocity ≤1.5 m/sec, with no subjective evidence of LV
hypertrophy or papillary muscle hypertrophy. Cats were
diagnosed with HCM if they had either an IVSd or
LVFWd >0.6 cm, measured by 2D and/or M-mode echo,
and concurrent findings indicative of HCM (ie, some
combination of diffuse or focal concentric hypertrophy
of the left ventricle, systolic anterior motion of the mitral
valve, left atrial enlargement or increased aortic veloc-
ity). Cats that did not fit into the HCM or normal catego-
ries were excluded from the study. All echocardiograms
were performed by a board-certified veterinary cardiol-
ogist (JR, BB or SC) and in any case where the diagnosis
of normal or HCM was in question, the echocardiogram
was reviewed by a second board-certified veterinary
cardiologist (JR, BB or SC).
Radiography was performed by use of a digital
radiography system for measurement of length of the
humerus, and fourth and twelfth vertebrae from a lateral
radiograph in which the left front leg was positioned to be
visible in its entirety on the radiograph. All measure-
ments of the humeri and vertebrae were performed by a
single investigator (LF). Blood was collected for a bio-
chemistry profile, T4 (if >7 years), insulin (radioimmu-
noassay: Human Insulin Specific; Millipore) and IGF-1
(high performance liquid chromatography; Endocrine
Section, Diagnostic Center for Population and Animal
Health, Michigan University). The homeostasis model
assessment (HOMA) — a calculation that has been used
as an estimate of insulin sensitivity in cats — was calcu-
lated using the formula: HOMA = (insulin × glucose)/
22.5.31 The biochemistry profile and T4 were performed
immediately, and serum for all other analyses was stored
at -80°C until batch analysis. DNA testing (blood) for the
MYBPC A31P mutation was performed at the Veterinary
Cardiac Genetics Laboratory at Washington State
University College of Veterinary Medicine.2 The study
was approved by the Tufts Cummings School of
Veterinary Medicine Clinical Studies Review Committee
and all owners signed an informed consent form before
enrolling cats in the study.
All data are presented as median (range) and skewed
data were transformed prior to analysis. Categorical var-
iables were compared between groups using χ2 analyses.
Continuous data were compared between groups using
independent t-tests. Correlation between continuous
variables was performed using Pearson correlation tests.
Any variables found to be P <0.10 on univariate analysis
also were analyzed using logistic regression analysis to
assess the independent effects of these variables. All
analyses were performed with commercial statistical
software (Systat 12.0, SPSS) and P <0.05 was considered
Eighty-five Maine Coon cats were screened for the study
between July 2010 and April 2011. Of these, two cats were
excluded for congestive heart failure (chronic: n = 1, acute:
n = 1), the echocardiogram was equivocal (ie, the heart
could not be clearly classified as either normal or HCM) in
16 cats and four cats had other cardiac abnormalities
(ie, tricuspid valve dysplasia, n = 2; ventricular septal
defect, n = 1; unexplained left ventricular dilation, n = 1).
These 22 cats were excluded from further evaluation.
Therefore, 63 cats qualified for the study: 16 had echo-
cardiographic evidence of HCM [hereafter designated as
HCM+ (MYBPC+, n = 3 and MYBPC–, n = 13)] and 47
were echocardiographically normal [HCM– (MYBPC+,
n = 17 and MYBPC–, n = 30)]. Echocardiographic meas-
urements for the HCM- group were similar to those
found in a previous study of healthy Maine Coon cats.32
There were no significant differences between MYBPC+
and MYBPC– cats in any measured parameter. Therefore,
all further comparisons are made between HCM+ and
HCM– cats. Most cats (52/63; 83%) were owned by
breeders. Two cats were receiving cardiac medication
(both in the HCM+ group and both were MYBPC–); enal-
april, n = 1; atenolol, n = 1; aspirin, n = 1). Cats with HCM
were significantly older (median = 9.1 years, range = 4.1–
11.4 years) compared with cats without HCM (median =
3.2 years, range = 2.0–10.9 years; P <0.001). Gender of the
HCM+ group (12 males, one female) was not signifi-
cantly different from the HCM– group (25 males, 22
females; P = 0.13). However, a significantly greater pro-
portion of the HCM+ group was neutered (15/16) com-
pared with the HCM– group (10/47; P <.001). Neuter age
was not significantly different between the two groups
(HCM+: median = 8 months, range 5–90 months;
HCM–: median = 6 months, range 5–72 months; P = 0.79).
