Adipose Cellularity Studies in Commercial Broiler Chicks

Adipose Cellularity Studies in Commercial Broiler Chicks J. A. CHERRY, W. J. SWARTWORTH, and P. B. SIEGEL Department of Poultry Science, Virginia Polytechnic Institute and State University, Blacksburg, Virginia 24061 (Received for publication April 6, 1983)

1984 Poultry Science 63:97-108 INTRODUCTION

Adipose tissue mass is dependent upon both number and size of individual adipocytes. In both broilers and Leghorns under ad libitum feeding (Pfaff and Austic, 1976; Hood, 1982), hyperplastic growth of adipose tissue appears to cease by 12 to 15 weeks of age. Although this age can apparently be altered by nutrient restriction (Pfaff and Austic, 1976; March and Hansen, 1977; Ballam and March, 1979), there is a lack of evidence that adipocyte hyperplasia persists in chickens beyond sexual maturity (March et al., 1982). Adult mammals are apparently capable of hyperplastic lipid deposition under some conditions (Lemonnier, 1972; Allen, 1976; Faust et al., 1978). Changes in adipose tissue cellularity in relation to fat deposition in the chicken prior to sexual maturity are not clear. Pfaff and Austic (1976) suggested that the contributions of cell size and cell number to the adiposity of White Leghorn chicks were similar to 7 weeks of age, after which cellular hypertrophy was the more predominant factor. In contrast, March and Hansen (1977) observed that adipocyte size in White Leghorn chicks remained constant to 6 weeks of age. This infers that lipid accumulation up to this age was primarily a hyperplastic phenomenon. Similar inconsistencies have been reported in studies with meat-type chickens. March and Hansen (1977) concluded that although lipid deposition was primarily due to adipocyte hyperplasia in broiler chicks prior to 21 days of age, some difference in cell size was also ob97

served. In contrast, the data of Hood (1982) indicated that adipocyte number increased rapidly while adipocyte hypertrophy proceeded slowly up to about 14 weeks of age. Subsequent to this time, adipose cell volume increased threefold while adipocyte number remained relatively constant. The objective of the study reported here was to examine further adipose cellularity in relation to fat deposition prior to the onset of sexual maturity. Commercial broiler stocks differing in adiposity were compared, and dietary effects were examined by feeding diets differing in the ratio of calories to protein. MATERIALS AMD METHODS

Experiment 1. Twenty-four male chicks of a commercial broiler strain were obtained at one day of age, vaccinated for Marek's disease, and caged in electrically heated battery brooders. The birds were subjected to continuous lighting and fed ad libitum a corn-soybean meal based diet containing 22% crude protein and 3200 kcal metabolizable energy /kg of diet. At 28 days of age, the chicks were transferred to wire-floored growing batteries. Otherwise, consistent management practices were maintained throughout the experiment, which was terminated when the chicks were 91 days of age. At 14, 21, 28,35,42,56,70, and 91 days of age, three chicks were randomly selected, weighed to the nearest gram, and killed by cervical dislocation. The abdominal fat pad and the sartorial (musculi sartorius) fat depot were

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ABSTRACT The development of adipose depots in broiler chickens prior to sexual maturity occurred as a consequence of both adipocyte hyperplasia and hypertrophy. Prior to about 28 days of age, increases in fat deposition were primarily associated with differences in adipocyte number while at later ages adipocyte hypertrophy became the primary influence. The feeding of diets containing a low calorie-to-protein ratio reduced fat deposition by decreasing adipocyte hypertrophy. The differences in adiposity between two commercial broiler stocks were due primarily to differences in adipocyte number prior to 28 days of age. Results at older ages were inconclusive for differences among populations. (Key words: broilers, lipid deposition, hyperplasia, hypertrophy)

98

CHERRY ET AL.

where i-I, 2 . . . 8 ages and j = 1, 2 ... 24 individuals. When significant differences were found among ages, the means were separated by Duncan's multiple range test. Product-moment correlation coefficients between the traits were calculated within ages and with ages pooled. Experiment 2, Male chicks from two com-

merciai strains believed to differ in;·,body fat content were reared in litter-covered floor pens under a continuous photoperiod. Chicks from each population were fed ad libitum each of two diets differing in the ratio of metabolizable calories to crude protein (Table 1). At intervals of 7 days from 0 to 56 days of age, adipose tissue samples were collected as described for Experiment 1 from five randomly selected male chicks of each population-diet subclass. Adipose tissue cellularity was then determined according to the procedures previously described. Comparisons within the various traits were made by an analysis of variance with population, diet and age considered to be fixed effects. The statistical model was: Yijkl

