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The Journal of Nutrition Vol. 127 No. 7 July 1997, pp. 1344-1348
Copyright ©1997 by the American Society for Nutritional Sciences

Genetic Variation in Cholesterol Absorption Efficiency among Inbred Strains of Mice1,2,3

Christopher P. Carter, Philip N. Howles, and David Y. Hui4

Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267

ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
FOOTNOTES
LITERATURE CITED

ABSTRACT

The initial study utilized the outbred Black Swiss, the inbred 129/SvEv and their hybrid mice to test for possible genetic difference in cholesterol absorption efficiency. Female mice (10-12 wk old) were fed a lipid test meal containing [3H]cholesterol and beta -[14C]sitosterol by stomach tube. The amount of [3H]cholesterol excreted in the feces was determined as nonabsorbed cholesterol and was normalized based on the recovery of the nonabsorbable beta -[14C]sitosterol. The Black Swiss mice absorbed significantly less cholesterol than the 129/SvEv mice within a 24-h period. Cholesterol absorption efficiency of the hybrid mice varied widely and did not segregate with either parental group. Differences in cholesterol absorption efficiency were also observed among six different inbred strains of mice fed either a basal low fat diet or a high fat/high cholesterol diet for 3 wk. Cholesterol absorption efficiency did not differ among DBA/2, C57BL/6, C3H/He, BALB/c and AKR/J mice under basal dietary conditions. However, cholesterol absorption was significantly lower in the DBA/2 mice than in C57BL/6 and C3H/He mice after mice were fed a high fat/high cholesterol diet. Cholesterol absorption by the C57L/J mice did not differ from that of C57BL/6, C3H/He, BALB/c and AKR/J mice under basal diet conditions, but was significantly lower when mice were fed a high fat/high cholesterol diet. Cholesterol absorption efficiency differed between DBA/2 and C57L/J mice under both dietary conditions. These results suggest that cholesterol absorption is controlled by multiple genetic factors.

KEY WORDS: cholesterol · mice · genetics · absorption · diet

INTRODUCTION

Epidemiological studies have documented a direct relationship between high plasma cholesterol concentration and the premature development of atherosclerosis. The cholesterol in circulation is derived from the diet by absorption through the intestine and from endogenous synthesis, primarily by the liver. Although many earlier studies showed a direct correlation between dietary and plasma cholesterol (Beynen et al. 1987), this correlation was demonstrated using mean plasma cholesterol concentrations of groups of individuals fed various diets. However, great variations in plasma cholesterol concentration exist within each group of individuals with a similar dietary cholesterol intake (reviewed by Beynen et al. 1987). These individual variations in susceptibility to diet-induced hypercholesterolemia were observed in many species including humans (McNamara et al. 1987, Safonova et al. 1993), primates (Bhattacharyya and Eggen 1988, Bhattacharyya et al. 1989), rabbits (Overturf et al. 1990), dogs (Mahley et al. 1974), and rodents (Aubert et al. 1988, Kirk et al. 1995, Paigen 1995).

Individual differences in plasma cholesterol response to dietary manipulations may be attributed to the large number of genes required for maintenance of plasma cholesterol homeostasis. (Lusis 1988, Lusis et al. 1987, Sing and Davignon 1993). Differences in susceptibility to diet-regulated expression of these genes may also contribute to individual variations in plasma cholesterol concentration among individuals fed a similar diet. For example, genetic differences in diet-regulated expression of genes for the LDL receptor (Dueland et al. 1993, Spady and Cuthbert 1992), hydroxy-methylglutaryl coenzyme A reductase (Clarke et al. 1983, Hwa et al. 1992) and various apolipoproteins (Chan and Dresel 1990, Grundy and Denke 1990, Spady et al. 1993) are well documented in animals and humans. The effects of fat and a cholesterol-rich diet on expression of lipolytic enzymes and lipid transfer proteins have also been demonstrated (Brodt-Eppley and Hui 1994, Jiang and Bruce 1995, Jiang et al. 1992, Rose and Juliano 1979). However, relatively little attention has been paid to the mechanism of dietary cholesterol absorption and whether individual differences in cholesterol absorption efficiency may account for some of the differences in plasma cholesterol response to specific diets. In view of the observation that up to 60% of daily body cholesterol input is derived from the diet instead of by endogenous biosynthesis (Dietschy and Wilson 1970), it is important to determine the mechanism of cholesterol absorption and establish whether differences in cholesterol absorption efficiency can account for individual variation in diet-induced hypercholesterolemia.

