digestion, absorption, transport Flashcards

0
Q

List all relevant enzymes, where they are produced, where they act, and their substrates and products.

A

a-amylase: produced by the salivary glands, act in the mouth, hydrolyses a-1,4 bonds of starches and glycogen produces dextrins.
pancreatic a-amylase: produced by the pancreas, acts in the small intestine, hydrolyses dextrins and produces maltose or glucose.
Maltase: produced by enterocytes, acts in small intestine, hydrolyzed maltose (a-1,4 bonds) forms 2 glucose molecules.
a-dextrinase: produced by enterocytes, acts in small intestine, hydrolyses a-1,6 bonds forming free glucose molecules

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1
Q

Describe the process of CHO digestion from the mouth to the brush border.

A

CHO undergo chemical transformations as they move through the GI tract. The glycosidic bonds that hold disaccharides and starches together are broken.
Process requires a serious of enzymes produced in the salivary glads, pancreas and small intestine.
Chemical digestion of starch begins in the mouth when the salivary glands release the enzyme a-amylase (breaks a-1,4 bonds) forming dextrins.
Once dextrins enter the stomach, the acidic environment stops the enzymatic activity of salivary a-amylase where dextrins then pass unchanged from the stomach into the small intestine.
Pancreatic a-amylase hydrolyzes a-1,4 glycosidic bonds transforming dextrins into disaccharide maltose.
Last maltase a brush border enzyme produced by enterocytes, finishes the job of starch digestion by hydrolyzing the last chemical bonds into two glucose molecules.
a-dextrinase, a brush border enzyme, hydrolysis a-1,6 glycosidic bonds .

**Now numerous glucose molecules are ready to be transported into the enterocytes.

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2
Q

Explain lactose intolerance and its treatment options.

A

Lactose intolerance: lactose enters the large intestine undigested. Bacteria ferment lactose producing
*gas
*abdominal cramps
*diarrhea
*bloating
Products such as lactose-free milk and over the counter lactase enzyme tablets

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3
Q

Describe the mechanisms by which each mono- is transported across the enterocyte. Specify all transporters and ions involved, whether each process is active, facilitated, and/or hormone mediated, and why?

A

Glucose and galactose are absorbed into the enterocyte by carrier-dependent, energy-requiring active transport. They move from a lower to higher concentration with assistance of transport proteins

Fructose is absorbed by facilitated diffusion. they move from a higher to lower concentration with the assistance of transport proteins

*once absorbed, mono- are circulated to the liver via hepatic portal system

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4
Q

Explain how insulin resistance could impact absorption.

A

Insulin resistance hinders glucose from being absorbed into cell membranes. This is called hyperglycemia when abnormally high levels of glucose is in the blood.

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5
Q

Describe what happens to mono- after they are absorbed.

A

After mono- are absorbed they circulate directly to the liver via the hepatic portal system, where the majority of galactose and fructose is converted into glucose.
Some mono- are converted to ribose (ATP, RNA, DNA)

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6
Q

Describe the glycemic response to CHO ingestion.

A

A rise in blood glucose levels can be detected shortly after we eat CHO-rich foods. Some foods cause blood glucose to rise quickly and remain elevated, while other elicit a more gradual increase.

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7
Q

Describe the terms glycemic index (GI) and glycemic load (GL), including how each is calculated, how they differ, and limitations of each.

A

glycemic index: a rating system used to categorize foods according to the relative glycemic responses they elicit
glycemic load: rating system used to categorize the bodies glycemic response to foods that takes into account GI as well as the amount of CHO

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8
Q

Explain how the glycemic index would affect glucose curves in individuals.

