Biochemistry Ch. 2 21-28
The Fed or Absorptive State
*Know Figure 2.2 on pg. 23
Carbohydrates – are converted to monosaccharide
-starch is a polymer of glucose and is digested by salivary alpha amylase and pancreatic alpha amylase.
-oligosaccharides produced by alpha amylase converted to glucose by digestive enzymes on intestine
-sucrase converts sucrose to glucose and fructose;; lactase converts lactose to glucose and galactose
-monosaccharides are absorbed by intestinal epithelium and released to hepatic portal vein for liver
Proteins – are cleaved to amino acids by proteases after ingestion (cleaving peptide bonds)
-Pepin acts in the stomach whereas trypsin, chymotrypsin, elastase, and carboxypeptidase (produced in
pancreas) acts in small intestine
-Digested amino acids are absorbed by intestinal epithelium and carried to liver by hepatic portal vein
Fats – triacylglycerols of diet are emulsified in intestine by bile salts (synthesized by liver and stored in
gallbladder)
-pancreatic lipase converts triacylglycerols to fatty acids and 2-monoacylglycerols in lumen of intestine,
which interact with bile salts to form microdroplets called micelles
-fatty acids are taken up by micelles and absorbed by intestinal epithelial cells, where they are
resynthesized into triacylglycerols
-these new triacylglycerols are combined with proteins, phospholipids and cholesterol to form
lipoprotein complexes called chylomicrons – secreted into LYMPH and enter bloodstream
Changes in Hormone Levels after a Meal – after carb-rich meal, pancreas releases insulin, and glucagon
is INHIBITED.
-endocrine hormones released into blood to carry messages between tissues and adjust the rate of
metabolic pathways to meet changing conditions
-Insulin is released by B-cells of pancreas and signals that glucose can be used
-Glucagon is released by A-cells of the pancreas and signals that glucose must be generated from
endogenous fuel stores (INHIBITED BY GLUCOSE AND INSULIN)
Fate of Glucose after a Meal – glucose first gets converted to glycogen, triacylglycerols and CO2 in liver.
-glucose leaves intestine through hepatic portal vein and enters the liver. Hepatocytes absorb some of
the glucose for their own needs, while the rest is stored as glycogen and triacylglycerols
-insulin promotes uptake of glucose by liver by increasing its use as fuel and storage
-glucose  pyruvate  Acetyl Co-A  enters TCA cycle  CO2 + ATP
-Co-enzyme A makes acetyl group more reactive and is derived from vitamin pantothenate
-liver glycogen stores reach max of approximately 200-300g after high carb meal (fat stores limitless)
-as liver stores become full, glucose becomes converted to triacylglycerols
-liver packages triacylglycerols with proteins, phospholipids and cholesterol into very low-density
lipoproteins (VLDL) and secreted into the bloodstream. These are stored in adipose tissue
Glucose Metabolism in Other Tissues – glucose not metabolized by liver travels to peripheral tissues
and oxidized for energy—muscle has very large glycogen stores
Insulin greatly stimulates uptake of glucose by muscle and adipose, but also other tissues need glucose
1. Brain and Neural Tissues – very dependent on glucose for ATP; except for starvation, glucose is
the only major fuel
a. Glucose major precursor of neurotransmitters
b. We become lightheaded with low glucose
2. Red Blood Cells – glucose is the only fuel used by RBCs because they lack mitochondria
a. RBCs rely on anaerobic glycolysis in the cytosol, which converts glucose to lactate
released in the blood
b. Without glucose, RBCs would not survive and would not be able to carry O2 to tissues
3. Muscle – skeletal muscles can use glucose from blood or from their own glycogen stores,
converting glucose to lactate through glycolysis or oxidizing completely to CO2 and H2O.
a. Muscle also uses other fuels such as fatty acids, but muscle uses glucose to replenish
glycogen stores depleted during exercise.
4. Adipose Tissue – insulin stimulates transport of glucose into adipose tissue which use them for
energy and as a source of glycerol to make triacylglycerols
Fate of Lipoproteins in Fed State – chylomicrons and VLDL are produced in the fed state and function to
provide blood a transport system for triacylglycerols and cholesterol (insoluble in H2O).
-Triacylglycerols from small intestine go into chylomicrons, those from VLDL come from liver
-As lipoproteins pass through blood vessels in adipose, triacylglycerols degraded to fatty acids and
glycerol, which enter the cells and combine with glycerol from blood glucose to reform triacylglycerols
and stored in large fat droplets in cells.
-Remaining chylomicrons cleared from blood by liver
-VLDL can be cleared by liver or converted to LDL which is cleared by liver or by peripheral cells
Fate of Amino Acids in the Fed State – Amino acids from dietary proteins travel from the intestine to
the liver by the hepatic portal vein for the synthesis of serum proteins, its own proteins, and Ncontaining compounds that need AA precursors such as nonessential AA, heme, hormones,
neurotransmitters, purine and pyrimidine.
-Liver can oxidize AA or convert them to glucose or ketone bodies and dispose of nitrogen as urea
-Many AA will go into peripheral circulation to be used for protein synthesis and biosynthetic processes
or oxidized for energy
-Proteins constantly undergo turnover, breakdown and synthesis to and from free pool of amino acids
Summary of Fed and Absorptive State –
-Glucose is major fuel for most tissues
-Excess glucose and other fuels are stored as glycogen in muscle and liver, or as triacylglycerols in
adipose tissue
-Amino acids from dietary proteins are converted to body proteins or oxidized as fuels
Anthropometric Measurements – use body parameters to monitor normal growth – height, weight,
triceps skinfold thickness, arm muscle circumference, waist circumference
Hypercholesterolemia – elevated cholesterol caused by specific mutation of a protein or excess
cholesterol intake
Hyperglycemia – high blood glucose caused by mutation to proteins or insulin resistance
Hyperlipidemia – high levels of blood lipids caused by mutation in proteins or ingestion of high-fat diets