A recent study by Overturf et al. (1990) showed that variations in cholesterol absorption efficiency could account for differences between hypo- and hyperresponding rabbits after rabbits were fed a cholesterol-rich diet. Moreover, Safonova et al. (1993) used human intestinal biopsy samples to show that cholesterol uptake by the intestine could be divided into three groups with low, medium and high rates of cholesterol transport. Taken together, these studies suggest that cholesterol absorption may be regulated by specific gene(s). The purpose of this study was to use inbred mice to determine if genetic factors contribute to dietary cholesterol absorption efficiency. The mouse is an ideal model for studying diet-gene interactions because its genetics are well characterized and differences in dietary cholesterol responsiveness among the various inbred strains have been documented (Kirk et al. 1995, Paigen 1995). Results of the current study extend this information to additional inbred strains and further support the hypothesis that cholesterol absorption is controlled by specific gene(s).

MATERIALS AND METHODS

Animals and diets. Black Swiss and 129/SvEv mice were obtained from Taconic Farms (Germantown, NY). The BALB/c, C57BL/6, C3H/He and DBA/2 mice were purchased from Harlan Bioproducts (Indianapolis, IN), and AKR/J and C57L/J mice were obtained from The Jackson Laboratories (Bar Harbor, ME). The (Black Swiss × 129)F2 mice were generated in our institutional facility by the procedure described previously (Howles et al. 1996). Briefly, male chimeric mice derived from cholesterol esterase gene-targeted embryonic stem cells, with a 129/SvEv genetic background, were mated with female Black Swiss mice. Heterozygotes from different parents were mated to produce the (Black Swiss × 129)F2 mice. Animals with the normal cholesterol esterase genotype were selected for the current study. The mice were housed at our facility in a temperature- and humidity-controlled room with a 12-h light:dark cycle for at least 7 d before experiments. Female mice between the ages of 10 and 12 wk were used for all experiments. The mice were fed either the basal nonpurified diet (Teklad LM485, Madison, WI) containing 5.7 g/100 g fat and no cholesterol, or a high fat/high cholesterol nonpurified diet (Purina Mouse Chow 5015 supplemented with 7.5 g/100 g cocoa butter and 1.25 g/100 g cholesterol to yield final concentrations of 15.8 g/100 g fat and 1.25 g/100 g cholesterol; Purina, St. Louis, MO). Mice were fed the high fat/high cholesterol diet for at least 3 wk before analysis. All experimental protocols described in the text were reviewed and approved by the Institutional Animal Care and Use Committee of the University of Cincinnati, in compliance with the National Institutes of Health guidelines (NRC 1985).

Cholesterol absorption studies. Female mice (10-12 wk old) fed either the basal diet or the high fat/high cholesterol diet were used to measure cholesterol absorption efficiency. The mice were transferred to metabolic cages at least 24 h before beginning the experiments to measure cholesterol absorption. On the day of the experiments, each mouse received, by stomach gavage, a bolus test meal of 50 µL of an emulsified test meal containing 1.3 GBq/L [3H]cholesterol (1.85 TBq/mmol, DuPont NEN, Boston, MA), 260 MBq/L beta -[14C] sitosterol (2 TBq/mmol, Amersham Life Science, Arlington Heights, IL), 2 g/L cholesterol, 8 g/L egg phosphatidylcholine and 50 g/L triolein. The trace amount of the nonabsorbable sterol beta -[14C]sitosterol was included in the test meal to normalize for recovery of the nonabsorbed radiolabeled sterols in the feces. The mice were returned to the metabolic cages where they had free access to their original diet and water. Feces were collected for 24 h after administration of the test meal. The samples were homogenized in water and then extracted with an equal volume of chloroform/methanol (2:1, v/v). An aliquot of the organic phase from each sample was used for scintillation counting to determine the amount of the radioactive sterols excreted in the feces. Counting efficiency was calculated by the channel ratio method based on external standards. The efficiency of cholesterol absorption was reported as a percentage of administered dose absorbed using the formula as described by Grundy et al. (1968) as follows: {1-[(3H-Bq/14C-Bq) in feces]/[(3H-Bq/14C-Bq) administered]} × 100.