=J1 + Pi + Dj + Ak + (PD)ij

+ (PA)ik + (DA)ik + (PDA)ijk + eijkl

where i = 1,2 populations, j = 1 ,2 diets, k = 1, 2 ... 8 ages and I = 1, 2 ... 5 individuals. When

TABLE 1. Composition and nutrient content oftbe experimental diets Energy: protein High Ingredient

(%)

Corn 56.91 Soybean meal (dehulled) 34.83 Fish meal 2.00 Hydrolyzed fat 2.75 Defluorinated phosphate 1.65 Ground limestone .68 Vitamin and trace mineral mix' .25 Salt .20 DL-Methionine .10 Coccidiostat .13 Antibiotic .50 Calculated composition Crude pro,tein, % Metabolizable energy, kcallkg Energy/protein

Low

23.09 3087 134

44.41 47.36 2.00 2.75 1.65 ,68 .25 .20 ,07 .13 .50 28.01 2981 106

'The premix supplied per kilogram of diet: 4400 IV vitamin A, 11 00 IV vitamin D 3' 4.4 IV vitamin E, 7.0 mg menadione sodium bisulfite, 8.8 mg riboflavin, 22 mg d-calcium pantothenate, 66 mg niacin, 500 mg choline chloride, 13.2 Jig vitamin B '2' 1. 2 mg folic acid, 250 mg ethoxyquin, 80 mg manganese, 112 mg zinc, 62 mg iron, 16 mg copper, 1 mg iodine,

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, removed with surgical scissors',and immediately placed in .15 M NaCI to prevent dehydration or cell lysis. The fat depots were then washed in saline to remove extra-cellular lipid droplets, blotted, and weighed to the nearest milligram. Tissue samples of 80 to 120 mg were then excised from each depot for cellularity determinations. Each fat sample was immediately placed onto a 5 cm square of 286 J1 polyethylene screen, which was then folded to contain the sample completely. These samples were subsequently placed into 50 ml polyethylene vials containing 25 ml of a 2% solution of osmium tetroxide in collidine-HCI buffer for fixation according to the procedure described by Hirsch and Gallian (1968). The vials were capped, placed into a water bath at 37 C, and incubated for 72 hr. The resulting mass of fixed adipocytes was sifted through a 286 J1 sieve using saline washing and gentle mechanical agitation. inc:tividual cells were collected on a 20 J1 screen to eliminate particulate matter of lesser diameters. The fixed cells were subsequently washed with 200 ml of an electrolyte solution into a 250 ml round bottom flask. The cells were homogeneously suspended in the electrolyte solution with constant stirring and were counted ~kctronically using a Coulter counter equipped with a 400 J1 aperture. The relative size of the adipocytes was also determined using a Coulter Channelyzer and Logarithmic Range Expander to produce a frequency distribution for each sample. Body weight, sartorial fat weight, abdominal fat weight, adipocyte number, and adipocyte size were determined for each broiler. These values were used to calculate additional parameters for each depot including cells per gram of fat, total adipocyte number per depot, and mean adipocyte diameter. Each trait measured was regressed on age using a polynomial model. Comparisons were made among ages for each trait by an analysis of variance with the statistical model:

99

ADIPOSE CELLULARITY IN CHICKS CELL

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50

NUt~BER

b

65

40

55

30

45

ab

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~ 20

35 ab

10

25

o Age SE

56

70

7.5

9.5

Age SE

4.3

7.7

b

43

8

40

S-

ab

<1> .0

E

"

z

37

b

ab

34

Age SE

.8

.5

.7 1.2 6.9

.6

14 21 28 35 42 .61.9 .5 3.54.2

Age SE

.3

56 3.6

70 .7

FIG. 1. The cellular development of the abdominal fat depot in Experiment 1. For each trait, means having the same letter were not significantly different (P
significant differences were found, the means were separated by Duncan's multiple range test. Product-moment correlation coefficients were also calculated between the various traits within

age-diet-population subclasses. RESULTS AND DISCUSSION

Experiment 1. Body weight, abdominal and

TABLE 2. Product-moment correlation coefficients among adipose cellularity traits in growing broilers Sartorial depot Weight

Cells /gram

Cells/ depot

.66**

.55' • .OS

Abdominal depot Cell diameter

Weight

Cells /gram

Cells/ depot

Cell diameter

-.69" .S3· • -.27 -.4S·

-.45 -.13 .47' .34

.72" -.76" .49 .41

-.72"

.51' • -.11

.61" -.76" .07

Sartorial Weight Cells/gram Cells/depot Cell diameter Abdominal Weight Cells/gram Cells/depot ·P
.72" -.76" .05

.S7*· -.57" .53" .42'

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CELL DIAMETER

46

CELL/GRAM

10

3.24.110.810.915.4

CHERRY ET AL.

