Body composition of inbred mice (Mus musculus)

Dawson, N. J.

doi:10.1016/0010-406x(70)90104-0

Cited by 13 publications

(4 citation statements)

References 12 publications

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“…We even found higher coefficients of variation of 10 to 15% for the organ weights of liver and heart in the majority of age groups. The considerably higher coefficients of variation between 11 and 28% for fat content are in good agreement with the data of Dawson (1970) and Kluge et a1. (1982).…”

Section: Discussionsupporting

confidence: 92%

Sex differences in age development of a mouse inbred strain: body composition, adipocyte size and organ weights of liver, heart and muscles

et al. 1995

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SummaryThe mouse inbred strain HLG has only recently been submitted for international registration. It has been widely used in radiological studies. Since these mice tend to become obese, they may be of interest for studies concerning fat metabolism. Therefore, the present ageing study examines the sex-specific development of body weight, body composition, adipocyte size as well as the organ weight of liver, heart and thigh muscles of the inbred strain HLG (54 males/53 virgin females) between day 40 and 360 of life.The body weight development showed a distinct sexual dimorphism, quickly increasing in the case of males but comparatively protracted in females until maturity. Significantly higher values for body and fat-free dry weight as well as body water were found in males of all ages. Body fat and adipocyte diameter were only higher in the 80 and 120 day-old males. Thus, the increase in female body weight resulted largely through a rise in body fat as additionally evidenced by the sex-specific correlation of characteristics. A 2-fold analysis of variance showed sex differences in the relative weights of liver and muscle, but not of the heart. A sex-specific close correlation was observed between body and liver weights in males until day 180. Correlations between body fat and other characteristics were only rarely found. Differences in coefficients of variation largely depended on the characteristics. A higher variability was also found for some characteristics in the youngest groups (40 days). A sex-specific difference was only seen in the case of body fat content for 60 day-old mice (female>male).

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Section: Discussionsupporting

confidence: 92%

Sex differences in age development of a mouse inbred strain: body composition, adipocyte size and organ weights of liver, heart and muscles

et al. 1995

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“…By rank-sum tests the small differences could be verified (P < 0.01). These results agree with Festing 4 and Jay, 5 and show the same tendency as the reports of Dawson 6 ; Oliverio et al, 7 Gärtner, 8 and Hagemann. 9 The standardization of different environmental components, such as food, temperature, group size, bedding, humidity, etc., does not substantially reduce the trait-specific, relative random variability.…”

Section: Effects Of Standardization On Random Variabilitysupporting

confidence: 90%

A third component causing random variability beside environment and genotype. A reason for the limited success of a 30 year long effort to standardize laboratory animals?1,2

Gärtner

2012

International Journal of Epidemiology

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This paper is a review of experiments, performed in our laboratory during the past 20 years, designed to analyse the significance of different components of random variability in quantitative traits in laboratory rats and mice. Reduction of genetic variability by using inbred strains and reduction of environmental variability by highly standardized husbandry in laboratory animals did not remarkably reduce the range of random variability in quantitative biological traits. Neither did a tremendous increase of the environmental variability (i.e., living in a natural setting) increase it. Therefore, the postnatal environment cannot be that important as the source of random variability. Utilizing methods established in twin research, only 20-30% of the range of the body weight in inbred mice were directly estimated to be of environmental origin. The remaining 70-80% were due to a third component creating biological random variability, in addition to the genetic and environmental influences. This third component is effective at or before fertilization and may originate from ooplasmic differences. It is the most important component of the phenotypic random variability, fixing its range and dominating the genetic and the environmental component. The Gaussian distribution of the body weights observed, even in inbred animals, seems to be an arrangement supporting natural selection rather than the consequence of heterogeneous environmental influences. In a group of inbred rats, the males with the highest chance of parenting the next generation were gathered in the central classes of the distribution of the body weight.

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“…Possibly, the actual fat content of the animals was below the value of 10% used for the estimation of Keq(th). Body fat fractions of mice in the range of 8.3% to 15.5% (Dawson 1970), of 9.8% (Tuey and Matthews 1980) and of rats between 7% (Caster et al 1956;Lutz et al 1977) and 11.4% (Geyer et al 1991) are published. A linear relationship between percentage composition of adipose tissue and body weight of rats giving a value of 9.6% for a 250 g rat has been reported by Anderson et al (1993).…”

Section: Partition Coefficient Whole Body : Airmentioning

confidence: 96%

Species-specific pharmacokinetics of styrene in rat and mouse

Filser¹,

Schwegler²,

Csanády

et al. 1993

Arch Toxicol

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The pharmacokinetics of styrene were investigated in male Sprague-Dawley rats and male B6C3F1 mice using the closed chamber technique. Animals were exposed to styrene vapors of initial concentrations ranging from 550 to 5000 ppm, or received intraperitoneal (i.p.) doses of styrene from 20 to 340 mg/kg or oral (p.o.) doses of styrene in olive oil from 100 to 350 mg/kg. Concentration-time courses of styrene in the chamber atmosphere were monitored and analyzed by a pharmacokinetic two-compartment model. In both species, the rate of metabolism of inhaled styrene was concentration dependent. At steady state it increased linearly with exposure concentration up to about 300 ppm; more than 95% of inhaled styrene was metabolized and only small amounts were exhaled unchanged. At these low concentrations transport to the metabolizing enzymes and not their metabolic capacity was the rate limiting step for metabolism. Pharmacokinetic behaviour of styrene was strongly influenced by physiological parameters such as blood flow and especially the alveolar ventilation rate. At exposure concentrations of styrene above 300 ppm the rate of metabolism at steady state was progressively limited by biochemical parameters of the metabolizing enzymes. Saturation of metabolism (Vmax) was reached at atmospheric concentrations of about 700 ppm in rats and 800 ppm in mice, Vmax being 224 mumol/(h.kg) and 625 mumol/(h.kg), respectively. The atmospheric concentrations at Vmax/2 were 190 ppm in rats and 270 ppm in mice. Styrene accumulates preferentially in the fatty tissue as can be deduced from its partition coefficients in olive oil:air and water:air which have been determined in vitro at 37 degrees C to be 5600 and 15. In rats and mice exposed to styrene vapors below 300 ppm, there was little accumulation since the uptake was rate limiting. The bioaccumulation factor body:air at steady state (K'st*) was rather low in comparison to the thermodynamic partition coefficient body:air (Keq) which was determined to be 420. K'st* increased from 2.7 at 10 ppm to 13 at 310 ppm in the rat and from 5.9 at 20 ppm to 13 at 310 ppm in the mouse. Above 300 ppm, K'st* increased considerably with increasing concentration since metabolism became saturated in both species. At levels above 2000 ppm K'st* reached its maximum of 420 being equivalent to Keq. Pretreatment with diethyldithiocarbamate, administered intraperitoneally (200 mg/kg in rats, 400 mg/kg in mice) 15 min prior to exposure of styrene vapours, resulted in effective inhibition of styrene metabolism, indicating that most of the styrene is metabolized by cytochrome P450-dependent monooxygenases.(ABSTRACT TRUNCATED AT 400 WORDS)

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Body composition of inbred mice (Mus musculus)

Cited by 13 publications

References 12 publications

Sex differences in age development of a mouse inbred strain: body composition, adipocyte size and organ weights of liver, heart and muscles

Sex differences in age development of a mouse inbred strain: body composition, adipocyte size and organ weights of liver, heart and muscles

A third component causing random variability beside environment and genotype. A reason for the limited success of a 30 year long effort to standardize laboratory animals?1,2

Species-specific pharmacokinetics of styrene in rat and mouse

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