Food Metabolism Flashcards
Fed State or…
post-absorptive state
Fasting State
pre-absorptive state
(gluconeogenesis,b-oxidation)
The Intestines Signal to your Brain and Pancreas via
Hormones
Hormonal Control of the “Fed State”
Insulin
Leptin
Leptin
released from fat cells and tells the brain that we are full and to suppress appetite
Insulin Triggers Cascades of Reactions in Many Tissues
liver, muscles, adiposites
Glucose Levels
Maintained at 4 – 7 mM in blood
(brain & RBC food)
Main Actions of Insulin
Stimulates gene expression
Upregulates glucose transporters on muscle and fat cells
Activates enzymes involved in FA and glycogen synthesis
Inhibits gluconeogenesis in the liver
Insulin Biosynthesis
starts w/ immature peptide Proinsulin to Mature Insulin Monomer
Insulin Signaling Leads to
Increased Gene Expression
Insulin Exocytosis by
Pancreatic b-cell
HIGH BLOOD GLUCOSE (FED STATE) TRIGGERS
SECRETION OF INSULIN BY THE PANCREAS
Insulin Promotes
Fatty Acid & Glycogen Synthesis
Net Result:
Insulin is Anabolic
Hormonal Control of the “Fasting or Starved State”
Glucagon
Epinephrine (adrenalin)
Glucagon and Epinephrine Oppose Insulin Action
Regulates gene expression
Inactivates enzymes involved in FA and glycogen synthesis
Stimulates gluconeogenesis in the liver
Stimulates FA and glycogen breakdown
Glucagon Release by
the Pancreatic a-cell
Glucagon Regulates Gene Expression and inhibits
pyruvate kinase gene expression
Glucagon Regulates Gene Expression
STOPS GLYCOLYSIS in liver
REDUCES FA SYNTHESIS
Fasting state favors gluconeogenesis because
F-2,6-BP is low (phosphatase active)
Glucagon/Epi Inhibit
Fatty Acid Synthesis
Glucagon/Epi Inhibit Fatty Acid Synthesis by
Reducing Malonyl CoA Levels
Glucagon/Epi Stimulate Fatty Acid b-Oxidation by
Reducing Malonyl-CoA Levels
Net Result: Glucagon/Epi
Catabolic
Hyperglycemia
high blood glucose
Diabetes Mellitus Increased reliance on
lipid metabolism
diabetes mimics the
starved state even though blood glucose is high!!!
Insulin Resistance (Type 2)
Obesity
Glucagon