Serum cholesterol analysis. Blood samples were collected from individual mice by severing the inferior vena cava after killing by CO2 asphyxiation. Sera were isolated after clotting of the blood samples and tested individually for total cholesterol after hydrolysis of the cholesteryl esters and oxidation of the free cholesterol to hydrogen peroxide, using the cholesterol C II colorimetric assay kit (catalog no. 276-64909) from Wako Chemicals (Richmond, VA).

Statistical analyses. Cholesterol absorption efficiency in Black Swiss mice and 129/SvEv mice was compared by Student's t test. Differences in cholesterol absorption efficiency and serum cholesterol concentration among various inbred strains of mice were evaluated by ANOVA followed by Duncan's post-hoc analysis for significance, using the program by Number Cruncher Statistical System, Version 5.03 (Kaysville, UT).

RESULTS

Differences between Black Swiss and 129/SvEv mice. The initial study compared cholesterol absorption efficiency in 10 Black Swiss mice with that observed in 10 129/SvEv mice fed a low fat, low cholesterol basal diet. Although cholesterol absorption efficiency in the Black Swiss mice was found to vary over a wide range, from 34 to 77% (Table 1), this variation was not observed in the 129/SvEv mice. Because Black Swiss is an outbred mouse line and 129/SvEv is an inbred strain, the difference in cholesterol absorption detected in these mice suggested that the efficiency of cholesterol absorption may be controlled by genetic factors. The potential for genetic differences in cholesterol absorption was further explored by examining cholesterol absorption efficiency in the (Black Swiss × 129)F2 mice. These hybrid mice displayed a cholesterol absorption efficiency ranging from 57 to 87% (data not shown). The identification of hybrid mice with more efficient cholesterol absorption than those observed in either parental strain suggests that cholesterol absorption may be controlled by more than one gene.

Table 1. Cholesterol absorption efficiency of Black Swiss and 129/SvEv mice fed a basal low fat/low cholesterol diet1

[View Table]

Studies with C57BL/6, C3H/He, BALB/c, DBA/2, AKR/J and C57L/J mice. The possible involvement of genetic factors in mediating dietary cholesterol absorption efficiency was further explored by expanding the study to six different inbred strains of mice. The mice absorbed cholesterol efficiently when fed the basal diet, with 65-76% of the [3H]cholesterol absorbed after 24 h (Fig. 1). No significant difference in cholesterol absorption efficiency was observed among the groups except that the efficiency of the DBA/2 mice was greater than that of the C57L/J mice (P < 0.05).
Fig. 1. Cholesterol absorption efficiency of inbred mice fed a basal diet. Six female mice from each strain of inbred mice were fed a basal nonpurified diet containing 5.7 g/100 g fat and no cholesterol for 3 wk. The mice were then fed 50 µL of an emulsified test meal containing 1.3 GBq/L [3H]cholesterol, 260 MBq/L beta -[14C]sitosterol, 2 g/L cholesterol, 8 g/L phosphatidylcholine and 50 g/L triolein. Feces were collected for 24 h. The percentage of cholesterol absorbed was calculated by the formula: 100 × {1 - [(3H/14C)excreted/(3H/14C)administered]}. Values are means ± SEM, n = 6. Values with different letters are significantly different at P < 0.05.
[View Larger Version of this Image (57K GIF file)]

Cholesterol absorption efficiency was quite different in mice fed a high fat/high cholesterol diet for 3 wk. The percentage of the [3H]cholesterol absorbed through the intestine was reduced from 65-76% to 11-31.8% (Fig. 2). In addition, strain-specific differences in cholesterol absorption efficiency were different than those observed when the mice were fed a low fat/low cholesterol diet. For example, under high fat/high cholesterol dietary conditions, the cholesterol absorption efficiency of the C57L/J mice was significantly less than that observed in all other strains (P < 0.01). Cholesterol absorption efficiency in the DBA/2 mice was not different than that in the BALB/c and AKR/J mice, but was lower than that observed in either the C57BL/6 or the C3H/He mice (P < 0.05). However, cholesterol absorption efficiency in BALB/c and AKR/J mice was not different than that of the C57BL/6 or the C3H/He mice.