100 WEIGHT

CELL NUMBER

12 10

ab ab ab ab

a Age SE

56 .44

70 .78

91 .45

CELLS/GRAM

Age SE

50

a

8

45

6

40

14 .7

21 .8

28 35 42 .2 1.2 1.9

56 2.7

79 1.9

91 1.3

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c

-

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4

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o Age SE

14 21 28 35 42 1.6 .8 .5 1.3 4.4

56 .9

70 .2

91 .1

Age SE

14 21 28 35 42 1.9 1.5 .5 1.0 3.5

56 .5

70 2.1

ql

1.9

FIG. 2. The cellular development of the sartorial fat depot in Experiment 1. For each trait, means having the same superscript were not significantly different (P";;.05).

sartorial fat weight, cell number, and cell size data were best fitted by a first degree polynomial model when regressed on age, indicating a linear relationship over time. Histograms for data obtained on individual birds revealed that these traits were generally normally distributed. There was no evidence of a bimodal size distribution similar to that observed in mature broiler-type females by March et at. (1982). The possibility of such a bimodal distribution, however, cannot be discounted, because the methods used in this experiment precluded the detection of adipocytes smaller than 20 J1 in diameter. For this reason, differences in the number of observable adipocytes also do not conclusively indicate hyperplastic cellular growth. The filling of small adipocytes, or preadipocytes, can be confounded with adipocyte hyperplasia when electronic counting techniques are used. When pooled across ages, the abdominal and sartorial fat weights were highly correlated (Table 2), and each of these depots was significantly correlated with body weight (r = .90 and .85 for abdominal and sartorial fat, re-

spectively). These results were consistent with those of Burgener et at. (1981) who demonstrated that the amount of sartorial fat was a reliable indicator of both abdominal fat weight and total carcass fat. The number of adipocytes per gram of adipose tissue and mean adipocyte diameters were also consistent between the sartorial and abdominal depots, indicating that the cellular development of these depots was similar. Within each depot, both total adipocyte number and mean adipocyte diameter were significantly correlated with the weight of the fat depot, suggesting that lipid deposition occurred through increases in both the number and size of adipocytes. In addition, the number of adipocytes per gram of adipose tissue and adipocyte diameter were negatively correlated. Thus, cells per gram of adipose tissue appeared to be a reasonable estimate of cell size in this experiment. The development of the abdominal fat depot with age is presented in Figure l. The increasing weights of the abdominal fat pad as the birds aged were associated with an increase in cell number until about 28 days of age. At older

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10

o 14 21 28 35 42 .04 .03 .05 .25 .28

ADIPOSE CELLULARITY IN CHICKS

,lEI GHT

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d

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x

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FIG. 3. The cellular development of the abdominal fat depot in Experiment 2. For each trait, means having the same letter were not significantly different (Po(.05).

ages, no substantial increases in cell number were observed. Conversely, cell size remained relatively constant during early stages of growth. Cells per gram of abdominal fat remained constant until 42 days of age, after which a significant decrease was observed. A significant increase in cell diameter was not observed until the birds reached 70 days of age. Total adipocyte number in the sartorial depot differed significantly only when the values at 56 days of age were compared with those obtained at 14 and 21 days of age (Fig. 2). Nonetheless, these results were similar to those pertaining to weight of abdominal fat in that there were no indications of increases in adipocyte number at the later ages. Cell size appeared to remain relatively constant at earlier

ages and appeared to increase at later ages. Cell diameters exhibited significant increases at 90 days of age and cells per gram of sartorial fat were significantly fewer at 70 and 91 days of age. This experiment suggested that fat deposition was primarily a hyperplastic phenomenon during early stages of growth while adipocyte hypertrophy appeared to be the principal factor at later ages. Data were not clear as to the specific age at which the transition from hyperplastic to hypertrophic growth occurred. Experiment 2. Two strains of commercial broilers chosen on the basis of being relatively fat or relatively lean were each fed diets differing in calorie-to-protein ratio to assess nutritional-genetic relationships involved in the

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Age

102

CHERRY ET AL.

