Journal of Nutrition OpenSOurce Diets- www.ResearchDiets.com

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Funkat, A.
Right arrow Articles by Andrikopoulos, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Funkat, A.
Right arrow Articles by Andrikopoulos, S.
© 2004 The American Society for Nutritional Sciences J. Nutr. 134:3264-3269, December 2004

Nutrient-Gene Interactions

Metabolic Adaptations of Three Inbred Strains of Mice (C57BL/6, DBA/2, and 129T2) in Response to a High-Fat Diet1

Alexandra Funkat, Christine M. Massa, Valentina Jovanovska, Joseph Proietto and Sofianos Andrikopoulos2

The University of Melbourne, Department of Medicine, (AH/NH), Heidelberg Repatriation Hospital, Heidelberg Heights, Victoria 3081 Australia

2To whom correspondence should be addressed. E-mail: sof{at}unimelb.edu.au.


   ABSTRACT
TOP
 ABSTRACT
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 LITERATURE CITED
 
Although it is now becoming more evident that the strain of mouse used to generate genetically modified models for the study of endocrine disorders contributes to the ensuing phenotype, metabolic characterization of these common strains used to produce genetically altered mice has been limited. The aim of this study therefore was to measure various metabolic parameters in C57BL/6, DBA/2, and 129T2 mice fed a control or a high-fat diet. Mice were fed either a control (7 g/100 g) or a high-fat (60 g/100 g) diet for 6 wk. During wk 6, spontaneous and voluntary physical activity and resting energy expenditure were determined. DBA/2 mice that consumed the control diet gained more weight and had larger regional fat pad depots than either C57BL/6 or 129T2 mice (P < 0.05). Spontaneous and voluntary activity was lower in 129T2 mice compared with DBA/2 or C57BL/6 mice (P < 0.05). Resting energy expenditure (corrected for body weight) was greater in C57BL/6 mice than in DBA/2 or 129T2 mice (P < 0.05), whereas glucose and fat oxidation did not differ among the 3 strains of mice. Plasma glucose concentrations in food-deprived mice were higher and insulin concentrations lower in 129T2 compared with C57BL/6 mice (P < 0.05), but were not affected by the high-fat diet in any of the 3 strains tested. This study shows that these 3 commonly used inbred strains of mice have different inherent metabolic characteristics. It further highlights that the background strain used to produce genetically modified mice is critical to the resultant phenotype.

KEY WORDS: • energy expenditure • physical activity • obesity • transgenics • knockout mice

Dramatic developments in the field of molecular genetics over the last 20 years have catapulted the humble rodent to the position of "biomedicine’s model mammal" (1). The advent of transgenic and gene-targeted models provided powerful and increasingly popular scientific tools with which to study the molecular and cellular mechanisms underlying the many varied metabolic and endocrine disorders, such as obesity and Type II diabetes. The science of ablating a gene or changing its expression has become remarkably simple. However, there are now a number of examples demonstrating that animals containing the same genetic change can exhibit profoundly different phenotypes when present on diverse genetic backgrounds.

The most notable of these for work associated with obesity and Type II diabetes is the mutation in either the leptin gene (Lepob mouse) or the leptin receptor gene (Leprdb mouse). When either of these mutations is present on the C57BL/6J inbred mouse background, a phenotype of massive obesity accompanied by insulin resistance with only transient diabetes is observed (2,3). In Sv129/J mice, which are the most common source of embryonic stem cells for targeted transgenesis, expression of the Leprdb mutation causes extreme hyperinsulinemia and massive obesity (4,5). In contrast, either mutation produces initial obesity and insulin resistance followed by life-shortening diabetes when present on the C57BL/KsJ strain.

Thus it is clear from the above discussion that to analyze properly the resultant phenotype of a specific genetic manipulation, the inherent phenotype of the particular mouse strain employed has to be known. Therefore, although it is now becoming recognized that different inbred strains harbor different susceptibilities to either obesity or diabetes, systematic metabolic characterization of most if not all strains is lacking. The importance of inbred strain background on phenotypic assessment has been well reviewed in the field of neurobiology and behavior (6,7). Although the Jackson Laboratory Mouse Phenome Database (8) contains a great deal of information on many strains, it does not yet have complete data on metabolic parameters pertinent to obesity and diabetes research and response to a high-fat diet. The aim of this study was to characterize the metabolic parameters of 3 of the most commonly used inbred mouse strains, i.e., C57BL/6, DBA/2, and 129T2 and their response to low- and high-fat diets.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 LITERATURE CITED
 
