Digestion Of Carbs

Front 1

Describe the various forms of carbs.

Back 1

1. Simple
- mono & di = glucose, fructose, sucrose & lactose
- rapidly reabsorbed
- rapidly increase BSL

2. Complex
- starch & fiber
- starch is more readily digested than non starch polysach.
- Fiber (cellulose) passes through GI, not digested, no nutritional value

Front 2

Describe the types of starch.

Back 2

Amylose;
o Unbranched, linear
o Alpha 1,4- glycosidic linkage
• Amylose can also form fat & proteins which further limit digestion
• Amylose degradation = slow rise in postprandial glucose = low glycemic index

Amylopectin;
o Branched
o Identical to glycogen but lower degree of branching
o Alpha 1,6-glycosidic
o Flour, rice, pasta & potatoes
• high glycemic index (possibly contributes to diabetes)

Front 3

Descrive the role of amylase.

Back 3

• Amylase degrades amylose much less than amylopectin

Front 4

Describe cellulose.

Back 4

• Long unbranched
• Beta 1,4-glycosidic (Humans lack beta 1,4 glycosidase)

Front 5

Describe the breakdown of carbs.

Back 5

Mouth; Salivary & pancreatic amylase cleaves alpha 1,4 links

Stomach; Very little carb digestion (amylase inactive at low pH)

Small intestine; Majority of carb digestion due to pancreatic amylase (neutral pH)
-poly (pancreatic lipase) --> disaccharide (Disacchridases) --> monosaccahride

Large intestine; Carbs that are not digested pass to large intestine. Serves as substrate for bacterial metabolism

Front 6

Types of Disacchridases.

Back 6

alpha-glucosidase, sucrose, lactase and maltase

Front 7

What are the circulatory consequences of carb digestion.

Back 7

1. complex carbs = slow rise in postprandial glucose = low glycemic index

2. simple carbs = fast rise in postprandisl glucose = high glycemic index.

Front 8

Evaluate the mechanism of monosacchrides to enter the cell.

Back 8

• glucose, galacose & fructose (monos) are more easily absorpbed by monosacchride-transport systems.

(They're highly water soluble and unable to pass into the enterocyte by simple diffusion)

Front 9

Describe primary lactase deficiency.

Back 9

• often minority children
• carb-malabsorption syndrome
• prevalent in Hispanics
• symptoms; diarrhea, bloating, abdominal pain and flatulence
• caused by metabolism of lactose by intestinal bacteria producing CO2, H2 and SCFA

Front 10

Describe lactose intolerance.

Back 10

• Absence of lactase or reduced activity
• Autosomal recessive or present secondary to intestinal damages

Front 11

Describe SGLT transport.

Back 11

• glucose absorption up conc. gradient
• uptake 2 Na+ down conc. gradient
• allows glucose to move into cell against its gradient
• secondary active transport (symport)

Front 12

Describe Glut I.

Back 12

• High capacity ubiquitous protein
• Found in every cell type
• Responsible for basal glucose uptake
• Main transporter in erythrocytes, fetal tissue, placenta, fat & brain
• High affinity (low Km = 2mM), completely saturated and working optimally at physio plasma glucose levels

Front 13

Describe Glut II.

Back 13

• Major in liver, kidney, B cells of pancreas, and small intestine
• Insensitive to insulin
• High km = never fully saturated at physiological blood glucose level
• low affinity for glucose

Front 14

Describe Glut III.

Back 14

• Present in all cells
• Predominately in kidney, brain and nerve cells
• Low km (1-2mM) allows constant rate of basal glucose uptake independent of fluctuation in blood glucose conc. (completely saturated w/ glucose)
• Functions alongside GLUT I to optimize glucose uptake

Front 15

Describe Glut IV.

Back 15

• Uptake by skeletal and heart muscle and adipose tissue
• Km of 5mM
• sensitive to insulin increasing uptake by 12 fold
• located in intracellular vesicles in the cytoplasm
• deficiency = insulin deficiency = hyperglycemia in diabetes

Front 16

Describe Glut V.

Back 16

• Apical membrane in enterocytes, brain and muscle
• Primarily fructose uptake
• Functions with SGLT I and the uptake of glucose by peripheral tissue

Front 17

Describe carb metabolism in an adipocyte.

Back 17

• Primary role of white adipose tissue = storage & mobilization of tags
• Enter adipocyte via GLUT I & IV
• Trapped by hexokinase-catalyzed phosphorylation forming G6P
o Some cytoplasmic G6P can be oxidize in the PPP with the production of NADPH
• Glycogen synthase activity = low

• Western diet, do not produce fats from carbs, large amount of consumed fats down regulate the expression of acetyl-SCoA carboxylase and F.A. synthesis

Front 18

Describe carb metabolism in hepatocyte.

Back 18

• Center of metabolic activity
• Exposed first to the pancreatic hormones, insulin and glucagon via pancreatic veins (diluted before circulating)
• Functions as a buffer, soaking up glucose & distributing it to other tissues when needed

1. After meal, glucose from hepatic portal vein (10m/mol)
2. GLUT II takes up glucose along a massive concentration gradient
3. Glucose in hepatocyte = glucose in blood, intracellular G6P will rise in blood due to glucokinase (high km ~12 and rarely saturated but DOES NOT obey M-M kinetics)
4. G6P -> glucose via glycogen synthase (stimulated by glucose [sole stimulant], insulin and G6)
o Does not inhibit glucokinase
o G6P may be oxidized in glycolysis & CAC with production of ATP

Front 19

Explain the role of glucose phosphorylation in intracellular trapping.

Back 19

Occurs via hexokinase-catalyzed phosphorylation forming G6P