WEI GHT

240

CELL NUMBER

7.2

d

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x

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12

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CELL DIAt1ETER

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d

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d

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6

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Age SE

7 .3

14 .2

21 .4

28 35 .61.2

42 .3

49 .3

56 .2

Aqe

sf:

7 .4

14 .6

21 .5

28 .8

35 42 49 56 1.0 1.2 1.2 1.2

FIG. 4. The cellular development of the sartorial fat depot in Experiment 2. For each trait, means having the same letter were not significantly different (P<.05).

cellular development of lipid stores. The effects of both diet and genome were significant while the interaction of diet by population was not significant, showing that the dietary response was similar in both populations. The results were pooled accordingly. The cellular development of the abdominal fat pad occurring with age is presented in Figure 3. Early growth of the abdominal fat pad was clearly associated with a rapid increase in cell number. Subsequent to 28 days of age, total cell number was remarkably constant, although the weight of this depot increased more than threefold between 28 and 56 days of age, which inferred that the accretion of fat at older ages was associated with adipocyte hypertrophy. Cells per gram of abdominal fat were significantly lower at 42, 49, and 56 days

of age and cell diameter was significantly elevated at 42 and 56 days of age. A substantial increase in cell diameter was also observed between 7 and 14 days of age, but cells per gram of abdominal fat did not reflect this difference. The cellular development of sartorial fat generally paralleled that of abdominal fat. Increases in the weight of this depot with age were associated with increasing cell numbers until 28 days of age (Figure 4). After 28 days of age, fat deposition appeared to be closely associated with cell size. Cell diameters also increased between 7 and 14 days of age but, similar to the results obtained with abdominal fat, this difference was not reflected in cells per gram of sartorial fat. These observations suggested that increases

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Age

103

ADIPOSE CELLULARITY IN CHICKS

10

100

WEIGfIT

. • LEAN

CELL NIJo1BER

~FAT

a

*

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x sQ)

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0 Age SE

14 .1

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Age SE

14 1.4

7

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21 2.0

28 3.0

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28

44

CELLS/GRAM

~

a

x E

'" s-

;:>

5

40

O>

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OJ

~

3b 0

0 Age SE

14 .3

7

.4

21 .4

Age SE

28 .6

7

14

.8

.5

.6

FIG. 5. Differences in the cellular development of the abdominal fat depot in relatively fat and lean strains of commercial broilers from 0 to 28 days of age. Asterisks (') indicate a significant difference (P';;;.05).

in the mass of adipose tissue up to about 28 days of age was accomplished primarily through adipocyte hyperplasia while subsequent increases in lipid deposition were primarily

associated with adipocyte hypertrophy. Product-moment correlation coefficients were consistent with this conclusion (Table 3). Weights of the fat depot were significantly correlated

TABLE 3. Product-moment correlation coefficients between fat depot weights and adipocyte number and diameter values from 7 to 56 days of age in Experiment 2 Days of age 14

21

28

Abdominal Weight and number .90" Weight and .15 diameter

.90'* .30

.89** .05

.62* .70*

-.42 .68*

Sartorial Weight and number .72*' Weight and .50 diameter

.86" .28

.73*' -.10

.80" .72'

.27 .50

7

*P';;;.05. "P';;;.Ol.

35

42

49

56

-.19 .87*'

-.63* .74'

-.39 .72*

-.15 .70*

-.40 . 70*

-.25 .75*'

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10

21 .3

104

CHERRY ET AL.

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10

8

Vl

80

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6

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0

.--<

60

x

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CELL NUMBER

100

WEIGHT

S-

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40

::J Z

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2 0

0

Age

7

SE

.1

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28 .3

Age

7

SE

.4

44

CELLS/GRAM

14 1.6

21 2.0

CELL DIAMETER

*

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10

28 3.6

~

0

x

40

8 ;:l.