    Mice and diets. C57BL/6, DBA/2 and 129T2 [formerly known as 129T2/SvEmsJ (9)] 8-wk-old mice were obtained from the Walter and Eliza Hall Institute of Research Animal facility, Kew Vic, Australia. Mice consumed a standard nonpurified rodent diet containing 6% of the energy as fat, 20% as protein and 74% as carbohydrate (Barastoc) with water freely available. Only male mice were used in this study. Lighting was artificial and maintained on a 12-h day:night cycle (lights on at 0600 h). The room temperature was kept at a constant 22°C. At 10 wk of age, the mice were randomly divided into the 2 diet groups. The control group was fed a diet containing 7% of the energy as fat, 18% as protein, and 75% as carbohydrate. The high-fat group was fed 60% of the energy as fat, 18% as protein, and 22% as carbohydrate (both diets were otherwise identical and manufactured by Glen Forrest Stockfeeders). The composition of the 2 diets is shown in Table 1. Ethics approval was obtained from Melbourne Health Animal Ethics Committee and all experiments were carried out in accordance with the guidelines stipulated by this board.


View this table:
[in this window]
[in a new window]
  		TABLE 1 Composition of diets provided to C57BL/6, DBA/2, and 129T2 mice

 
    Measures of energy balance. Mice were housed in pairs and body weights were determined weekly for 5 wk. Food intake was determined daily during wk 6 with mice housed individually. The bedding used in the cage was cellulose bedding (Fibercycle) to enable identification of food particles. Food intake was corrected for spillage. Energy intake was determined as the mean of 5-d measurements and was estimated from the calculated energy in each diet. Physical activity was measured during wk 6 after the commencement of the dietary regimen and presented as total counts (or cycles) over a 24-h period.

Voluntary physical activity levels were determined in a separate group of mice and were measured by continuous monitoring of the use of the running wheels using a computerized meter as previously described (10). Mice were individually housed for 7 d in rat boxes containing a 15-cm diameter running wheel and had free access to food. The first 2 d were allowed for acclimation, and readings were taken over the following 5 d, averaged, and expressed as cycles/d.

Spontaneous physical activity levels were measured in individually housed mice that had free access to food using an infrared light beam monitor (Columbus Instruments) as previously described (11). Again, mice were allowed 2 d of acclimation to the activity meters; readings were taken over the next 5 d, averaged, and expressed as counts/d.

In wk 6, after the activity measurements were completed, and after 2 h of food deprivation to minimize effects from food digestion, rates of resting energy expenditure, glucose oxidation, and fat oxidation were measured during the light cycle as previously described (12) using indirect calorimetry (Columbus Instruments). Mice were placed in the calorimetry chambers for a 30-min acclimation period followed by measurement of expired oxygen and carbon dioxide every minute over the following 30 min.

    Tissue collection. At the end of wk 6, mice were deprived of food overnight and anesthetized with pentobarbitone sodium (Nembutal) administered by i.p. injection (100 mg/kg body weight); 30 min later, the mice were bled from the eye using heparinized capillary tubes. Plasma was collected and stored at –20°C. Epididymal, inguinal subcutaneous, and retroperitoneal adipose tissues were removed and the wet mass was weighed. Because the same person performed the procedure on all mice, the dissection of the adipose tissue depots was standardized.

    Measurement of plasma glucose and insulin levels. The glucose oxidase method was used to measure plasma glucose using a GM7Analox glucose analyzer (Helena Laboratories). Plasma insulin was measured by RIA (Linco Research Immunoassay).

    Statistical analysis. Data are expressed as means ± SEM. Data were analyzed by 2-way ANOVA with Tukey’s Honestly Significant Difference post-hoc test (SPSS 11 for Windows). Comparisons were made between the 2 diets in mice from the same strain and among the 3 mouse strains fed the same diet. Differences were considered significant at P < 0.05.


   RESULTS
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 LITERATURE CITED
 
    Weight gain and food intake. The initial body weights did not differ among the 3 strains of mice. DBA/2 mice gained significantly more weight than either the C57BL/6 or 129T2 mice when fed either the control or high-fat diet (Fig. 1). However, although the high-fat diet enhanced weight gain relative to the control diet in C57BL/6 and 129T2 mice, it did not have this effect in DBA/2 mice (Fig. 1).