A

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9
Q

List examples of low and high GL and GI foods

A
High GL: 
*French fries
*baked potato
*white rice
Low GL:
*oat bran bread 
*apple
*cherries
High GI:
*baked potato
*french fries
*waffles
Low GI:
*oat bran bread
*cherries
*apple
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10
Q

Explain how one food item could be both high GI and a low GL food

A

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11
Q
Define: 
absorptive state 
postprandial state
postabsorptive state 
fasted state
A
absorptive state: when full, proceeds anabolic process 
postprandial state: 3-4 hours 
post-absorptive state: 12-18 hours
fast state: 18 hours up to 2 days
starvation: several weeks
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12
Q

Describe how blood glucose levels are maintained, how cells take up glucose, and how energy storage in the body is regulated.

A

Blood glucose levels are maintained by the hormones insulin (b-cells) & glucagon (a-cells) that are secreted from the pancreas. Cells take up glucose through transport proteins.

^glucose - ^ insulin - v glucose
v glucose - ^ glucagon - ^ glucose

when meals provide more glucose than required, insulin stimulates storage of glycogen. Once muscle & liver reach storage capacity excess glucose is converted to fat.

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13
Q

Describe the GLUT transporters, including how they function, which subtypes are expressed in which tissue; which subtypes are insulin resistant.

A

GLUT 2: monosaccharides facilitated transportation
GLUT 5: enables fructose to be transported to the intestinal lumen into enterocyte by facilitated transportation
GLUT 4: insulin responsive, skeletal muscle
SGLT-1: Active transport, glucose and galactose, apical membrane of kidney

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14
Q

Explain how insulin and glucagon work to maintain homeostasis. List where and which state each is produced.

A

Insulin and glucagon assist in blood glucose regulation and energy storage. When blood glucose levels increase, the pancreas takes action by releasing more insulin. Insulin in return lowers blood glucose by facilitating the uptake of glucose into many kinds of cells.
glucagon stimulates the breakdown of glycogen stores in the liver.

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15
Q

Describe functions of insulin in the metabolic tissues discussed in class.

A

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16
Q

Explain where CHO are stored in the body (tissues)

A

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17
Q

List the three primary fates of glucose after it is transported into the liver.

A

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18
Q

Discuss the primary function of glycogen stores (specific to tissue type)

A

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19
Q

Explain how glycogenesis and glycogenolysis are regulated.

A

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20
Q

compare and contrast glycogenesis and glycogenolysis in the liver and the muscle

A

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21
Q

Describe gluconeogenesis, including when it happens and the primary purpose.

A

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22
Q

List the precursors of gluconeogenesis.

A

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23
Q

Describe which three steps of glycolysis are bypassed during gluconeogenesis explain how/why they are key regulatory steps

A

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24
Q

Discuss how fructose metabolism is different from glucose metabolism

A

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25
Q

Discuss the differences in the effects insulin has on the liver, skeletal muscle, and adipose tissue

A

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26
Q

Explain how insulin, an anaerobic hormone, leads to the breakdown of glucose via glycolysis.

A

Insulin leads to the breakdown of glucose via glycolysis………….

27
Q

Define type 1 and type 2 diabetes and explain the chief differences

A

Type 1 diabetes: insulin is not produced in B-cells of the pancreas
Type 2 diabetes: sedentary lifestyle, insulin resistance, overweight

28
Q

convert the following glucose values to mg/dl
4mmol/L
6.5mmol/L
9mmol/L

list values that outside the normal range

A

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29
Q

compare blood glucose curves for diabetic and normal individuals following a meal

A

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30
Q

Define insulin resistance, describe how insulin function is affected in the various metabolic tissues in individuals with insulin resistance

A

Insulin resistance: insulin receptors have difficulty recognizing or responding to insulin.
Insulin function is affected in various metabolic tissues in individuals with insulin resistance……..

31
Q

Describe how insulin resistance, blood glucose, and blood insulin levels change over the natural history of type 2 diabetes

A

Type 2 diabetes is caused by insulin resistance, because insulin is not able to do its job, the transport of glucose across the cell membrane is impaired, which results in the accumulation of glucose in the blood. Elevated blood glucose levels cause the pancreas to release more insulin into the blood. Over a period of time the pancreas becomes worn out and can no longer produce insulin.