S-

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::J Z

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4

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0

Age

7

SE

.3

14 .2

21 .3

28

Age

7

.5

SE

.4

14 .6

21 .5

28 .6

FIG. 6. The cellular development of the abdominal fat depot from 0 to 28 days of age in response to feeding diets containing high (H) or low (L) ratios of calories to protein. Asterisks (*) indicate a significant difference (P<.05).

with adipocyte number at younger ages and with adipocyte size at older ages. Although no attempt was made to monitor adipose cellularity up to the time of sexual maturity, our data suggested that adipocyte hyperplasia was arrested at ages considerably earlier than those previously reported for both Leghorn and broiler stocks (Pfaff and Austic, 1976; Hood, 1982). Adipocyte hyperplasia, however, may not have permanently ceased. In humans, there appears to be multiple stages of adipose tissue growth, which differ in normal and obese subjects (Knittle and Hirsch, 1968; Hager et al., 1977). In obese cattle and pigs, adipocyte hyperplasia also occurs in phases over an extended period of time (Allen, 1976). It is also possible that sexual dimorphism contributed to the discrepancies between laboratories. Older males carry little abdominal fat while fat increases as females age (Gyles et aI., 1982). Hood (1982) observed sex differences in adipose cellularity in meat-type chickens.

When summarized by population, the body weights differed significantly only at 7 days of age, at which time the chicks from the leaner strain were heavier than those from the fatter strain. Interestingly, the leaner chicks had significantly more abdominal fat at both 7 and 14 days of age when compared to the chicks from the fatter strain (Figure 5). At 28 days of age, the chicks from the fatter strain exhibited the anticipated increase in abdominal fat in comparison with the leaner chicks. As might be expected from the longitudinal data, population differences in abdominal fat at these ages were associated with differences in adipocyte number. Total adipocyte number was significantly reduced at seven days of age and significantly increased at 28 days of age when the fat strain was compared to the lean one. There was no indication that differences in cell size contributed to population differences in adiposity at these ages. Sartorial fat data were generally consistent

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12

14 .2

105

ADIPOS E CELLUL ARITY IN CHICKS

.H

1000 800

NU~1BER

8

~L

6

~

600

0

x

0>

E

4

0

z

400

2

200

0

0

Age

7

SE

.1

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21 .1

Age

28 .1

SE

.1

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21 .2

28 .4

40

6 ;:1

x

4

38

2

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0

Age SE

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Age SE

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0 to 28 days of age in response to feeding FIG. 7. The cellular developm ent of the sartorial fat depot from Asterisks (*) indicate a significa nt differenc e diets containin g high (H) and low (L) ratios of calories to protein. due to diet (P";;.OS).

some differen ce in cell size was with those for abdomi nal fat. Sartoria l fat leaner strain but is possible, therefor e, that It d. observe also ally numeric were weights for the fatter strain contrib uted to popophy smaller at 7 days of age and signific antly larger adipocy te hypertr size during this cell in ces differen at 28 days of age in compar ison to those for the ulation differen ces in ant signific no Because period. in ces differen leaner strain. These populat ion d, these data obtaine ity were sartoria l fat weight appeare d to be associat ed adipose cellular d. presente with increases in cell number , althoug h these were not March and Hansen (1977) observe d that differen ces were not significant. There was tes were both smaller and fewer in adipocy difsize te adipocy dearly no indicati on that in broiler chicks. Hood and fered between the two populat ions prior to 28 White Leghorn than adipose tissue cellular ity ed compar (1982) days of age. For purpose s of brevity, these data Pym s selected for body chicken of lines among were not present ed. ption, or feed efconsum feed gain, the weight both age, of days 28 to Subsequ ent was greatest volume te adipocy sartoria l and abdomi nal fat depots were con- ficiency. Average ption consum feed for selected line the in leaner sistently larger in the fatter than in the of basis the on selected birds in t smalles sigand were r, howeve strain. These differen ces, ces differen ed attribut They nificant only for sartoria l fat at 42 days of age. feed efficien cy. adipocy te number to difNo significant populat ion differen ces in cell among the lines in rate. To our knowled ge, growth in ferences cell or number , cells per gram of adipose tissue isons among comcompar ity cellular adipose depot fat either for d diamete r were observe been previou sly not have stocks at ages older than 28 days. Adipoc yte number s mercial broiler the differen ces that show data Our . tended to be higher in the fatter than in the reported

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CELL DIAMETER

42

8 'b

7

44

CELLS/GRAM

10

z0

CELL

10

WE I GfIT

106

CHERRY ET AL.