View larger version (14K):
[in this window]
[in a new window]
  		FIGURE 1 Cumulative weight gain of C57BL/6, DBA/2 and 129T2 mice fed a control or high-fat diet for 5 wk. Initial weights (g) of mice fed the control (C57BL/6: 24.9 ± 0.6, DBA/2: 25.5 ± 0.6, 129T2: 26.9 ± 0.7) and high-fat diets (C57BL/6: 25.5 ± 0.4, DBA/2: 24.8 ± 0.6, 129T2: 25.9 ± 1.1) did not differ among the 3 strains. Values are means ± SEM, n = 10. Means within a strain or diet group with a common letter do not differ, P ≥ 0.05.

 
Food intake did not differ among the 3 strains of mice regardless of the diet (Table 2). All 3 strains consumed less of the high-fat diet than of the control diet, showing that the strains did not differ in this adaptive response to limiting weight gain (Table 2).


View this table:
[in this window]
[in a new window]
  		TABLE 2 Food and energy consumed by C57BL/6, DBA/2, and 129T2 mice fed a control or high-fat diet for 6 wk1

 
    Fat pads. DBA/2 mice fed the control diet had larger epididymal, subcutaneous, and retroperitoneal depots than either the C57BL/6 or 129T2 mice (Fig. 2, P = 0.001). When exposed to a high-fat diet, all 3 strains had larger epididymal, subcutaneous, and retroperitoneal fat pads than mice of the same strain fed the control diet (Fig. 2, P = 0.01). Thus, although DBA/2 mice did not gain more body weight when they consumed a high-fat diet, they did accumulate more fat.



View larger version (13K):
[in this window]
[in a new window]
  		FIGURE 2 Epididymal (A), subcutaneous (B), and retroperitoneal (C) fat depot weights of C57BL/6, DBA/2 and 129T2 mice fed the control or high-fat diet for 6 wk. Values are means ± SEM, n = 10. Means within a strain or diet group with a common letter do not differ, P ≥ 0.05.

 
    Spontaneous physical activity. DBA/2 mice fed the control diet displayed less vertical and ambulatory activity compared with C57BL/6 but not 129T2 mice (Fig. 3). Although dietary manipulation did not affect any spontaneous activity measurement in DBA/2 mice, vertical activity was decreased in C57BL/6 mice and increased in 129T2 mice fed the high-fat diet compared with their counterparts fed the control diet (Fig. 3B). 129T2 mice displayed lower spontaneous activity than the other 2 strains.



View larger version (17K):
[in this window]
[in a new window]
  		FIGURE 3 Spontaneous physical activity of C57BL/6, DBA/2 and 129T2 mice fed the control or a high-fat diet for 6 wk: Horizontal (A), Vertical (B), Ambulatory (C). Values are means ± SEM, n = 10. Means within a strain or diet group with a common letter do not differ, P ≥ 0.05.

 
    Voluntary physical activity. Similar to spontaneous activity measurements, 129T2 mice fed either diet exhibited less voluntary activity compared with both C57BL/6 and DBA/2 mice (Fig. 4). The high-fat diet decreased voluntary activity in both C57BL/6 and DBA/2 mice, but there was no further decrease in activity in the 129T2 mice (Fig. 4).



View larger version (12K):
[in this window]
[in a new window]
  		FIGURE 4 Voluntary physical activity of C57BL/6, DBA/2 and 129T2 mice fed the control or high-fat diet for 6 wk. Values are means ± SEM, n = 10. Means within a strain or diet group with a common letter do not differ, P ≥ 0.05.

 
    Calorimetric measurements. C57BL/6 mice fed both diets had greater resting energy expenditure than DBA/2 and 129T2 control mice and mice fed the high-fat diet when corrected for body weight (Table 3, P < 0.05). Resting energy expenditure was not affected by the diets in any strain tested (Table 3).


View this table:
[in this window]
[in a new window]
  		TABLE 3 Resting energy expenditure in C57BL/6, DBA/2, and 129T2 mice fed a control or high fat diet for 6 wk1

 
Dietary manipulation also did not affect substrate oxidation in the 3 strains of mice (Fig. 5). Furthermore, glucose and fat oxidation did not differ among the 3 strains regardless of dietary fat intake.



