Table 1. Comparison of metabolic studies in mouse models with disrupted GH axis.

Mouse	Phenotype	VCO 2	VO 2	RE R	EE	Food Intake	ActivityAmbulatory	ActivityTotal	Reference
SIGFRKOyoung	Incr. GH, weight gain velocity	↓	↑	↓	↑	↔	↔	↔
SIGFRKOolder	Incr. GH, weight gain velocity	↑	↑	↑	↑	↔	↔	↔
FIGIRKO	marked decr WAT/BAT, no differences IGF-1 (presume no change GH)	NR	↑	↔	↑?	↔	NR	↔	14
GHR−/−	dwarf mice, incr total fat mass	NR	↑	↔	↓/↑ *	↓	NR	NR	13
mGHRKO	Inactivation of the GH receptor in mouse skeletal mouse (data based on mice given HFD)	↑	↑	↑(lig ht) ↔(d ark)	↑	NR	NR	NR	15
bGH	excess GH (>50 fold nl), incr growth	NR	↔	↔	↑	↑	NR	NR	13
HiGH	Incr. GH & IGF-1, No weight difference (decr. Visceral fat depot)	↔	↔	↓ **	↔	↔	NR	↔	19
LiGHRKO	Incr. GH, Decr. IGF-1, decr. Body weight and length decreased.	NR	↔	↔	↔	NR	NR	NR	29

A summary of metabolic findings in the SIGFRKO mouse model at younger and older ages is graphed along with metabolic findings reported in several previously characterized genetically modified mouse models in which there is disruption or alteration of the GH axis. The table is a compilation of the reported metabolic changes for each model; therefore, comparisons are possible for all parameters. Of note, metabolic studies on the mGHRKO only were reported on a high fat diet (HFD). SIGFRKO (somatotroph IGF-1R knockout), FIGIRKO (double tissue-specific knockout of insulin and IGF-1 receptors in fat), GHR−/− (GH receptor/binding protein knockout), bGH (bovine GH transgene overexpression), mGHRKO (skeletal muscle GH receptor knockout), HiGH (somatotroph inactivation of IGF-1R and Insulin receptor), LiGHRKO (liver-specific GHR gene knockout), ↑ - increase, ↓ - decrease, ↔ – no difference, NR – not reported.

^*The calculated EE was reported differently in the citations.

^**Significant difference were more pronounced during the light cycle vs. dark cycle [13-15, 19, 29].