The answer is pretty straightforward. My body’s insulin would drop while glucagon would rise (1p246). Muscle and fat tissue would also become a bit resistant to insulin (1p246). Protein synthesis would drop (1p246). Glycogen from my liver would start becoming used up and muscles would release a mix of amino acids for gluconeogenesis (stimulating the glucagon) (1p246). The liver would keep my blood sugar level stable (1p246). If I didn’t eat for awhile, then my tissues would keep using fatty acids and glucose, but also start using ketones (from the fatty acid oxidation) for gluconeogenesis too (1p246). This is an important step to limit to conserve body protein, but does increase acidosis (1p246). The body has a way to deal with that too: more glutamine directed to the kidneys produces ammonia that combines with hydrogen ions to make urea for excretion (1p246). Acidosis is corrected and the kidney simply uses the carbon skeleton of glutamine to make glucose (1p246).
Summary of Starvation –
- Glucagon up, insulin down
- Reduced mRNA for translate of proteins
- Protein synthesis drops
- Increased starvation leads to decrease in secretion of glucocorticoids including cortisol
- Few days of fasting or starvation, glycogen is depleted and muscles undergo proteolysis for gluconeogenesis
- As fasting continues, tissues use fatty acids and glucose, but also ketones from fatty acids.
- Decrease in protein catabolism.
Apart from hurting pretty bad, stress from trauma like from a gun shot wound or burn would cause a bunch of problems. Mainly, it would send hormones in my body into a frenzy; glutocorticoids (primarily cortisol), catecholamines, cytokines, insulin and glucagon would all shoot up (1p246). Unlike starvation, the insulin presence would inhibit use of ketones for energy, thus, leaving me defenseless against muscle wasting (1p246). I’d lose more fast-twitch muscle than slow-twitch muscle (1p247). And yet, because tissues would be resistant to insulin, it would be useless in guarding against hyperglycemia caused partly by elevated cortisol (1p247). The cortisol, in fact, would be promoting the proteolysis (1p247). Cytokines would mediate proteolysis as well as hormonal response (1p247). The cytokines and glucocorticoids are thought to start synthesizing proteins including acute phase reactant and acute phase response proteins that cause fever, further hormonal changes and blood cell count changes (1p247). Other protein synthesis would decrease (1p247). To cope with possible loss of blood or to restore circulation depressed by shock, luckily, I’d have release of aldosterone and antidiuretic hormone to promote renal sodium and fluid reabsorption (1p247).
Summary of Stress –
- Glutocorticoids (primarily cortisol), catecholamines, cytokines, insulin and glucagon all up
- Tissues becomes resistant to insulin and hyperglycemia results
- Cytokines change substrate use
- Cortisol remains elevated causing proteolysis and hyperglycemia
- Cytokines and cortisol thought to increase synthesis of some proteins in liver to modulate body’s response; albumin and transferring to diminish stress
- Release of aldosterone causing sodium and fluid reabsorption and increasing blood volume (helps diminish fluid loss)
- Basal metabolic rate elevated
- Protein catabolism and lipolysis
- Lipolysis does not produce ketones for ketogenesis because of insulin presence and cannot defend against muscle catabolism
- Muscle wasting – white first, then red
- Protein turnover worsened by immune and acute phase responses (fever, etc.)
- Protein degradation exceeds starvation
Reference List
1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
