Conjugated linoleic acid evokes de-lipidation through the regulation of genes controlling lipid metabolism in adipose and liver tissue.

Conjugated linoleic acid (CLA) is a unique lipid that elicits dramatic reductions in adiposity in several animal models when included at < or = 1% of the diet. Despite a flurry of investigations, the precise mechanisms by which conjugated linoleic acid elicits its dramatic effects in adipose tissue and liver are still largely unknown. In vivo and in vitro analyses of physiological modifications imparted by conjugated linoleic acid on protein and gene expression suggest that conjugated linoleic acid exerts its de-lipidating effects by modulating energy expenditure, apoptosis, fatty acid oxidation, lipolysis, stromal vascular cell differentiation and lipogenesis. The purpose of this review shall be to examine the recent advances and insights into conjugated linoleic acid's effects on obesity and lipid metabolism, specifically focused on changes in gene expression and physiology of liver and adipose tissue.

Single-trait and antagonistic index selection for litter size and body weight in mice.

INDIVIDUAL SELECTION BASED ON FEMALE PERFORMANCE ONLY WAS CONDUCTED IN FOUR LINES OF MICE: L(+) for increased litter size, W(+) for increased 6-week body weight, L(-)W(+) for a selection index aimed at decreasing litter size and increasing 6-week body weight and L(+)W(-) for a selection index aimed at increasing litter size and decreasing 6-week body weight. A fifth line (K) served as an unselected control. All litters were standardized to eight mice at one day of age. Expected heritability was based on twice the regression of offspring on dam (h(2) (d)), which contains additive genetic variance due to direct (sigma(2) (A(o) )) and maternal (sigma(2) (A(m) )) effects and their covariance (sigma(A(o)A(m) )). Responses and correlated responses were measured either deviated (method 1) or not deviated (method 2) from the control line. Realized heritabilities (h(2) (R)) for litter size were 0.19 +/- 0.04 (1) and 0.16 +/- 0.03 (2), which were similar to h( 2) (d) of 0.17 +/- 0.04. The h(2) ( R) for 6-week body weight of 0.55 +/- 0.07 (1) and 0.44 +/- 0.07 (2) agreed with h(2) (d) of 0.42 +/- 0.02. Realized genetic correlations (r*(G(R) )) between litter size and 6-week body weight calculated from the double-selection experiment were 0.52 +/- 0.10 (1) and 0.52 +/- 0.13 (2), which were not significantly different from the base population estimate of r*( G(d) ) = 0.63 +/- 0.14. Divergence (L(-)W( +) minus L(+)W(-)) in the antagonistic index selection lines was 0.21 +/- 0.01 index units (I = 0.305 P(W) - 0.436 P(L), where P( W) and P(L) are the phenotypic values for 6-week body weight and litter size, respectively.). The h(2) ( R) of index units of 0.14 +/- 0.02 calculated from divergence agreed with h(2) (d) of 0.14 +/- 0.04. Divergences in litter size (-0.19 +/- 0.07) and 6-week body weight (0.46 +/- 0.10) were in the expected direction. Antagonistic index selection yielded about one-half the expected divergence in litter size, while divergence in 6-week body weight was only slightly less than expected. Realized genetic correlations indicated that litter size, 6-week body weight and index units each showed positive pleiotropy with 3-week body weight, postweaning gain and weight at vaginal introitus and negative pleiotropy with age at vaginal introitus. Sex ratio and several components of fitness (days from joining to parturition, percent fertile matings and percent perinatal survival) did not change significantly in the selected lines.

Population size and selection intensity effects on long-term selection response in mice.