Fig. 2. Cholesterol absorption efficiency of inbred mice fed a high fat/high cholesterol diet. Six female mice from each strain of inbred mice were fed a diet containing 15.8 g/100 g fat and 1.25 g /100 g cholesterol for 3 wk. The mice were then fed 50 µL of an emulsified test meal containing 1.3 GBq/L [3H]cholesterol, 260 MBq/L beta -[14C]sitosterol, 2 g/L cholesterol, 8 g/L phosphatidylcholine, and 50 g/L triolein. Feces were collected for 24 h. The percent of cholesterol absorbed was calculated by the formula: 100 × {1 - [(3H/14C)excreted/(3H/14C)administered]}. Values are means ± SEM, n = 6. Values with different letters are significantly different at P < 0.05.
[View Larger Version of this Image (38K GIF file)]

There was no correlation between cholesterol absorption efficiency and plasma cholesterol concentration in these mice when fed either diet. When mice were fed the basal low fat/low cholesterol diet, the lowest concentration was observed in the C57L/J mice and the highest level observed in the C3H/He mice (Fig. 3). When they were fed the high fat/high cholesterol diet, C57BL/6, C3H/He, BALB/c, AKR/J and C57L/J mice had higher serum cholesterol concentrations than those fed a basal low fat/low cholesterol diet (Fig. 3). In contrast, serum cholesterol level was not significantly different in the DBA/2 mice fed the high fat/high cholesterol diet than in those fed the basal low fat diet (Fig. 3).

Fig. 3. The effects of dietary fat and cholesterol on serum cholesterol concentration in inbred mice. Six female mice from each strain of inbred mice were fed either a basal diet containing 5.7 g/100 g fat and no cholesterol or a high fat/high cholesterol diet with 15.8 g/100 g fat and 1.25 g/100 g cholesterol for 3 wk. Serum was obtained and used for determination of total cholesterol concentration. Values are means ± SEM, n = 6. Values with different letters differed significantly (P < 0.05).
[View Larger Version of this Image (44K GIF file)]

DISCUSSION

The well-defined genetics of inbred strains has made the mouse a popular model for studying the genetic influence on serum cholesterol responsiveness and susceptibility to atherosclerosis as a result of a high fat/high cholesterol diet (reviewed in Paigen 1995). In early studies, Thompson and colleagues examined 13 strains of inbred mice and found substantial interstrain variations in susceptibility to atherosclerosis in response to a high fat/high cholesterol diet (Roberts and Thompson 1976, Thompson 1969). In general, their results showed positive correlations among cholesterol absorption, serum cholesterol level and susceptibility to atherosclerosis. Paigen and co-workers performed similar but more comprehensive studies to relate serum cholesterol responsiveness and susceptibility to atherosclerosis in various inbred mice (reviewed in Ishida and Paigen 1989). They found differences in dietary cholesterol responsiveness in both serum cholesterol concentration and atherosclerotic lesion formation among the various inbred mouse strains. However, the Paigen studies failed to demonstrate a correlation between serum cholesterol level and the severity of atherosclerosis. In fact, strain pairs with high or low cholesterol levels and high or low susceptibility to atherosclerosis in all possible combinations were observed (Paigen et al. 1985). Although these inconsistencies may be interpreted to indicate that no relationship exists between serum cholesterol level and susceptibility to atherosclerosis, it must be noted that none of the mice developed atherosclerosis unless they were fed a high fat/high cholesterol diet. Therefore, the contribution of dietary fat and cholesterol to serum cholesterol concentration and to the development of atherosclerosis cannot be minimized.

