Table 1.

Phenotypic summary of GH clinical conditions and comparable mouse ones.

	Elevated GH		GH deficiency (GHD)				GH insensitivity
	Clinical	Mouse	Clinical	Mouse	Mouse	Mouse	Clinical	Mouse	Mouse
	Acromegaly Gigantism	bGH	GHD *	GHA **	AOiGHD	Ames	Laron	aGHRKO ****	GHR-/-
GH defect	Hypersecretion of GH commonly due to pituitary adenoma	Transgenic for bovine GH	Many variations depending on age and etiology	Transgenic for GHR antagonist gene	Ablation of somatotrophs with an inducible system	Mutation in Prop1	Hereditary conditions usually caused by GHR receptor defects	Knockdown of Ghr gene via an inducible system	Disruption of Ghr gene
GH action	↑↑ with onset of adenoma	↑↑ from birth	↓ onset varies based on etiology	↓ throughout life due to GH antagonism	↓ beginning at time of induction (10–12 weeks)	GH deficiency (as well as prolactin and TSH)	Absent from birth	↓ beginning at time of induction (6 weeks)	Absent GHR from birth
GH	↑↑	↑↑	↓	↑		↓	↑	↑	↑
IGF-1	↑↑	↑↑	↓	↓		↓↓	↓↓	↓	↓↓
Growth and body weight	↑↑ *	↑↑	↓ ↔ *	↓	↔	↓↓	↓↓	↓	↓↓
Insulin sensitivity	↓	↓	↑	↑	↓↔	↑	↑↓ ***	↓	↑
Lifespan	↓	↓	↔	No data	↔	↑↑	↔	↔ male; ↑ female	↑

↑ increase, ↔ no change, ↓ decrease; * depends on the age of onset; ** while technically not GH deficient, this mouse line is unique in that it produces a GHR antagonist that blocks endogenous GH, resulting in mice with a dramatic reduction in GH action from birth; *** depends on Israeli or Ecuadorian cohort; Israeli cohort tends to have higher insulin levels [63]; **** GHR disruption is not equivalent in all tissues. Adapted with permission from [38]. Copyright 2017 John Wiley & Son.