Long-term response to within full-sib family selection for increased postweaning gain was evaluated in lines having different effective population sized (Ne) and selection intensities (i). Line designations were I4(4), I8(2), I16(2), M4(4), M8(2) and M16(2), where I and M indicate selection of the top 50% and 25%, respectively; 4, 8 and 16 represent the number of parental pairs per replicate and number of replicates is given in parentheses. Realized within full-sib family heritabilities (hR-2) in the first phase of selection (0-14 generations) were larger in 16-pair lines than in 4- and 8-pair lines. In the second phase of selection (greater than 14 generations), hR-2 declined significantly (P smaller than .01) in all lines, and only the I16 and M16 lines had hR-2 values significantly (P smaller than .01) greater than zero. Realized genetic correlations involving number born, 12-day litter weight, weaning weight and six-week weight tended to decline in the second phase of selection. The I16, M16 and control (C16) replicates were crossed in all combinations at generation 14. Crosses were then selected within litters for high postweaning gain. The hR-2 values in the crossbred lines were all larger than those in the second selection phase for M16-1. M16-2 and I16-1, but not for I16-2. Within each Ne level, total response was significantly (P smaller than .01) less for I lines compared with M lines. Total response increased as Ne increased, within each level of i. Relatively small differences in realized i values among Ne lines could not account for this result. The difference in total response among the Ne lines at a given selection intensity may be due to inbreeding depression and a combination of interactions involving "drift" and selection. By crossing replicates of the M lines with the C16 control, the effects of inbreeding depression were removed. Inbreeding depression and genetic drift, as defined herein, were equally important in accounting for differences among Ne lines in total response.

Long-term selection response for 12-day litter weight in mice.

Long-term selection for increased 12-day litter weight in two replicate lines (W(2), W(3)) of mice resulted in an apparent selection limit at about 17 generations. Quadratic polynomial and exponential models were fitted to the data in order to estimate the plateaued response and half-life of the selection process. Using the polynomial results, the half-life estimates were 4.5 and 8.6 generations for W(2) and W(3), respectively. The plateaued responses were 5.1 and 5.8 g which, when expressed in phenotypic standard deviation units, became 1.1 and 1.3. The exponential model provides similar estimates. A negative association between 12-day litter weight and fitness was not considered to be an adequate explanation for the plateau since there was no decrease in fertility of the selected lines. Evidence that exhaustion of genetic variability was not the cause of the plateau came from the immediate response to reverse selection. It was proposed that the plateau may be due to a negative genetic correlation between direct and maternal genetic effects, which would be expected to occur after many generations of selection. There were positive correlated responses in both replicates for adult body weight, which was in agreement with the positive genetic correlation between preweaning and postweaning body weight. The expected positive correlated response for number born was realized in only one of the replicates.

Genetic analysis of brown adipose tissue, obesity and growth in mice.

The hypothesis developed from single-gene mutant obese rodents that brown adipose tissue (BAT), through its thermogenic ability, is an important factor in the development of obesity, was tested in a randombred population of mice in which degree of adiposity is polygenically determined. Additive direct genetic parameters for measures of body size, lean, fatness and BAT at 6 wk of age were estimated under control and high-fat postweaning dietary regimens. Heritabilities were generally similar for the two diets. However, the lipid-free dry (LFD) component of BAT had a heritability estimate of 0.70 +/- 0.26 on the control diet, but only 0.09 +/- 0.20 on the high-fat diet. For all traits, genotype by diet interactions indicated that additive direct genetic rankings were not significantly different for the two diets. Based on estimates of genetic parameters in the control diet, selection for 6-wk body weight or 3- to 6-wk gain is expected to increase body size and adiposity. Selection for BAT weight is predicted to result in large, lean individuals. However, selection for the LFD content of BAT, generally believed to be a better indicator of thermogenic ability, is predicted to increase fatness as well as body size. Selection for LFD as a proportion of 6-wk body weight reduced the expected correlated response in fatness. It was concluded that BAT does not play a major role in determining the correlated response in obesity that is often found in populations selected for large body size.

Correlated responses in male reproductive traits in mice selected for litter size and body weight.

