LIPID-LEVEL AND TYPE ALTER STEAROYL-COA DESATURASE MESSENGER-RNA ABUNDANCE DIFFERENTLY IN MICE WITH DISTINCT SUSCEPTIBILITIES TO DIET-INFLUENCED DISEASES
Ei. Park et al., LIPID-LEVEL AND TYPE ALTER STEAROYL-COA DESATURASE MESSENGER-RNA ABUNDANCE DIFFERENTLY IN MICE WITH DISTINCT SUSCEPTIBILITIES TO DIET-INFLUENCED DISEASES, The Journal of nutrition, 127(4), 1997, pp. 566-573
Chronic diseases develop in susceptible individuals following exposure
to environmental conditions including high fat diets. Inbred strains
of mice differing in susceptibility to atherosclerosis, diabetes, obes
ity and certain cancers are models for understanding the genetic basis
and molecular mechanisms whereby diet influences these polygenic and
multifactorial disorders. Expression sequence tags (EST) and disease q
uantitative trait loci (QTL) are also being identified with these stra
ins. Reported here are comparisons of food intake, growth, nonfasting
serum lipids and expression of mRNA for hepatic apolipoprotein E (ApoE
), hepatic stearoyl CoA desaturase (Scd1) and heart lipoprotein lipase
(Lpl) in a 2 x 2 x 2 design with C57BL/6J and BALB/cByJ mice fed semi
purified diets with 4 or 20% saturated (coconut) or unsaturated (corn)
oils for 4 mo. Histological studies of aortas and coronary arteries a
re also reported for these animals. After 4 mo, BALB/cByJ mice were si
gnificantly heavier and had significantly higher total serum cholester
ol, HDL cholesterol and triglyceride concentrations in the fed state t
han C57BL/6J mice. Efficiency of utilizing dietary energy did not diff
er consistently between strains. Oil level affected serum total choles
terol, triglycerides and HDL cholesterol, which were significantly gre
ater in mice fed high fat diets. Lpl and ApoE mRNA expression levels w
ere not significantly affected by mouse strain, oil source or oil leve
l. Scd1 mRNA expression, however, was significantly higher in C57BL/6J
than in BALB/cByJ mice and was lower in all mice fed 20% compared wit
h those fed 4% fat diets. Genes regulated differently by diet among st
rains with distinct susceptibility to diet-influenced disease may be a
ssociated with molecular pathways contributing to incidence or severit
y.