25

H

65

WEIGIfr

20

VI

60

a

15

E

'"C">

CEll NUMBER

55

x

<-

0

10

z

50 45

5 0

0

Age SE

35 .8

42 1.6

49 2.4

SE

35 8.0

42 7.1

49 8.6

56 7.6

CELL DIAMETER

50

* 48

8 ~

0

46

6 ;oJ.

x 0

z

44

4

42

1i

0

Age SE

35 2.0

42 1.2

49 .6

56 .3

Age SE

35 1.0

42 1.0

49 1.2

56 1.2

FIG. 8. The cellular development of the abdominal fat depot from 28 to 56 days of age in response to feeding diets containing high (H) and low (L) ratios of calories to protein. Asterisks (*) indicate a significant difference due to diet (P<.05).

in adiposity between two such populations were primarily due to differences in adipocyte number up to 28 days of age. Results obtained at subsequent ages were inconclusive. Differences in adiposity due to diet appeared to be the result of differences in adipocyte size. The body weights of chicks fed a relatively low (L) ratio of calories to protein were significantly greater at 28, 35,49, and 56 days of age than were those of chicks fed diets containing a relatively high (H) calorie to protein ratio. Although heavier, the chicks fed the L diet tended to have smaller fat depots; sartorial and abdominal fat weights were significantly smaller by 21 and 28 days of age, respectively (Figures 6 and 7). These dietary differences in adiposity appeared to be the result of differences in cell size. Furthermore, significant dietary differences in cell size were not obtained until the birds were about 28 days of age, an age that

appeared to be near the transitIOn stage from adipocyte hyperplasia to hypertrophy. No significant dietary differences in adipocyte number were obtained during the initial period of 28 days. Subsequent to 28 days of age, dietary differences in fat deposition clearly appeared to be a hypertrophic response (Figures 8 and 9). In experiments with White Leghorn pullets, Pfaff and Austic (1976) also observed that the feeding of low energy or high protein diets depressed hypertrophic lipid deposition. Observations that adipocyte hyperplasia proceeds under nutrient restriction, although the cells remain smaller, are also consistent with our results (March and Hansen, 1977). Pfaff and Austic (1976), however, observed a reduction in cell number as well as cell size when they fed diets differing in calorie to protein ratios. Our results suggest that adipose tissue

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CELLS/GRAM

10

1.'{ Age

56 2.2

107

ADIPOSE CELLULARITY IN CHICKS

30

V>

8

-

~

20

0

E

'"<-

0

z

5

10

4

0

0 35 .2

6

42 .2

49 .3

56 .2

Age SE

CELLS/GRAM

35 .8

50

5

42 1.0

49 1.0

56 .8

CELL 0 I AMETER

48

4

46 "-

x 0

44

z

2 0

42

L; Age SE

0 35 1.9

42 2.0

49 .8

56 2.0

L,t Age SE

35 .8

42 1.0

49 1.0

56 .8

FIG. 9. The cellular development of the abdominal fat depot from 28 to 56 days of age in response to feeding diets containing high (H) or low (L) ratios of calories to protein. Asterisks (.) indicate a significant difference due to diet (P<.05).

development in chickens follows trends similar to those reported for other species. Early growth of adipose tissue appeared to be influenced predominantly by increases in cell number while later lipid accumulation appeared to be primarily associated with increases in cell size. Differences in adiposity between two commercial broiler strains appeared to be primarily a hyperplastic phenomenon prior to 28 days of age, but the results at older ages were inconclusive. Dietary differences were clearly associated with adipocyte hypertrophy but not adipocyte number. Thus, genetic and nutritional influences on fat deposition are probably manifested through disparate mechanisms. Clarification of metabolic and hormonal influences on fat deposition is needed before the significance of adipose cellularity studies can be completely assessed.

REFERENCES Allen, C. E., 1976. Cellularity of adipose tissue in meat animals. Fed. Proc. 35:2302-2307. Ballam, G. C., and B. E. March, 1979. Adipose size and number in mature broiler-type female chickens subjected to dietary restriction during the growing period. Poultry Sci. 58: 940-948. Burgener, J. A., J. A. Cherry, and P. B. Siegel, 1981. Sartorial fat as a predictor of fat deposition in meat-type chickens. Poultry Sci. 60: 54-62. Faust, I. M., P. R. Johnson, J. S. Stern, and J. Hirsch, 1978. Diet-induced adipocyte number increase in adult rats: A new model of obesity. Am. J. Physiol. 235:E279-E286. Gyles, N. R., A. Maeza, and T. L. Goodwin, 1982. Regression of abdominal fat in broilers on abdominal fat in spent parents. Poultry Sci. 61: 1809-1814. Hager, A., L. Sjostrom, B. Arvidsson, P. Bjorntorp, and U. Smith, 1977. Body fat and adipose tissue cellularity in infants: A longitudinal study. Metab. Clin. Exp. 26:607-614.

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Age SE

0

6

x

0>

~

CELL NUMBER

108

CHERRY ET AL.

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