Correlated responses in male reproductive traits were determined at 4, 6 and 8 weeks of age in lines of mice selected for large litter size (L+), large 6-week body weight (W+), large litter size and small body weight (L+W-) and small litter size and large body weight (L-W+), and in an unselected control (K). Concentration of serum testosterone and weights of testes, seminal vesicles, epididymides and adrenal glands increased with age. Line differences in testosterone concentration were not detected. L+ and W+ males exhibited positive correlated responses in testes, epididymides and seminal vesicle weights. Testis weight adjusted for body weight was significantly larger for L+ than controls and approached significance for W+. Realized genetic correlation be-testis weight and litter size was 0.60 +/- 0.04, and the realized partial genetic correlation holding body weight constant was 0.42. Therefore, pleiotropic loci, acting via the hypothalamic-pituitary axis, affect testis weight and litter size independently of body weight. Additionally, genes influencing overall growth have a pleiotropic effect on testis weight and litter size in mice; the realized genetic correlations of body weight with testis weight and with litter size were 0.60 +/- 0.03 and 0.52 +/- 0.10. Testis weight increased in both L+W- and L-W+ males. The positive correlated response in L+W- may have resulted from changes in frequency of genes controlling reproductive processes; whereas, in L-W+ it could have been the result of changes in the frequency of genes associated with body weight.

Partitioning average and heterotic components of direct and maternal genetic effects on growth in mice using crossfostering techniques.

Crossfostering was performed using lines selected for increased 6-week body weight (H6) and increased 3-to 6-week postweaning gain (M16) and their reciprocal F1 crosses as nurse dams in the selected crossfostering group, and base population controls (C2, ICR) and their reciprocal F1 crosses in the control group. The offspring suckled were H6, M16 and F2 crosses in the selected group, and C2, ICR and their F2 crosses in the control group. Measurements taken on the individual offspring were body weights at birth (WB) and at 12, 21, 31, 42, and 63 days (W12, W21, W31, W42 and W63, respectively) and weight gains between adjacent ages (GB-12, G12-21, G21-31, G31-42 and G42-63, respectively). Least squares constants fitted to populations of genetic and nurse dams were used to calculate specific linear contrasts. Correlated responses to selection in average direct genetic effects were significant and positive for all traits examined in both H6 and M16, while the correlated responses in average maternal genetic effects were negative in M16 and negligible in H6. Selection response was primarily due to average direct genetic effects while the contribution of average maternal genetic effects was of secondary importance. The response in average direct genetic effects was smaller in M16 for postweaning weights (W31, W42 and W63). The correlated responses in average maternal genetic effects were consistently smaller in M16 than in H6. Direct heterosis was significant for all traits except for G12-21 and G42-63 in the control group, whereas maternal heterosis was significant for weight gains at early ages and for body weights. Direct heterosis tended to be larger than maternal heterosis in both selected and control crosses. Percent direct heterosis for body weight was larger in the selected crosses relative to the control crosses through 31 days of age, but the trend was reversed by 63 days. Percent maternal heterosis was consistently larger in the selected crosses.

Selection for nursing ability and adult weight in mice.

Three selection treatments were conducted for 12 generations in each of two base populations (P and Q): (1) increased nursing ability of the mother (n12), as measured by mean 12-day weight of eight young within a crossfostering set (M(P) and M(Q) lines), (2) increased adult (42-day) body weight of the offspring (w42) (W(P) and W( Q) lines), and (3) performance combining the two traits (n12 and w42) into a selection index (B(P) and B(Q) lines). Lines C( P) and C(Q) were maintained as unselected controls in each population. In each line-generation subclass, 92 single-pair matings were made and the offspring assigned to balanced crossfostering sets of four dams each. Regression coefficients of mean performance (in grams) on generations were 0.080 +/-0.029 and 0.054 +/- 0.031 for n12 in M(P) and M(Q), and 0.680 +/- 0.039 and 0.868 +/- 0.051 for w42 in W(P) and W(Q), respectively. The B(P) and B(Q) lines showed genetic gains in n12 (0.090 and 0.053, respectively) and w42 (0.576 and 0.696) intermediate between the performance of M(P) and W(P), and M(Q) and W(Q), respectively, except for n12 of B(Q). Realized heritabilities for n12 were 0.16 +/- 0.05 and 0.11 +/- 0.06 and those for w42 were 0.40 +/- 0.02 and 0.43 +/- 0.03 for P and Q, respectively. The realized genetic correlations between n12 and w42 were 0.70 +/- 0.07 and 0.73 +/- 0.08 in P and Q, respectively. The ratios of the predicted to observed responses in M(P), B(P) and B(Q) were 0.99, 1.03 and 0.89, respectively. However, the predicted and observed responses differed in M( Q), W(P) and W(Q); the ratios were 1.29, 0.65 and 0.65, respectively. The observed combined responses for n12 and w42 in the index lines (B(P) and B(Q)) were smaller than the optimum expected from index selection. A possible cause was that the estimated genetic correlations (0.22 +/- 0.16 and -0.17 +/- 0.16 for B(P) and B( Q), respectively) and heritabilities (0.39 +/- 0.03 and 0.28 +/- 0.02, respectively) for w42 that were used to construct the selection index were smaller than the respective realized parameters.

