Table 1.
Phenotypic comparison of genetically modified mice with altered GH action.
| Variable | GHR−/− [49, 50] |
Ames[51, 63, 88]* |
Snell[48, 63]* |
Lit/Lit[89] | GHA[49, 50] | AOiGHD[44] | FaGHRKO[46] | MacGHRKO[73 ] |
LiGHRKO[45] | bGH[50, 52] |
|---|---|---|---|---|---|---|---|---|---|---|
| GH action | absent | ↓↓ | ↓↓ | ↓↓ | ↓ | ↓ (adult) | ↔ | ↓ | ↑ | ↑↑ |
| Defect | Gene disrupti on of GHR gene |
homozygo us recessive mutation in prop-1 gene |
homozygo us recessive mutation in the Pit- 1 gene |
GH-defic ient due to recessive mutation in the Ghrhr gene |
Transgenic for GHR antagonist gene |
adult GH deficient mouse |
Fat-specific gene disruption of GHR gene |
Macrophage specific gene disruption of GHR gene |
Liver-specific gene disruption of the GHR gene |
Transgenic for bovine GH |
| GH | ↑ | ↓↓ | ↓↓ | ↓↓ | ↑ | ↓ | ↔ | ↑ | ↑↑ | |
| IGF-1 | ↓↓ | ↓↓ | ↓↓ | ↓↓ | ↓ | ↓ | ↔/↑ | ↓ | ↑↑ | |
|
Body weight and growth |
↓↓ | ↓↓ | ↓↓ | ↓↓ | ↓ | ↔ | ↑ | ↔ | ↓ | ↑ |
|
Insulin sensitivity |
↑ | ↑ | ↑ | ↑ | ↔ (young) ↓(older) |
↑ | ↔ | ↓ | ↓ | ↓ |
| Lifespan | ↑ | ↑ | ↑ | ↑ | ↔ | No data | No data | ↔ | ↓ | |
|
Fat mass (Depot Differences) |
↑↑ (subQ mainly) |
↑ | ↑ (subQ mainly) |
↑ | ↑↑↑ (subQ mainly) |
↑ (subQ & retro) |
↑↑↑ (all depots) |
↑ (Epi) | ↑(young) ↓(older) (all depots) |
↑(young) ↓(older) (all depots) |
| Adipocyte Size | ↑ | ↓ (Epi) | No data | ↑ | No data | ↑ | ↑ | ↔ | ↓ | |
|
Adipokine Leptin Adiponectin Resistin |
↑ ↑↑ ↑ |
↔ ↑ No data |
↑ ↑ No data |
↔/↑ ↑ No data |
↑↑ ↑ ↑ |
↑ ↔ No data |
↔/↑ ↔/↓ ↔ |
No data No data No data |
↑(female) ↑ ↑ |
↓ ↓ ↓ |
| Senescence | ↓ | ↓ | No data | No data | ↔ | No data | No data | No data | No data | ↑ |
*
Ames dwarfs and Snell dwarf mice are deficient in GH, PRL, and TSH