Biochemistry Objectives 43
1.
Glucose/fatty acid/ketone body cycle in starvation: since glucose is not being
taken in exogenously in early starvation, it must be synthesized from fatty acid
stimulation and amino acid components for use in the brain and RBCs. The rest
of the body utilizes fatty acids to meet metabolic demand. In late starvation,
gluconeogenesis slows to preserve proteins as ketone bodies from fatty acid
oxidation displace brain glucose. Fatty acids are still used to meet the metabolic
demands of the body, and glucose is still utilized by RBCs.
2.
Pattern of changes in major food sources in well-fed to prolonged starvation:
a.
Insulin: high levels are important for glucose storage during the well-fed
state; in post-absorptive to prolonged starvation, insulin levels decline
drastically due to the increased need for blood glucose.
b.
Glucagon: low levels are maintained during the well-fed state due to the
abundance of exogenous glucose; however, during the post-absorptive
state and early starvation, where glycogenolysis is necessary, glucagon
synthesis and release is stimulated. Glucagon levels drop off during
prolonged starvation, where glucose is no longer used by the brain.
c.
Cortisol: low levels are maintained during the well-fed state due to the
abundance of exogenous glucose; however, during the late post-absorptive
state and early starvation, where protein catabolism for gluconeogenesis is
necessary, cortisol synthesis and release is stimulated. Cortisol levels drop
off during prolonged starvation in an effort to conserve proteins.
3.
Fatty acid maintenance of blood glucose during starvation: fatty acids are
important during starvation because their oxidation in the body provides energy to
meet metabolic demand while conserving glucose for tissues that depend on it.
Fatty acids also stimulate gluconeogenesis by providing acetyl CoA and inhibiting
pyruvate dehydrogenase.
4.
Fuel mobilization:
a.
Liver epinephrine to 1 or 2 receptors: both IP3/DAG  Ca2+ (1, via
CaM-kinase phosphorylation of phosphorylase kinase) and cAMP (2)
inhibit glycogenesis and stimulate glycogenolysis to glucose and
subsequent glucose release
b.
Muscle epinephrine to 2 receptors: cAMP increase causes
glycogenolysis to glucose-6-phosphate, which can then be used by the
muscle cell for fuel
c.
Muscle acetylcholine and Ca2+ release: neural impulse depolarized the
cell, causing increased Ca2+, and glycogenolysis to glucose-6-phosphate,
which can then be used by the muscle cell for fuel
d.
e.
Hormonal changes with trauma:
a. Ebb phase (acute response): think of this phase as an urgent call for
glucose and fuel use; glucagon, cortisol, epinephrine, and thyroid
hormone (increased metabolism) increase while insulin decreases.
Also, ADH and aldosterone increase to control fluids and sodium,
respectively, while sex hormones decrease.
b. Flow phase (chronic response): think of this phase as a need to repair
tissues, requiring glucose mobilization, and utilization in tissue. Thus,
cortisol and glucagon are upregulated to mobilize glucose, and insulin
is upregulated to deliver it to the damaged tissues.
Glucose recovery from trauma:
a. Insulin resistance and hyperinsulinemia and hyperglycemia: because
insulin is upregulated, non-damaged tissues develop an insulin
resistance, and the increased plasma glucose causes a hyperglycemia.
b. Accelerated protein catabolism: to synthesize glucose during trauma,
proteins are broken down without inhibition (emergency response).
This can lead to severe consequences, as response to prolonged trauma
can lead to breakdown of respiratory muscles leading to pneumonia
and death.
c. Increased gluconeogenesis: increased need for glucose to repair
trauma