Effects of population size and selection intensity of short-term response to selection for postweaning gain in mice.

The effects of population size and selection intensity on the mean response was examined after 14 generations of within full-sib family selection for postweaning gain in mice. Population sizes of 1, 2, 4, 8 and 16 pair matings were each evaluated at selection intensities of 100% (control), 50% and 25% in a replicated experiment. Selection response per generation increased as selection intensity increased. Selection response and realized heritability tended to increase with increasing population size. Replicate variability in realized heritability was large at population sizes of 1, 2 and 4 pairs. Genetic drift was implicated as the primary factor causing the reduced response and lowered repeatability at the smaller population sizes. Lines with intended effective population sizes of 62 yielded larger selection responses per unit selection differential than lines with effective population sizes of 30 or less.

Effects of population size and selection intensity on correlated responses to selection for postweaning gain in mice.

Correlated responses to selection for postweaning gain in mice were studied to determine the influence of population size and selection intensity. Correlated traits measured were three-, six- and eight-week body weights, litter size, twelve-day litter weight, proportion infertile matings and two indexes of reproductive performance. In general, the results agreed with observations made on direct response: correlated responses in the body weight traits and litter size increased as (1) selection intensity increased and (2) effective population size increased. Correlated responses in the body weight traits and litter size were positive in the large population size lines (16 pairs), as expected from the positive genetic correlation between these traits and postweaning gain. However, several negative correlated responses were observed at small population sizes (one and two pairs). Within each level of selection intensity, traits generally associated with fitness tended to decline most in the very small populations (one and two pairs) and in the large populations (16 pairs) for apparently different reasons. The fitness decline at the small effective population sizes was attributable to inbreeding depression. In contrast, it was postulated that the fitness decline at the large effective population size was due to selection moving the population mean for body weight and a trait positively correlated genetically with body weight (i.e., percent body fat) away from an optimum.

An experimental evaluation of genetic correlation.

Heritability and genetic correlations realized from both single-trait and antagonistic index selection were compared with paternal half-sib estimates. Primary attention was focused on the genetic correlation between six-week body weight and six-week tail length. Parameters realized from single-trait selection were in excellent agreement with paternal half-sib estimates. However, the realized genetic correlation between six-week body weight and six-week tail length obtained from index selection was significantly greater than the other estimates. Differential inbreeding levels and realized selection intensities were considered and rejected as being causative factors for these results. Linkage disequilibrium probably was not a factor either, as the base population had been randomly mated and randomly selected with a large effective population size for many generations. It was concluded that with antagonistic index selection, the pleiotropic effects of genes may be more powerful in retarding response in aggregate genotype than current theory would suggest. Replication of all selected and control lines allowed the use of between-line estimators of sampling variances of realized genetic parameters in the above comparisons. Generally, standard errors of realized genetic parameters were much smaller than corresponding paternal half-sib standard errors. Thus, selection was an efficient method of estimation.

The impact of maternal uterine genotype on postnatal growth and adult body size in mice.