Blood pressure was not significantly different between
groups (HCM+: median = 140 mmHg, range 109–167 mmHg;
Freeman et al
HCM–: median = 141 mmHg, range 100–170 mmHg; P =
0.84). Cats with HCM had a significantly higher median
murmur grade (median = 2, range 0–4) compared with
controls (median = 0, range 0–2; P <0.001). On M-mode
echocardiography, cats with HCM had significantly
thicker IVSd/s and LVWd/s measurements (all P <0.001)
and significantly smaller left ventricular internal dimen-
sion in diastole/systole (LVID) in systole (P <0.001; Table
1). The IVSd and LVWd measured by 2D echocardiogra-
phy were also significantly thicker in the HCM+ group
(both P <0.001). All measures of left atrial size were sig-
nificantly larger in the HCM+ group compared with the
HCM– group [M-mode left atrial diameter (P = 0.02) and
2D left atrial diameter (P = 0.007)]. Systolic anterior
motion of the mitral valve was present in 4/16 HCM+
cats and 0/47 HCM– cats (P <0.001). Cats with HCM had
significantly higher aortic velocity (P <0.001), A wave (P
= 0.03), E/E’ LVW (P = 0.01) and E/E’ IVS (P = 0.007;
Table 1) compared with controls. Cats with HCM had
significantly lower E/A (P = 0.02), E’ LVW (P = 0.02),
E’ IVS (P = 0.001), E’/A’ LVW (P = 0.001) and E’/A’ IVS
(P = 0.02).
Morphometric measurements of the cats revealed
significantly higher median body weight (P = 0.006),
BCS (P = 0.008) and abdominal circumference (P = 0.004)
in the HCM+ group compared with the HCM– group
(Table 2). Cats in the HCM+ group also had significantly
longer humeri (P = 0.02). The median length of the fourth
and twelfth vertebra was not significantly different
between groups (P = 0.07 and P = 0.22, respectively).
The HCM+ group had higher serum glucose (P = 0.01)
and HOMA (P <0.001), although insulin and insulin/
glucose ratios were not significantly different between
groups (Table 3). IGF-1 concentrations were higher in
the HCM+ cats (P = 0.01; Table 3). Cholesterol and tri-
glyceride concentrations were not significantly differ-
ent in the HCM+ cats compared with the HCM– cats
(both P = 0.32).
Table 1 Echocardiographic measurements for cats without (HCM–; n = 47) and with hypertrophic cardiomyopathy
(HCM+; n = 16). Data are presented as median (range)
Left atrium (cm)
IVSd 2D (cm)
LVWd 2D (cm)
Aorta 2D (cm)
Left atrium 2D (cm)
Aortic velocity (m/s)
E′ LVW (m/s)
A′ LVW (m/s)
E′ IVS (m/s)
A′ IVS (m/s)
Isovolumetric relaxation time (ms)
IVSd/s = interventricular septal thickness in diastole/systole, LVIDd/s = left ventricular internal dimension in diastole/systole, LVWd/s = left
ventricular free wall thickness in diastole/systole, E = early diastolic velocity of mitral inflow, A = late diastolic velocity of mitral inflow, E′ = early
peak diastolic myocardial velocity, A′ = late diastolic myocardial velocity
78 Journal of Feline Medicine and Surgery 15(2)
Historical data could be obtained from some cat own-
ers [size at 6 months, n = 57 (88% were breeders); litter
size, n = 55 (86% were breeders); feeding method for kit-
tens, n = 54 (85% were breeders); weight at 1 year, n = 42
(86% were breeders)]. Litters from which the HCM+ cats
were born were significantly smaller (median = 4, range
2–6) compared with those of the HCM– cats (median = 5,
range 2–8; P = 0.04). HCM+ cats were also judged subjec-
tively by their owners/breeders to be larger at 6 months
of age (P = 0.02) and weighed more at 1 year of age
(HCM+: 6.1 kg, range 3.2–8.6 kg; HCM–: median = 5.5
kg, range 3.6–7.5 kg; P = 0.03). The percentage of cats fed
ad libitum as kittens (HCM–: 37/41 vs HCM+: 11/13; P
= 0.57) and adults (HCM–: 41/44 vs HCM+: 10/13; P =
0.09) was not significantly different between groups.
As cats in the HCM+ group were significantly older
than cats in the HCM– group, multivariate analysis was
performed and age (P <0.001), BCS (P = 0.03) and HOMA
(P = 0.047) remained significantly associated with HCM.
Maine Coon cats with echocardiographic evidence of
HCM (HCM+) were older, more likely to be neutered,
heavier and more obese, and had longer humeri
compared with cats without HCM. This is similar to
findings from a study of cats of breeds other than Maine
Coons, in which cats with HCM also were heavier and
had longer humeri.26 However, the current results of
higher abdominal circumference and BCS in HCM+ cats
differ from the results of this previous study.26 The
reason for the differences in obesity in these two studies
is not clear but may be related to the age difference
between groups in the current study, which was not pre-
sent in the study by Yang et al. Although not evaluated
in the current study, distribution of adipose tissue (ie,
central vs peripheral adiposity) can confer different
metabolic effects in humans;33 this would be interesting
to evaluate in future studies. Morphometric differences
have not been studied in humans with HCM so it is
unknown whether this is a species-specific finding. In
addition, the current study did not find differences in
head width or length, in contrast to the previous study
by Yang et al26 in which cats with HCM had signifi-
cantly longer and wider heads compared with healthy
controls. This difference between studies may be related
to the single breed (Maine Coon cats) in the current
study compared with the previous study, which specifi-
cally excluded Maine Coon cats.
