Table 1.
Modulation of select endocrine factors during the transition from catabolism (fasting) to hyperanabolism (refeeding).
| Catabolism (fasting) |
Hyperanabolism (refeeding) |
|||||
|---|---|---|---|---|---|---|
| Response | Effect | Reference | Response | Effect | Reference | |
| GH | Elevated levels | Lipolysis (protein sparing) | Sheridan (1986), Deng et al. (2004), Albalat et al. (2005), Small and Peterson (2005), Norbeck et al. (2007), Picha et al. (2009) | Residually high, then decreasing | Elevated IGF production, enhanced protein uptake | Collie and Stevens (1985), Foster et al. (1991), Sun and Farmanfarmaian (1992), Fine et al. (1993), Norbeck et al. (2007), Picha et al. (2009), Pierce et al. (2011), Kling et al. (2012) |
| GHR (liver) | Downregulated | Hepatic GH resistance | Gray et al. (1992), Mori et al. (1992), Duan (1998), Deng et al. (2004), Saera-Vila et al. (2005), Norbeck et al. (2007), Picha et al. (2008b) | Upregulated | GH-induced IGF production | Gray et al. (1992), Small et al. (2006), Picha et al. (2008b) |
| IGFs | Suppressed | Growth stasis | Duan and Plisetskaya (1993), Picha et al. (2008b) | Elevated/Overcompensated | Enhanced somatic growth | Uchida et al. (2003), Beckman et al. (2004), Picha et al. (2008a); Picha et al. (2008b) |
| Ghrelin | Elevated levels | Increased appetite, GH secretion | Kaiya et al. (2003a); Ran et al. (2004), Unniappan and Peter (2004); Fox et al. (2007), Picha et al. (2009) | Residually high, then decreasing | Hyperphagia | Riley et al. (2005), Matsuda et al. (2006), Miura et al. (2006) |
| NPY | Elevated levels | Increased appetite | Peng et al. (1994), Silverstein et al. (1998), Leonard et al. (2001) | Residually high, then decreasing | Hyperphagia | Lopez-Patino et al. (1999), Narnaware et al. (2000), Volkoff and Peter (2001), Aldegunde and Mancebo (2006), Kiris et al. (2007) |
| Leptin | Species/tissue dependent | Regulation of energy metabolism? | Kling et al. (2009), Rønnestad et al. (2010), Fuentes et al. (2012), Frøiland et al. (2012), Trombley et al. (2012), Zhang et al. (2012) | Species/tissue dependent | Lipostatic signal? | Johnson et al. (2000), Nieminen et al. (2003), Volkoff et al. (2003), Murashita et al. (2008), Gorissen et al. (2009), Won et al. (2012) |
| Cortisol | Elevated levels | GH secretion, hepatic GH resistance, IGF-I suppression | Nishioka et al. (1985), Kajimura et al. (2003), Small and Peterson (2005), Leung et al. (2008), Pierce et al. (2011) | Low levels | Enhanced somatic growth | Kajimura et al. (2003), Leung et al. (2008) |
| Somatostatin | Elevated levels | Hepatic GH resistance, IGF-I suppression | Very and Sheridan (2002), Sheridan and Kittilson (2004) | Low levels | Enhanced somatic growth | Very and Sheridan (2002) |
The response, or relative presence of a component, during a particular metabolic state is paired with what is estimated to be the relevant effect it has in eliciting compensatory growth (GH, growth hormone; GHR, growth hormone receptor; IGFs, insulin-like growth factors; NPY, neuropeptide Y).