Embryo transfers were used to demonstrate that the genotype of the mother providing the uterine developmental environment significantly influences postnatal growth and adult body size of her progeny. Irrespective of their own genotype, mouse embryos transferred into the uterus of an inbred strain with large body size (C3H) had greater body weights, longer tails and higher growth rates than those transferred into the uterus of a strain with small body size (SWR). Uterine heterosis on body size was smaller than progeny heterosis, and both progeny and uterine heterosis persisted in adult mice. Uterine litter size was significantly negatively associated with body weight, tail length, growth rate and the timing of developmental events. The inbred SWR strain was more sensitive to the embryo transfer procedure than the C3H strain, but effects due to embryo transfer were moderate. Prenatal uterine effects have ramifications for biotechnologies utilizing embryo transfer as well as predictions about evolutionary change by selection.

Pleiotropy of quantitative trait loci for organ weights and limb bone lengths in mice.

We investigated the genetic basis of several limb bone lengths and weights of organs in mice produced from a cross of the F1 between CAST/Ei (wild strain) and M16i (selected for rapid growth rate) back to M16i. From previous correlation studies, we hypothesized that quantitative trait loci (QTLs) would exhibit greater pleiotropy within than between the limb length and organ weight character sets. Using interval mapping procedures and significance testing at the chromosome-wise level, we discovered 14 putative QTLs affecting weight of the liver, spleen, heart, and/or kidney, 9 of which affected more than one organ; and 12 QTLs for limb lengths, all of which affected the length of two or more of the limb bones in these mice. As was hypothesized, most QTLs affected either organ weights or limb lengths independently of each other, although five QTLs were found that affected both sets of characters. The direction of the effect of these QTLs was almost always consistent within and between characters, with little evidence for antagonistic pleiotropy.

Differential effects of fat and sucrose on body composition in A/J and C57BL/6 mice.

The C57BL/6 (B6) mouse is more sensitive to the effects of a high-fat diet than the A/J strain. The B6 mouse develops severe obesity, hyperglycemia, and hyperinsulinemia when fed this dietary regimen. This study was conducted to determine the effects of dietary fat and sucrose concentrations on body composition and intestinal sucrase (EC 3.2.1.48) and maltase (EC 3.2.1.20) activity in these two mouse strains. High-fat diets, regardless of sucrose content, resulted in significant weight gain, higher body fat, and lower body protein and water content in both strains of mice. The shift toward higher body fat and lower protein and water content was far greater in the B6 strain. Low-fat, high-sucrose diets resulted in lower body weight in both strains, as well as significantly greater body protein content in B6 mice. Analysis of intestinal sucrase showed that the enzyme was less active in B6 mice when the diet was high in sucrose. Both sucrase and maltase had lower activity in the presence of high dietary fat in both mouse strains. The percent reduction of intestinal enzyme activity due to dietary fat was similar in both strains. The B6 mouse exhibits disproportionate weight gain and altered body composition on a high-fat diet. This coupled with the reduced body weight and increased body protein on a low-fat, high-sucrose diet suggests that factors-relative to fat metabolism rather than sucrose metabolism are responsible for obesity.

Factors influencing maternal behavior in the hubb/hubb mutant mouse.

We examined the maternal behavior of hubb/hubb mutant mice and normal control (+/hubb) siblings. From previous observations we noted that mutants groom their pups less, suckle less than normal, and often cannibalize the young. To date, these observations had not been quantified. Although prolactin (PRL) is linked to maternal behavior, it was difficult to measure because of the hyperirratibility of the mutant mice. Consequently, dopamine (DA) and its metabolite, dihydroxyphenylacetic acid (DOPAC), were measured in the median eminence in brains of both normal and mutant mice. Tyrosine hydroxylase, the rate-determining step in dopamine synthesis, was localized in the brain by immunohistochemistry. Five mutant and nine normal dams were observed for pup retrieval and crouching. Mean time for pup retrieval was slower (p < 0.06) for mutants (28.09 s) than for normal dams (18.49 s). Crouching was the same for both strains. Mutant pups were cold to the touch, and not well groomed. Brains from both strains were examined at Day 11 and Day 18 of gestation and Day 2 and Day 11 of lactation. Qualitatively, tyrosine hydroxylase localization in the arcuate nucleus and median eminence was the same in both strains for the gestation samples. The decrease in staining observed from gestation to lactation in the normal mice was increased in the mutants. Dopamine was similar in both strains at all stages, but DOPAC was significantly higher at early lactation in the mutants. We do not assume an absolute inverse relationship between dopaminergic activities and prolactin, but it is likely that the increase in DOPAC in the mutant reflects a decrease in prolactin, which could contribute to the diminished maternal care in the mutants.

