TABLE 1  Knockout and congenic mouse models used to study the interaction between fat, adrenergic signaling and bone.

From the following article:

Mechanisms of Disease: is osteoporosis the obesity of bone?

Clifford J Rosen and Mary L Bouxsein

Nature Clinical Practice Rheumatology (2006) 2, 35-43
doi:10.1038/ncprheum0070

Model	Body composition	Skeletal phenotype	Comment
BMC, bone mineral content; BW, body weight; AR, -adrenergic receptor; IGF, insulin-like growth factor; KO, knockout; OB, osteoblast; OPX, oophorectomy; PPAR, peroxisome proliferative activated receptor; +/-, heterozygous.
ob/ob12	BW, fat mass	Trabecular bone volume	Leptin deficiency
db/db12, 13	BW, fat mass	Trabecular bone volume	Leptin resistance (leptin-receptor deficiency)
AR2 KO20	Normal	Trabecular bone volume at 6 months	Resistant to deleterious effects of OPX and -adrenergic agonists on skeleton
AR1,2 KO20	BW	Total body BMC; normal trabecular bone volume; mid-diaphyseal cross-sectional area	Resistant to deleterious effects of -adrenergic agonists on skeleton
AR123 KO (beta-less)20	BW, fat mass	Total body BMC, trabecular bone volume; mid-diaphyseal cross-sectional area	Not resistant to deleterious effects of OPX on skeleton
Congenic 6T25	Normal BW fat mass	Trabecular bone volume; mid-diaphyseal cross-sectional area; OB apoptosis, bone-marrow fat	Serum/skeletal IGFI; PPAR activation
PPAR+/-22	body fat	Trabecular bone volume; OB number	PPAR null lethal
SAMP625	body fat	Trabecular bone volume; bone-marrow fat	Accelerated aging model

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