View larger version (17K):
[in this window]
[in a new window]
  		FIGURE 5 Substrate oxidation by C57BL/6, DBA/2 and 129T2 mice fed the control or high-fat diet for 6 wk. Values are means ± SEM, n = 10. Means within a strain or diet group with a common letter do not differ, P ≥ 0.05.

 
    Fasting plasma glucose and insulin concentrations. Fasting plasma glucose concentrations were significantly higher in 129T2 mice fed the control diet compared with C57BL/6 mice fed the control diet (Table 4). Conversely, plasma insulin levels were lower in 129T2 mice compared with the other 2 strains (Table 4). Surprisingly, the high-fat diet did not affect either plasma glucose or insulin levels in any of the 3 strains, despite causing weight gain in C57BL/6 and 129T2 mice.


View this table:
[in this window]
[in a new window]
  		TABLE 4 Fasting plasma glucose and insulin concentrations in C57BL/6, DBA/2, and 129T2 mice fed a control or high fat diet for 6 wk1

 

   DISCUSSION
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
LITERATURE CITED
 
Normal development and physiology can vary greatly from one mouse strain to the next, and in the analysis of mutants, it is often not possible to distinguish subtle effects due to the mutation itself from effects due to other genes within the background of the mutant strain. To make this distinction, it is essential to be able to compare animals in which differences in the genetic background have been eliminated as a variable in the experiment. Until recently and for a number of reasons, including techniques used to increase hybrid vigor, such as the conditional expression system Cre/LoxP (which requires a tissue-specific Cre expressing and a LoxP-containing gene targeted mouse), the resultant genetically modified mouse was usually a conglomeration of 2 or more strains. Although clear phenotypic differences can be observed only in pure inbred strains, the conundrum now has become which strain provides the optimum isogenic environment on which to place a mutation. This warrants studies of the inherent physiologic and biochemical parameters of commonly used mouse strains to provide a more informed choice on the background strain on which a genetic manipulation should be placed. Although information on many mouse strains is available via the Mouse Phenome Database on the Jackson Laboratory website (8), it does not yet contain extensive information on metabolic parameters that would be determined when studying mechanisms for obesity and diabetes and the effect of a high-fat diet.

In this study we chose 3 inbred mouse strains commonly used to generate genetically altered mice for the study of metabolic disorders (obesity and diabetes), i.e., C57BL/6, DBA/2, and 129T2. The C57BL/6 and DBA/2 strains were widely used as the hybrid backgrounds for transgenics and, as stated above, the 129 strain was used to derive embryonic stem cells for use in homologous recombination for the production of "knockout" mice. The results show that these seemingly similar mouse strains displayed differences in 2 metabolic parameters and responded differently to a high-fat diet. The first was that weight gain over 6 wk when consuming the control diet and regional fat pad weight regardless of diet were greater in the DBA/2 mice compared with the other 2 strains. An increase in carcass lipid and fat pad weight was shown previously in DBA/2 compared with C57BL/6 mice (13). Intrauterine effects may contribute to the increase in fat accumulation because it was reported that DBA/2 litter sizes are smaller than those of C57BL/6 and 129 (14). Studies showed that mice arising from small litters were heavier and had more carcass fat than mice produced from larger litters (15,16).

The second important finding of this study is that DBA/2 mice displayed decreased ambulatory and voluntary activity as well as reduced resting energy expenditure compared with C57BL/6 but not 129T2 mice; this might partially but not completely explain the increase in adiposity. Moreover, spontaneous and, more profoundly, voluntary activity was decreased in 129T2 mice compared with both C57BL/6 and DBA/2 mice. Although less locomotor activity as assessed by video tracking systems in an open field was reported (17,18), to our knowledge this is the first report of decreased spontaneous and voluntary activity of 129T2 compared with C57BL/6 mice. DBA/2 mice had lower voluntary activity as assessed by running wheels compared with C57BL/6 mice, a finding corroborated by a previous report showing that running duration, distance, and average speed were lower in DBA/2 compared with C57BL/6 mice (19). Together, these data suggest that 129T2 mice are inherently sedentary, and this should be a consideration when physical activity is determined in genetically manipulated models containing the 129T2 background strain. Furthermore, 129T2 mice displayed decreased energy expenditure, which, together with decreased physical activity, should have resulted in increased fat accumulation compared with the other 2 strains. This could be explained by decreased fat uptake by the digestive system as was reported previously for other mouse strains (20).