Ascorbic acid decreases heat shock protein 70 and plasma corticosterone response in broilers (Gallus gallus domesticus) subjected to cyclic heat stress.

It is known that ascorbic acid (AA) supplementation can ameliorate the chicken's responses to heat stress. The influence of AA on heart heat shock protein 70 (hsp70) and plasma corticosterone (CS) was evaluated in young male broiler chickens fed either no AA (N-AA) or 500 mg AA /kg (AA) and exposed to cyclic high temperatures (21 to 30 to 21 degrees C) over a 3.5 h period on three consecutive days. Dietary AA supplementation elevated plasma AA and maintained it at high levels after heating, but in N-AA birds, only heat elevated plasma AA. In N-AA fed chickens, plasma CS was elevated and was further increased by heat stress as compared with AA-fed birds. Heart hsp70 expression was greater in N-AA-fed chickens compared to AA-fed chickens, and heat stress further elevated hsp70 in both N-AA- and AA-fed birds. The hsp70 increase after heat was two-fold greater in N-AA- vs. AA-fed birds. Plasma CS and heart hsp70 were positively correlated, plasma AA and heart hsp70 were negatively correlated, and plasma CS and AA were negatively correlated. It was concluded that chickens experience a less severe stress response after exposure to high temperatures when they are provided dietary AA.

Effects of consuming endophyte-infected tall fescue on growth, reproduction and lactation in mice selected for high fecundity.

Effects of a diet containing endophyte-infected tall fescue seed (83% infected) were investigated using 2 lines of mice, one line selected for fecundity (L(+)) and the other a randomly selected control line (K). Treatments included a commercial stock diet (C), 50% stock plus 50% non-infected tall fescue seed (N), and 50% stock plus 50% infected tall fescue seed (I). The experiment was conducted using mice on respective treatments in 2 phases (successive generations), with 15 to 23 mated females per line and diet subgroups. Mated females of Phase 1 were assigned at random within line to experimental diets which were fed during gestation and through 21 d of lactation. Litters were standardized to 10 pups 1 d after birth. Stock diets were fed to all groups from Day 21 to weaning on Day 28. Weaned male and female pups were allotted to previous diets. Mated females in Phase 2 were managed as in Phase 1 through weaning at 28 d. Diets of males did not affect reproduction and data were pooled within female diets. Selected (L(+)) dams gave birth to more live pups than K dams (P<0.05) during both phases (+3.4 and +2.8 +/- 0.4 pups, respectively). Diet but not line affected littering rate of mated females in Phase 1 (71.3%, I; < 87.1%, C or 93.0%, N; P<0.05) and Phase 2 (82.1%, I < 93.8%, N or 97.1%, C; P<0.05). Diet had no effect on fecundity during Phase 1 but females on I diet had reduced (P<0.05) litter size by 1.9 and 3.2 +/- 0.5 pups compared with the females on N and C diets, respectively, in Phase 2. Feed consumption and weights of dams during lactation generally ranked C>N>I. Growth of pups during both phases also ranked C>N>I. Vaginal opening at 28 d differed by line (71.4%, K < 89.3%, L(+), P<0.05) and diet (56.8%, I < 92.0%, C or 92.2%, N, P<0.05). These results suggest both acute and chronic effects of consumption of endophyte-infected diets. Absence of line-by-diet interactions demonstrates that adverse effects were unrelated to genetic differences between lines.

Effects of selection for rapid postweaning gain on maturing patterns of fat depots in mice.