Cats with HCM in the current study also had higher
serum glucose and IGF-1 concentrations, and a higher
HOMA compared with HCM– cats, although this could
be related to differences in age between groups. Glucose
and IGF-1 concentrations were not significantly different
between cats with HCM and healthy controls in a previ-
ous study, which included only breeds other than Maine
Coon cats,26 so this finding may be specific to Maine
Coon cats. The higher median glucose concentration and
HOMA in the current study may also be related to the
Table 2 Morphometric measurements for cats without (HCM–; n = 47) and with hypertrophic cardiomyopathy
(HCM+; n = 16). Data are presented as median (range)
Body weight (kg)
Body condition score (1–9)
Head length (cm)
Head width (cm)
Humerus length (cm)
Fourth vertebra length (cm)
Twelfth vertebra length (cm)
Table 3 Laboratory analyses in cats without (HCM–; n = 47) and with hypertrophic cardiomyopathy (HCM+; n = 16).
Data are presented as median (range)
Homeostasis model assessment
Insulin-like growth factor-1 (nmol/l)
Freeman et al
fact that HCM+ cats had a higher median BCS than
HCM– cats, as obese cats have been shown to be more
insulin resistant than lean cats.34 The previous study by
Yang et al did not evaluate HOMA, so it is unknown
whether this calculated estimate of insulin sensitivity
would have differed in breeds other than Maine Coon.
The use of HOMA is not well studied in cats so future
studies of HCM should not only include assessment of
insulin, glucose and HOMA, but also of other, more spe-
cific measurements of insulin resistance which also take
into account more than just a single time point. The lack
of difference in IGF-1 concentrations in the previous
study by Yang et al compared with the differences found
in IGF-1 in the current study may be a breed-specific
finding, or may be related to growth and overall size dif-
ferences. In the current study, HCM+ cats came from
smaller litters and were already larger than HCM– cats
at 6 months and 1 year of age. Whether these historical
factors contributed to higher glucose, IGF-1 concentra-
tions and obesity, or were independent factors is not
known. Further prospective investigation is needed to
better understand these findings.
The higher percentage of neutered cats in the HCM+
cats compared with HCM– cats could also play a role in
the greater risk of obesity in this group, as neutering is
known to significantly reduce the energy requirements of
cats.35–38 The percentages of cats fed ad libitum during
growth and as adults was not different between the HCM+
and HCM– groups, but was very high overall (89% during
growth, 90% as adults). The high percentage of cats in this
study that were overweight suggests that enhanced owner
education regarding optimal body condition is needed.
There are a number of limitations to this study. One is
the significant difference in age between the HCM+ and
HCM– cats. Although body weight and HOMA concen-
trations were determined to be associated indepen-
dently with HCM in the multivariate statistical analysis,
it would have been desirable to have age-matched groups.
This proved to be difficult in the current study in order
to enroll as large a population as possible. However, this
should be a goal of future studies.
The difference in age also raises the question of
whether younger cats in the HCM– group would remain
free of HCM later in life, as this was a cross-sectional
study. In the article by Kittleson et al on HCM in Maine
Coon cats, the age at which left ventricular hypertro-
phy became moderate-to-severe was 24 ± 13 months.6
Therefore, it would be likely that Maine Coon cats >2
years of age would show some echocardiographic signs
of HCM. However, longitudinal studies are needed to
determine the proportion of MYBPC+ and MYBPC–
Maine Coon cats that will ultimately develop HCM over
the course of their lifetimes.
Another limitation is that historical information on
cats was not available for all cats and some of it was sub-
jective (eg, 67% could provide the cat’s weight at 1 year
of age and 91% were able to provide a subjective assess-
ment of the cat’s size at 6 months of age). For the subjec-
tive question on size at 6 months, 88% of the respondents
were breeders (and some of the others who were not
breeders obtained the information from the cat’s
breeder). Cat breeders may be more likely than the aver-
age cat owner to be able to assess size, but this question
was still subjective. Prospective studies of Maine Coon
cats during growth would provide valuable information
on the role of early nutrition and growth on the pheno-
type of HCM. The population enrolled in the study may
have been biased as many cats were owned by breeders.
Therefore, some were from related lines and owners
with cats already determined to be MYBPC+ or to have
HCM may have been more or less likely to have volun-
teered for the study. Finally, the genotype and pheno-
type of cats in this population reflects cats from the
Northeast and mid-Atlantic regions, and may be differ-
ent from cats in other parts of the country and the world.
These data support the hypothesis that early growth and
nutrition, larger body size and obesity may be environ-
mental modifiers of genetic predisposition to HCM.
Further studies are warranted to evaluate the effects of
early nutrition and growth on the phenotypic expression
Acknowledgements The authors gratefully acknowledge
the contributions of Dr Gordon S Huggins and Dr Martin S
Maron to this research.
Funding This project was supported by the American
Association of Feline Practitioners and by grant number UL1
RR025752 from the National Center for Research Resources
(NCRR). The content is solely the responsibility of the authors
and does not necessarily represent the official views of NCRR
Conflict of interest The authors do not have any potential
conflicts of interest to declare.
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