Chp8 Digestion And Absorption Of Cho

Front 1

۞ -----Common CHO’s in diet

Back 1

monosacchrides
disaccharides
polysaccharides

Front 2

۞ ----- monosaccharides

Back 2

glucose, fructose, galactose

Front 3

۞ ----- • Disaccharides:

Back 3

sucrose, lactose, maltose

Front 4

۞ -----Polysaccharides:

Back 4

amylose, amylopectin, glycogen

Front 5

۞ -----Digestible CHO’s

Back 5

•Easily digested

•cleavage of the bond between the hexose units

•final transport across the intestine as free hexose

Front 6

(Digestible CHO’s)

۞ -----PROCESS MAINLY

Back 6

1) duodenum with secretion of amylase

2) enterocyte enzymes ( brush border)

3)

Front 7

(Digestible CHO’s)

۞ -----The average diet contains about 300 gms of CHO

Back 7

20-35% of fat
10-15 % protein
55% CHO's in diet

Front 8

۞ -----Other dietary CHO’s include:

Back 8

Corn syrup –
maltodextrins

Invert sugar –

mixture of hydrolyzed sucrose which contains free glucose and fructose and is sweeter than sucrose due to the free fructose

Front 9

۞ -----Non-digestible CHO’s

Back 9

•alpha-galactosidic linkage (raffinose and stachyose) no human enzyme to break this linkage found in many legumes and dried beans


• beta-linked glucosyl – non-digested------ go to the large intestine and fermented---

Front 10

۞ -----Non-digestible CHO’s (2)

Back 10

*go to the large intestine produce SCFA’s, H+, Co2, methane (can be resorbed)

**increase the osmolarity in the large intestine – increase stool output

Front 11

۞ -----DIGESTION

Back 11

* Starts in the mouth --Alpha amylase in saliva

**duodenum--- pancreatic amylase

***enterocyte final bond cleavage

Front 12

۞ -----DIGESTION 2
Starch
process and refined

Back 12

Starch in association with protein or non-digestible CHO may hinder the intestinal luminal interaction

•processing of starch;

cracking, milling, heating increases the availability for ALPHA -amylase to breakdown the starch

• refined starches –

hydrolyzed efficiently

Front 13

۞ -----DIGESTION 3
starch inhibitors
infants and starch

Back 13

There may be other inhibitory factors that prevent the breakdown of the starch so about 1-10% passes to the colon

Infants have delayed maturation of pancreatic amylase and poor starch digestion if fed in early infancy

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۞ -----Brush border

Back 14

breaks down
*maltriose
**maltose
***alpha-limit dextrin

Front 15

۞ -----Primary Hypolactasia

Back 15

• In many lactose-producing mammals lactase is high in infants and declines after weaning


• In humans lactase decreases in late childhood or the second decade of life in many – autosomal recessive trait


• Adult level is 5-10% of the level newborns (can tolerate about 1 cup of milk per day) ( Lactose hydrolyzed milk often tolerated)


• Some populations maintain high lactase in adult life- dominant gene feature

Front 16

۞ -----Primary Hypolactasia
SYMPTOMS

Back 16

• abdominal distention

• gas

• nausea

• osmotic diarrhea

• irritable bowel

• recurrent abdominal pain

Front 17

۞ -----Primary Hypolactasia

(DIAGNOSIS)

Back 17

• remove lactose – symptoms stop

• reintroduce lactose – symptoms return

• loading (usually 50 gms) this is higher than individuals with low lactase level;

• rise in blood glucose (if normal)

*****if glucose is high, it means that lactose is being digested and turned into glucose

• breath hydrogen – lactose in colon fermented and high H+

• acidification of the colonic contents because of scfa’s produced by fermentation

• assay of jejunum

Front 18

۞ -----Congenital lactase
deficiency

Back 18

• autosomal recessive inheritance

• lactase gene is absent or not working

• symptom is diarrhea

• need a lactose-free diet (even trace amounts)

******primary congenital
"baby is born with it"
**Autosomal recessive rr

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۞ -----Lactose Intolerant

Back 19

*adults having low levels of lactose

**usually ppl know their limits

*** most can tolerate about one cup of milk daily

****milk in coffee is OK, but not a whole glass of milk

Front 20

۞ -----Secondary disaccharidase
deficiency

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• celiac disease*****alergic to some grains, so the intestine swells and does not transfer things well.

• cow milk protein intolerance

• infectious diarrhea***** Sloughing of villi = lactase becomes affected so they lose the ability to metabolize milk.

• lactase is the most severely affected

• treatment of the primary problem alleviates the problem

*** cause of other disease of the intestine

Front 21

۞ -----Absorption

Back 21

• lined by a single layer of columnar cells, attached by tight junctions – impermeable even to small molecules

• transporters or carriers must promote entry and exit to cell

Front 22

۞ -----Absorption
HEXOSE TRANSPORTERS

Back 22

• glu and gal use the same sodium glucose transporter – SGLT1
• SGGLT1 supports binding and transfer of 2 sodium and 1 glu or gal into cell
• Entry dependent on NA
• Active transport using Na+, K+, ATPase requires energy
• Glu and gal accumulate and exit down a concentration gradient to the capillary beds of the portal system

Front 23

۞ -----Absorption
FRUCTOSE

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• Facilitated diffusion
• Supported by GLUT5 a brush border membrane protein
• Proceeds down a concentration gradient

Front 24

۞ -----Absorption
Factors affecting CHO
assimilation

Back 24

• Luminal hydrolysis is a rate limiting step

• Monosaccharide transport rate limiting
• Rate of chewing and time in the mouth for starch

• Nutrient composition; fat, fiber and high osmolarity will slow gastric emptying

• Pancreatic excretions are usually 10 times greater than needed and lack of hydrolysis is related to physical characteristics (eg. milling) ****can be used as a protein source

• Lactase in people who maintain ability to digest lactose is 1/3 that of sucrase