Furthermore, although none of the spontaneous activities measured were affected in DBA/2 mice, a high-fat diet decreased vertical and ambulatory activity in the C57BL/6 mice, whereas it increased vertical activity in 129T2 mice. Moreover, voluntary activity was decreased in response to a high-fat diet in C57BL/6 and DBA/2 but not 129T2 mice. A decrease in physical activity is associated with increased adiposity and weight gain (11,21,22) and this could explain the increase in body and fat pad weights in C57BL/6 and DBA/2 mice in response to the high-fat diet. The reason for the increase in body and fat pad weights in 129T2 mice as a result of a high-fat diet is not clear. A possible mechanism is enhanced fatty acid transport, which could contribute to the increased weight gain in 129T2 mice consuming the high-fat diet. What is clear, though, is that the 3 strains used in this study have different basal physical activity parameters and respond differently to a high-fat diet.

Finally, dietary manipulation did not affect either fasting plasma glucose or insulin concentrations in any of the 3 strains of mice. In contrast, previous studies demonstrated that insulin resistance and diabetes developed in C57BL/6 mice when a high-fat diet was fed (23–25). In fact, the studies by Burcelin and colleagues (23–25) differentiated a number of phenotypes in C57BL/6 mice fed a high-fat diet for 9 mo, i.e., lean normoglycaemic, lean diabetic, and obese diabetic. Furthermore, they found that the C57BL/6 mice that remained lean and normoglycemic after consumption of the high-fat diet displayed increased glucose clearance (23–25). The reason that we did not a see a change in plasma glucose or insulin concentrations in mice fed the high-fat diet could be due to the length of time (6 mo or longer vs. 6 wk in our study) and type of dietary fat (saturated vs. polyunsaturated used in our study). It was suggested that SFA cause a greater reduction in insulin sensitivity than polyunsaturated fats (26,27). Furthermore, it was shown recently that although a high-fat diet caused glucose intolerance, insulin sensitivity in peripheral tissues was not affected in C57BL/6 mice (28).

Interestingly, plasma glucose concentrations were higher and plasma insulin levels were lower in 129T2 compared with C57BL/6 mice, suggesting differences in pancreatic islet insulin secretory function among strains of mice. In fact, we showed recently that glucose-mediated insulin secretion is enhanced in DBA/2 compared with C57BL/6 mice both in vivo and in vitro (29).

The ease with which the mouse genome can be manipulated makes it an invaluable tool in the discovery of the etiopathogenesis of complex disorders such as obesity and Type 2 diabetes. However, although the methodology has become surprisingly simple, the science and the interpretation have become more complex than ever. This study clearly shows that detailed inherent metabolic information, as well as careful and strategic planning, are required before undertaking the long and arduous road of characterizing a transgenic or "knockout" animal.


   ACKNOWLEDGMENTS
 
Dedicated to Peter Andrikopoulos (d. 7 September 2004).


   FOOTNOTES
 
1 Supported by the National Health and Medical Research Council of Australia (project numbers 145769, 209001 and 209002 to J.P. and S.A.). Back

Manuscript received 13 July 2004. Initial review completed 26 August 2004. Revision accepted 24 September 2004.


   LITERATURE CITED
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 LITERATURE CITED
 

1. Malakoff, D. (2000) The rise of the mouse, biomedicine’s model mammal. Science (Washington, DC) 288:248-252.[Free Full Text]

2. Beisel, W. R. (1982) Single nutrients and immunity. Am. J. Clin. Nutr. 35:417-468.[Free Full Text]

3. Coleman, D. (1978) Obese and diabetes: two mutant genes causing diabetes-obesity syndromes in mice. Diabetologia 14:141-148.[Medline]

4. Coleman, D. L. & Hummel, K. P. (1973) The influence of genetic background on the expression of the obese (Ob) gene in the mouse. Diabetologia 9:287-293.[Medline]

5. Leiter, E. H., Coleman, D. L. & Hummel, K. P. (1981) The influence of genetic background on the expression of mutations at the diabetes locus in the mouse. III. Effect of H-2 haplotype and sex. Diabetes 30:1029-1034.[Abstract]

6. Crawley, J. N. (2003) Behavioral phenotyping of rodents. Comp. Med. 53:140-146.[Medline]

7. Bachmanov, A. A., Reed, D. R., Beauchamp, G. K. & Tordoff, M. G. (2002) Food intake, water intake, and drinking spout side preference of 28 mouse strains. Behav. Genet. 32:435-443.[Medline]

8. Mouse Phenome Database Web Site, The Jackson Laboratory, Bar Harbor, Maine. World Wide Web http://www.jax.org/phenome [accessed October, 2003].

