Lecture 34: Absorptive and Postabsorptive Nutrient Utilization-2 Flashcards
What happens to glucose and glucagon during the postabsorptive phase
Blood glucose decreases, stimulates glucagon and inhibits insulin secretion
Describe the liver transition from absorptive to postabsorptive phase
Liver switches from glucose utilization to glucose production by glycogen and gluconeogenesis
What tissues are using glucose during postabsorptive phase
All tissues, including brain. Muscle and adipose tissue at a diminished rate
How does the liver mobilize its stores during postabsorptive phase
Decrease glucose stimulates glucagon secretion
Glucagon stimulated glycogenolysis and gluconeogenesis
How long does glycogen depot last during rest/moderate ecercise
8-12 hrs
How long does glycogen depot last during high demand/severe exercise
30 minutes
How does glucagon act on adipose tissues
Stimulates lipolysis
__ and ___ stimulate lipolysis and FA release through B-adrenoreceptors
Epi and NE
___ peptide from the heart stimulate lipolysis during exercise
Natriuretic
__ and ___ reinforce increased lipolysis during and after prolonged exercise
Growth hormone and cortisol
How are FA mobilized and released from adipose tissue
- Epi or Glucagon bind B-adrenergic receptor
- Activate hormone sensitive lipase
- NEFA are transported out as free FA, bound to albumin or VLDL
- Taken up by liver and skeletal muscle
NEFA’s are used for synthesis of ___ and ___
Ketones and VLDL
Why are there multiple transport mechanisms for NEFA’s
Albumin decreases during long phases of nutrient deficiency. VLDL’s are independent of AA availability
What transporters FA into cells
CD36
Describe the steps in transportation of FA into cells—> kreb cycle
- NEFA’s bind albumin and are transported
- CD36 transporters NEFA’s into cell
- After absorption enter B-oxidation in Krebs cycle
How does the absorption of fatty acids and glucose in the absorptive phase vs postabsorptive (what receptors are used)
Absorptive: GLUT4
Post-absorptive: CD36
How are muscle stores/proteins utilized during postabsorptive phase
- Decrease AA entry into AA pool
- Degrade and use AA pool for energy
During the postabsorptive phase what enzymes does glucagon activate and deactivate
Deactivate: glycogensynthase and phosphofructokinase
Activate: fructose-1,6 biphosphate and glycogenophosphorylase
Without food for 24 hrs or more the body forms ___
Ketone bodies
After 24 hours without food all glycogen stores are exhausted and the body utilized ___ for energy
FA (which get converted to ketones)
Brain can’t use __ too large so for first 48hrs without food the brain uses ___
FA, glucose
> 48hrs without food the liver metabolizes FA to ___ which can be used by the brain
Ketone bodies
How does the fuel oxidation shift in prolonged energy deficiency
Carbs to mainly lipids as oxidative source
During prolonged energy deficiency what happens to lipolysis
Increases to provide body with FA—> TG and ketone bodies
during prolonged energy deficiency __ are released from adipose tissue
NEFA’s
What are the three mechanisms by which liver utilizations NEFA’s
- Oxidation
- Triglycerides
- Ketones
During the prolonged energy deficiency phase, the goal is to preserve ___ and ___ and utilize ___
Glucose, AA and utilize fat
Liver can produce FA from glucose and AA during absorptive phase or consume fatty acids and channel them to krebs or into ketogenesis. What determines pathway to use
Levels of malonyl Co-A, decreased levels enter ketogenesis
During the absorptive phase (insulin high) malonyl CoA suppresses ___
CPT-1
During postabsorptive phase and prolonged deficiency malonyl-CoA is __ because glugacon inhibits glycolysis
Low
When malonyl CoA is low what happens to FA
- FA are released from adipose tissues and transported to mitochondria via CPT-1
- FA into mitochondria-> B oxidation and ketone body synthesis
What is happening during hepatic lipodosis
Can’t convert NEFA to VLDL because hepatocytes become overwhelmed by NEFA
Hepatic lipodosis leads to build up of TG’s which results in ___
Fatty liver
What diseases are associated with hepatic lipodosis
Old age, obesity, DM, pancreatitis, DKA, IBD, cholangitis, hepatitis, cancer
What are some symptoms of hepatic lipodosis in cats
Anorexia, obesity, icterus, liver enlargement, vomiting
What is the treatment for H. Lipodosis
High protein diet
How doe s a ruminant maintain glucose homeostasis
Production of propionate which results in gluconeogenesis
What is negative energy balance in dairy cows
Usually occurs post calving and during lactation when they start spending lots of energy to produce milk and not gaining enough energy via feed3
What happens to electrolytes during starvation (clinical correlation: refeeding)
Shift from intracellular space to extra cellular space
What causes refeeding syndrome
Surge of insulin movement of electrolytes back to intracellular space and overwhelm, leading to severe hypokalemia
What effect does insulin play in electrolyte homeostasis in regards to refeeding syndrome
Activates Na/K+ pump, movement of K+ to intracellular space—> hypokalemia—> effects on membrane potential for nervous tissue and cardiac muscle
What is the therapy strategy for refeeding syndrome
Low carb/high fat diet
Adequate K, PO4, MG