Correlated responses to selection for rapid 3 to 6-wk postweaning gain in male mice were estimated for five fat depots weighed at specific degrees of maturity in body weight (37.5, 50.0, 62.5, 75, 87.5 and 100%). Fat pads measured were from regions of the subcutaneous hindlimb, subcutaneous forelimb, epididymides, mesentery and kidneys. At the same degree of maturity, selected mice (M16) were older (P less than .01) than controls (ICR). M16 had heavier (P less than .01) fat depots than ICR for all sites at each degree of maturity. From 62.5 to 100% maturity, M16 was larger than ICR in fat depot weight as a percentage of body weight at all sites. Mesenteric fat made up the largest percentage of total fat in both lines and perirenal fat the smallest percentage. Development of degree of maturity in each fat depot relative to degree of maturity in body weight was studied using the constrained quadratic and standardized allometric models. Both models showed similar trends, but the latter identified more significant line differences. The standardized allometric analysis indicated that total fat and all individual fat depots except mesenteric fat matured at a slower rate (P less than .01) in M16 than in ICR. Bivariate allometric analyses of ln fat depot weight on ln body weight showed that M16 exceeded (P less than .01) ICR in relative growth of all fat depots except mesenteric fat; at lower body weights, ICR had larger fat depots than M16, but the reverse was true at higher body weights.(ABSTRACT TRUNCATED AT 250 WORDS)

Estimates of genetic parameters and predicted selection responses for growth, fat and lean traits in mice.

Heritabilities (h2) and genetic correlations (rG) were estimated by regression of offspring on sire in two replicate, unselected lines of mice. Traits were associated with growth, feed efficiency, fat deposition and lean tissue. The h2 for growth traits ranged from .34 to .42, except for 3-wk body weight, which was only .05. The h2 for feed efficiency was .28. Ranges in h2 were .45 to .50 for fat deposition traits and .36 to .42 for lean tissue traits. The rG involving 3-wk to 6-wk feed efficiency with hind carcass and fat measurements at 12 wk were small. Antagonisms were found between the sign of rG and the direction of usual breeding goals for pairs of traits (e.g., rG greater than 0 between fat deposition and hind carcass weight and rG less than 0 between hind carcass as a percentage of body weight and body weight). Selection indexes were developed to counteract these antagonisms. Modified selection indexes were compared where responses in individual traits rather than the aggregate breeding value were of major importance. The aggregate breeding values and selection indexes included: 1) epididymal fat pad weight and body weight, 2) hind carcass weight and body weight, or 3) all three traits. Economic weights in retrospect were calculated for the modified selection indexes. In some cases, expected correlated responses in component traits were not influenced greatly over a wide range of ratios of economic weights, but in other cases the component traits changed sharply over a narrow range of ratios.

Direct and maternal genetic differences between lines of mice selected for body weight and litter size: traits of dams.

Genetic differences in performance of dams were estimated by linear contrasts using means of two selected lines of mice and reciprocal F1's, F2's and backcrosses. The lines were selected for increased 6-wk body weight (W) or increased litter size (L). Genetic differences estimated were direct average (gD), direct heterosis (hD), maternal average (gM), progeny average (gP), and progeny heterosis (hP). For dam weight and feed consumption from 12 to 21 d postpartum (pp), gD was the largest genetic difference and favored line W. For litter size, litter weight at birth, litter efficiency (litter weight gain/dam feed consumption) from birth to 12 d pp and within litter mortality from 1 to 21 d pp, gD favored L and, except for hD in litter efficiency, was the most important genetic difference for these traits. Direct heterosis was the only significant difference for litter weight at 21 d pp, litter efficiency from 12 to 21 d pp and within litter mortality at parturition. The gM were larger in W than in L for dam weight and feed consumption, and for litter size and weight at birth, but they were usually of smaller magnitude than gD. The gP were significant only in litter traits measured before 12 d pp and favored W. For no trait measured was hP of consequence. Line differences in dam and litter weight accounted for genetic differences in dam feed consumption. Genetic differences in litter size at birth were not due to line differences in dam weight. The lower mortality within litters nursed by crossbred dams was responsible for hD on litter weight and litter efficiency. Within but not among lines, higher mortality rates were associated with larger litters.