9. Simpson, E. M., Linder, C. C., Sargent, E. E., Davisson, M. T., Mobraaten, L. E. & Sharp, J. J. (1997) Genetic variation among 129 substrains and its importance for targeted mutagenesis in mice. Nat. Genet. 16:19-27.[Medline]

10. Thorburn, A. W., Holdsworth, A., Proietto, J. & Morahan, G. (2000) Differential and genetically separable associations of leptin with obesity-related traits. Int. J. Obes. Relat. Metab. Disord. 24:742-750.[Medline]

11. Jones, M. E., Thorburn, A. W., Britt, K. L., Hewitt, K. N., Wreford, N. G., Proietto, J., Oz, O. K., Leury, B. J., Robertson, K. M., Yao, S. & Simpson, E. R. (2000) Aromatase-deficient (ArKO) mice have a phenotype of increased adiposity. Proc. Natl. Acad. Sci. U.S.A. 97:12735-12740.[Abstract/Free Full Text]

12. Heffernan, M. A., Jiang, W. J., Thorburn, A. W. & Ng, F. M. (2000) Effects of oral administration of a synthetic fragment of human growth hormone on lipid metabolism. Am. J. Physiol. 279:E501-E507.

13. West, D. B., Boozer, C. N., Moody, D. L. & Atkinson, R. L. (1992) Dietary obesity in nine inbred mouse strains. Am. J. Physiol. 262:R1025-R1032.

14. Blake, J. A., Richardson, J. E., Bult, C. J., Kadin, J. A. & Eppig, J. T. (2003) MGD: the Mouse Genome Database. Nucleic Acids Res. 31:193-195.[Abstract/Free Full Text]

15. Roberts, J. L., Whittington, F. M. & Enser, M. (1988) Effects of litter size and subsequent gold-thioglucose-induced obesity on adipose tissue weight, distribution and cellularity in male and female mice: an age study. Br. J. Nutr. 59:519-533.[Medline]

16. Koopman, J. P., Scholten, P. M., Van Den Brink, M. E. & Beynen, A. C. (1990) Availability of solid feed and growth rates of pre-weaned mice of different litter size. Z. Versuchstierkd. 33:217-219.[Medline]

17. Paulus, M. P., Dulawa, S. C., Ralph, R. J. & Mark, A. G. (1999) Behavioral organization is independent of locomotor activity in 129 and C57 mouse strains. Brain Res. 835:27-36.[Medline]

18. Ralph, R. J., Paulus, M. P. & Geyer, M. A. (2001) Strain-specific effects of amphetamine on prepulse inhibition and patterns of locomotor behavior in mice. J. Pharmacol. Exp. Ther. 298:148-155.[Abstract/Free Full Text]

19. Lerman, I., Harrison, B. C., Freeman, K., Hewett, T. E., Allen, D. L., Robbins, J. & Leinwand, L. A. (2002) Genetic variability in forced and voluntary endurance exercise performance in seven inbred mouse strains. J. Appl. Physiol. 92:2245-2255.[Abstract/Free Full Text]

20. Keelan, M., Hui, D. Y., Wild, G., Clandinin, M. T. & Thomson, A. B. (2000) Variability of the intestinal uptake of lipids is genetically determined in mice. Lipids 35:833-837.[Medline]

21. Pedrazzini, T., Seydoux, J., Kunstner, P., Aubert, J. F., Grouzmann, E., Beermann, F. & Brunner, H. R. (1998) Cardiovascular response, feeding behavior and locomotor activity in mice lacking the NPY Y1 receptor. Nat. Med. 4:722-726.[Medline]

22. Coyle, C. A., Jing, E., Hosmer, T., Powers, J. B., Wade, G. & Good, D. J. (2002) Reduced voluntary activity precedes adult-onset obesity in Nhlh2 knockout mice. Physiol. Behav. 77:387-402.[Medline]

23. Surwit, R. S., Kuhn, C. M., Cochrane, C., McCubbin, J. A. & Feinglos, M. N. (1988) Diet-induced type II diabetes in C57BL/6J mice. Diabetes 37:1163-1167.[Abstract]

24. Ahren, B. (2001) Reducing plasma free fatty acids by acipimox improves glucose tolerance in high-fat fed mice. Acta Physiol. Scand. 171:161-167.[Medline]

25. Burcelin, R., Crivelli, V., Dacosta, A., Roy-Tirelli, A. & Thorens, B. (2002) Heterogeneous metabolic adaptation of C57BL/6J mice to high-fat diet. Am. J. Physiol. 282:E834-E842.

