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Chapter eight: Fasting
8.1.3.2 Other marine mammals
Polar bears likely exhibit episodes of metabolic depression throughout the year, and perhaps episodes of hibernation during denning (Nelson et al. 1983). Curiously, there are no
published studies of energy-saving strategies among any other types of marine mammals.
Hence, our vision of what makes up a “marine mammal” response is likely highly skewed.
This is obviously an important area for future comparative research into the bioenergetic
strategies of fasting among marine mammals.
8.1.4 Hormonal controls
Changes in an animal’s physiology during a fast—including metabolic rate, appetite,
growth, and choice of metabolic substrate—are all part of a controlled shift that is mediated by a suite of hormones. In this section, we will focus on those hormones thought to
be most important in fasting physiology of marine mammals, but the list is by no means
exhaustive.
Glucocorticoids are steroid hormones, known most commonly as a biochemical
marker of physiological stress (“stress hormone”). However, they have multiple specific purposes (such as within the immune system) including serving an important
regulatory role during fasting. In marine mammals, the primary glucocorticoid is cortisol. Plasma cortisol levels increase during prolonged fasting. Among its functions,
cortisol helps to provide energy by increasing lipolysis and the associated mobilization of FFA. However, it also assists in maintaining circulating glucose concentrations
via increased gluconeogenesis from protein stores. It is believed that during fasts the
impacts of increased cortisol on lipid mobilization predominate over protein wasting
effects (Ortiz et al. 2001).
The increase in lipolysis and lipid oxidation during extended fasting is thought to be
regulated by increased levels of growth hormone (GH) and decreased levels of leptin. GH
is a peptide hormone that, true to its name, stimulates cellular growth. However, it also
functions as a “stress hormone,” increasing in response to fasting in most species. It is
important in the conservation of protein during fasting by raising the concentration of free
fatty acids (via increased lipolysis). In non-fasting animals it also stimulates production of
the hormone IGF-1 (insulin-like growth factor 1), which is important in protein anabolism.
However, during fasting there is both an elevation of GH and suppression of IGF-1 (possibly due to reduced hepatic GH receptors) (Crocker et al. 2012). Inhibition of IGF-1 secretion
allows hypersecretion of GH during fasting without diverting energy to tissue growth
(Crocker et al. 2012).
Leptin is a relatively recently discovered hormone that is often referred to as the “satiety hormone.” It is made by fat cells, and in feeding animals it regulates the amount of fat
stored in the body through adjustment of the hunger response. In fed animals, as fat deposition surpasses a critical point, the fat cells release increasing levels of leptin, decreasing
the sensation of hunger (increasing satiety), and increasing energy expenditures, promoting lipid oxidation and reducing triacylglycerol synthesis. However, episodes of fasting
are usually associated with lowered leptin concentrations as part of an animal’s strategy
for limiting energy expenditures (Crocker et al. 2012).
This is partly because decreases in leptin are also associated with decreases in the thyroid hormones T3 (triiodothyronine) and T4 (thyroxine) in fasted animals. These hormones,
produced by the thyroid gland, are primarily responsible for regulation of metabolism,
and therefore decreased levels facilitate the decreases in metabolic expenditures associated with metabolic depression. This is despite the fact that the energy-demanding process
Chapter eight: Fasting
8.1.3.2 Other marine mammals
Polar bears likely exhibit episodes of metabolic depression throughout the year, and perhaps episodes of hibernation during denning (Nelson et al. 1983). Curiously, there are no
published studies of energy-saving strategies among any other types of marine mammals.
Hence, our vision of what makes up a “marine mammal” response is likely highly skewed.
This is obviously an important area for future comparative research into the bioenergetic
strategies of fasting among marine mammals.
8.1.4 Hormonal controls
Changes in an animal’s physiology during a fast—including metabolic rate, appetite,
growth, and choice of metabolic substrate—are all part of a controlled shift that is mediated by a suite of hormones. In this section, we will focus on those hormones thought to
be most important in fasting physiology of marine mammals, but the list is by no means
exhaustive.
Glucocorticoids are steroid hormones, known most commonly as a biochemical
marker of physiological stress (“stress hormone”). However, they have multiple specific purposes (such as within the immune system) including serving an important
regulatory role during fasting. In marine mammals, the primary glucocorticoid is cortisol. Plasma cortisol levels increase during prolonged fasting. Among its functions,
cortisol helps to provide energy by increasing lipolysis and the associated mobilization of FFA. However, it also assists in maintaining circulating glucose concentrations
via increased gluconeogenesis from protein stores. It is believed that during fasts the
impacts of increased cortisol on lipid mobilization predominate over protein wasting
effects (Ortiz et al. 2001).
The increase in lipolysis and lipid oxidation during extended fasting is thought to be
regulated by increased levels of growth hormone (GH) and decreased levels of leptin. GH
is a peptide hormone that, true to its name, stimulates cellular growth. However, it also
functions as a “stress hormone,” increasing in response to fasting in most species. It is
important in the conservation of protein during fasting by raising the concentration of free
fatty acids (via increased lipolysis). In non-fasting animals it also stimulates production of
the hormone IGF-1 (insulin-like growth factor 1), which is important in protein anabolism.
However, during fasting there is both an elevation of GH and suppression of IGF-1 (possibly due to reduced hepatic GH receptors) (Crocker et al. 2012). Inhibition of IGF-1 secretion
allows hypersecretion of GH during fasting without diverting energy to tissue growth
(Crocker et al. 2012).
Leptin is a relatively recently discovered hormone that is often referred to as the “satiety hormone.” It is made by fat cells, and in feeding animals it regulates the amount of fat
stored in the body through adjustment of the hunger response. In fed animals, as fat deposition surpasses a critical point, the fat cells release increasing levels of leptin, decreasing
the sensation of hunger (increasing satiety), and increasing energy expenditures, promoting lipid oxidation and reducing triacylglycerol synthesis. However, episodes of fasting
are usually associated with lowered leptin concentrations as part of an animal’s strategy
for limiting energy expenditures (Crocker et al. 2012).
This is partly because decreases in leptin are also associated with decreases in the thyroid hormones T3 (triiodothyronine) and T4 (thyroxine) in fasted animals. These hormones,
produced by the thyroid gland, are primarily responsible for regulation of metabolism,
and therefore decreased levels facilitate the decreases in metabolic expenditures associated with metabolic depression. This is despite the fact that the energy-demanding process