A recent study identified one specific strain of mice, namely, DBA/2 mice, as resistant to hypercholesterolemia when fed a diet containing high fat, high cholesterol and sodium cholate (Kirk et al. 1995). This study further demonstrated that the resistance to diet-induced hypercholesterolemia in DBA/2 mice was due to their low rate of cholesterol absorption after consuming this atherogenic diet (Kirk et al. 1995). Based on these results, Kirk et al. (1995) proposed that cholesterol absorption efficiency is controlled by genetic factor(s). They also proposed that variations in the expression of cholesterol absorption genes may in part account for individual differences in plasma cholesterol level in mice fed a high fat/high cholesterol diet. In agreement with the data reported by Kirk et al. (1995), results of the current study also showed that cholesterol absorption efficiency was low in DBA/2 mice after consuming a high fat/high cholesterol diet. An important distinction between the current study and the Kirk study was the type of diet used. The Kirk study used a high fat/high cholesterol diet containing sodium cholate, whereas the high fat/high cholesterol diet used in the current study did not contain any bile salt. Because similar results were obtained in both studies, the low cholesterol absorption efficiency in DBA/2 mice was not due to secondary effects of the bile salt. Dueland et al. (1993) also showed that adding taurocholate to a cholesterol-rich diet had no influence on cholesterol absorption by C57BL/6 and BALB/c mice. Taken together, these results support the hypothesis that cholesterol absorption is controlled by genes in response to fat and/or cholesterol in the diet.

The current study also extended the previous study by Kirk et al. (1995) by examining cholesterol absorption efficiency in additional inbred strains of mice. Our data revealed differences between C57L/J mice and the other inbred strains when they were fed the high fat/high cholesterol diet. Under these dietary conditions, the C57L/J mice absorbed significantly less cholesterol from the diet, yet their serum cholesterol concentration was higher than that of mice fed the low fat/low cholesterol basal diet, similar to serum cholesterol concentrations observed in the other inbred strains. The latter results documented that, although dietary cholesterol absorption may be one variable controlling serum cholesterol level in mice, other metabolic variables are also involved in determining cholesterol homeostasis. For example, differences in serum cholesterol clearance and/or endogenous cholesterol biosynthetic rates may account for the observed differences between the C57L/J and the other inbred strains of mice. Additional metabolic studies will be required to verify this hypothesis.

The survey of six different inbred strains of mice also revealed that the C57L/J mice consistently absorbed less cholesterol than other strains, indicating that cholesterol absorptionefficiency is controlled by at least one gene and that the C57L/J mice are different from the other mice at this locus. Our results also showed that although the DBA/2 mice absorbed dietary cholesterol with efficiency similar to that of the C57BL/6, C3H/He, BALB/c and AKR/J mice when they were fed the basal low fat/low cholesterol diet, the DBA/2 mice had significantly lower cholesterol absorption efficiency than did the C57BL/6 and C3H/He mice when they were fed a high fat/high cholesterol diet. Thus, these results indicated that cholesterol absorption efficiency is a highly regulated process and the regulation may also be controlled by distinct genetic factors. Based on these observations, we postulate that cholesterol absorption efficiency is controlled by at least two distinct genes.

The literature has suggested several candidate genes that may control cholesterol absorption efficiency. For example, it has been suggested that pancreatic cholesterol esterase plays a role in mediating dietary cholesterol absorption (Gallo et al. 1977 and 1984, Lopez-Candales et al. 1993). However, our recent studies with cholesterol esterase gene-knockout mice did not support this hypothesis (Howles et al. 1996). Other proteins that mediate lipid transport and metabolism in the intestine have also been implicated in the cholesterol absorption process. These proteins include the intestinal acyl coenzyme A:acyltransferase (Clark and Tercyak 1984, Krause et al. 1993), pancreatic lipase (Fernandez and Borgstrom 1989), intestinal cholesterol transfer proteins (Lipka et al. 1995, Thurnhofer et al. 1991), and fatty acid binding proteins (Schroeder et al. 1993). However, the physiological importance of these proteins in dietary cholesterol absorption remains unconfirmed. Genetic manipulation, either by transgene expression or gene knockouts, is necessary to test the hypothesis of their involvement. Alternatively, gene locus mapping and positional cloning of specific genes may also be used to confirm the involvement of these and other genes in controlling the efficiency of cholesterol absorption.

FOOTNOTES

1   Presented in part at Experimental Biology 96, April 1996, Washington, DC [Carter, C. P., Howles, P. N. & Hui, D. Y. (1996) Variation in cholesterol absorption among inbred strains of mice. FASEB J. 10: A237 (abs.)].
2   Supported by National Institutes of Health grant RO1 DK40917.
3   The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.
4   To whom correspondence should be addressed.

Manuscript received 23 September 1996. Initial reviews completed 5 November 1996. Revision accepted 28 February 1997.

LITERATURE CITED

0022-3166/97 $3.00 ©1997 American Society for Nutritional Sciences



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