26. Rivellese, A. A., De Natale, C. & Lilli, S. (2002) Type of dietary fat and insulin resistance. Ann. N.Y. Acad. Sci. 967:329-335.[Abstract/Free Full Text]

27. Hu, F. B., van Dam, R. M. & Liu, S. (2001) Diet and risk of Type II diabetes: the role of types of fat and carbohydrate. Diabetologia 44:805-817.[Medline]

28. Rossmeisl, M., Rim, J. S., Koza, R. A. & Kozak, L. P. (2003) Variation in type 2 diabetes–related traits in mouse strains susceptible to diet-induced obesity. Diabetes 52:1958-1966.[Abstract/Free Full Text]

29. Kooptiwut, S., Zraika, S., Thorburn, A. W., Dunlop, M. E., Darwiche, R., Kay, T. W., Proietto, J. & Andrikopoulos, S. (2002) Comparison of insulin secretory function in 2 mouse models with different susceptibility to beta-cell failure. Endocrinology 143:2085-2092.[Abstract/Free Full Text]




This article has been cited by other articles:


Home page
 DiabetesHome page
E. D. Berglund, C. Y. Li, G. Poffenberger, J. E. Ayala, P. T. Fueger, S. E. Willis, M. M. Jewell, A. C. Powers, and D. H. Wasserman
Glucose Metabolism In Vivo in Four Commonly Used Inbred Mouse Strains
Diabetes, July 1, 2008; 57(7): 1790 - 1799.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
M. Bjursell, A.-K. Gerdin, C. J. Lelliott, E. Egecioglu, A. Elmgren, J. Tornell, J. Oscarsson, and M. Bohlooly-Y
Acutely reduced locomotor activity is a major contributor to Western diet-induced obesity in mice
Am J Physiol Endocrinol Metab, February 1, 2008; 294(2): E251 - E260.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. GenomicsHome page
A. Wagener, A. O. Schmitt, S. Aksu, W. Schlote, C. Neuschl, and G. A. Brockmann
Genetic, sex, and diet effects on body weight and obesity in the Berlin Fat Mouse Inbred lines
Physiol Genomics, November 21, 2006; 27(3): 264 - 270.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
C. Gelegen, D. A. Collier, I. C. Campbell, H. Oppelaar, and M. J. H. Kas
Behavioral, physiological, and molecular differences in response to dietary restriction in three inbred mouse strains
Am J Physiol Endocrinol Metab, September 1, 2006; 291(3): E574 - E581.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
R. A. Davey and H. E. MacLean
Current and future approaches using genetically modified mice in endocrine research
Am J Physiol Endocrinol Metab, September 1, 2006; 291(3): E429 - E438.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
B. J. Lamont, S. Visinoni, B. C. Fam, M. Kebede, B. Weinrich, S. Papapostolou, H. Massinet, J. Proietto, J. Favaloro, and S. Andrikopoulos
Expression of Human Fructose-1,6-Bisphosphatase in the Liver of Transgenic Mice Results in Increased Glycerol Gluconeogenesis
Endocrinology, June 1, 2006; 147(6): 2764 - 2772.
[Abstract] [Full Text] [PDF]

Home page
 J EndocrinolHome page
S. Andrikopoulos, C. M Massa, K. Aston-Mourney, A. Funkat, B. C Fam, R. L Hull, S. E Kahn, and J. Proietto
Differential effect of inbred mouse strain (C57BL/6, DBA/2, 129T2) on insulin secretory function in response to a high fat diet
J. Endocrinol., October 1, 2005; 187(1): 45 - 53.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Funkat, A.
Right arrow Articles by Andrikopoulos, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Funkat, A.
Right arrow Articles by Andrikopoulos, S.

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]