Evaluation of Growth Patterns and Body Composition in C57Bl/6J Mice Using Dual Energy X-Ray Absorptiometry

Abstract

The normal growth pattern of female C57BL/6J mice, from 5 to 30 weeks of age, has been investigated in a longitudinal study. Weight, body surface area (BS), and body mass index (BMI) were evaluated in forty mice. Lean mass and fat mass, bone mineral content (BMC), and bone mineral density (BMD) were monitored by dual energy X-ray absorptiometry (DEXA). Weight and BS increased linearly (16.15 ± 0.64–27.64 ± 1.42 g; 51.13 ± 0.74–79.57 ± 2.15 cm2, P < 0.01), more markedly from 5 to 9 weeks of age (P < 0.001). BMD showed a peak at 17 weeks (0.0548 ± 0.0011 g/cm2∗ m, P < 0.01). Lean mass showed an evident gain at 9 (15.8 ± 0.8 g, P < 0.001) and 25 weeks (20.5 ± 0.3 g, P < 0.01), like fat mass from 13 to 17 weeks (2.0 ± 0.4–3.6 ± 0.7 g, P < 0.01). BMI and lean mass index (LMI) reached the highest value at 21 weeks (3.57 ± 0.02–0.284 ± 0.010 g/cm2, resp.), like fat mass index (FMI) at 17 weeks (0.057 ± 0.009 g/cm2) (P < 0.01). BMI, weight, and BS showed a moderate positive correlation (0.45–0.85) with lean mass from 5 to 21 weeks. Mixed linear models provided a good prediction for lean mass, fat mass, and BMD. This study may represent a baseline reference for a future comparison of wild-type C57BL/6J mice with models of altered growth.

Knockout of the X‐linkedFgf13in the hypothalamic paraventricular nucleus impairs sympathetic output to brown fat and causes obesity

“…We compared theFgf13 +/2 mice's daily EE (previously corrected by ANCOVA for LBM, with that of WT mice and converted the deficit to grams by dividing by the caloric content of fat to obtain a predicted fat gain per day. We used the caloric content of fat because of the observations that weight gain of the Fgf13 +/2 mice was almost all fat mass and that there was no difference in the lean mass of the WT and Fgf13 +/2 mice and because it has been shown that from 13 to 17 wk, the majority of weight gain in female C57BL/6J mice is fat mass (34). Using these parameters, we extrapolated the change in weight to 16 wk of age by multiplying the daily fat gain by the number of days.…”

Knock-In of the Recurrent R368X Mutation of PRKAR1A that Represses cAMP-Dependent Protein Kinase A Activation: A Model of Type 1 Acrodysostosis

“…After acquisition, 3D reconstructions were performed using the Rigaku software and morphometric analyses were performed using the OsiriX imaging software (v.5.6 64 bit; OsiriX, Geneva, Switzerland) from stacks of 2D images. Body mass index (BMI) was calculated by dividing the weight (in g) by the square root of the tail‐less length (in cm), and body surface was calculated by dividing the tail‐less length (in cm) by the cube root of the weight (in g), as described …”

“…Body mass index (BMI) was calculated by dividing the weight (in g) by the square root of the tail-less length (in cm), and body surface was calculated by dividing the tail-less length (in cm) by the cube root of the weight (in g), as described. (34) Hormonal and biochemical measurements in plasma and urine Plasma and urinary calcium, phosphorus, and creatinine were determined using a Modular P Roche analyzer. Plasma intact PTH and thyroid-stimulating hormone (TSH) were measured by ELISA (Immutopics, San Clemente, CA, USA and Cloud-Clone Corp, Houston, TX, USA, respectively).…”

Individual housing of male C57BL/6J mice after weaning impairs growth and predisposes for obesity

“…Indeed, profound abnormalities in brain structural and functional development due to social isolation occur specifically during adolescence, disrupting cognitive and behavioural function at later life stages (22–24). Adolescence is also a period of rapid lean body growth (25), which is accompanied by a high energy demand. Moreover, this period also represents a critical phase for the development and maturation of (visceral) white adipose tissue (26–28) and the structural and functional maturation of the hypothalamic circuits that control food intake (29).…”