L15 Flashcards

1
Q

how does digestion of carbohydrates begin?

A

in the mouth, salivary alpha-amylase breaks down polysaccharides
continues in the small intestine with pancreatic a-amylase breaking it down to monosaccharides

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2
Q

glucose and galactose leave the cell via ______

A

GLUT-2

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3
Q

contrast how glucose/galactose and fructose are absorbed

A

glucose/galactose - secondary active transport
fructose - facilitated diffusion

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4
Q

fructose enters the epithelial cells via ____ and enters the blood via _____

A

GLUT-5; GLUT-2

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5
Q

glycogenesis

A

synthesis of glycogen, stimulated by insulin

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6
Q

glycogenolysis

A

glycogen –> glucose
stimulated by glucagon and epinephrine

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7
Q

gluconeogenesis

A

synthesis of glucose from noncarbohydrates, such as fats and amino acids

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8
Q

____ ATPs generated per glucose

A

38

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9
Q

When blood glucose levels begin to fall, glucagon does 3 things:

A
  1. stimulates glycogenolysis in the liver by activating enzymes that hydrolyze glycogen and release
    glucose
  2. activates hepatic gluconeogenesis - amino acids –> glucose
  3. enhances lipolysis of triglyceride in adipose tissue as an additional way of conserving blood glucose.
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10
Q

______ and ______ are the primary sites where glycogen is found

A

liver and skeletal muscle

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11
Q

[alpha/beta] cells secrete [insulin/glucagon]

A

alpha cells secrete glucagon; beta cells secrete insulin

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12
Q

delta cells secrete _______

A

somatostatin

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13
Q

three enzymes required for glycogen breakdown

A
  • Glycogen phosphorylase
    – Glycogen debranching enzyme
    – Phosphoglucomutase
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14
Q

what is PEPCK?

A

key enzyme in gluconeogenesis, catalyzes the conversion of oxaloacetate to phosphoenolpyruvate.

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15
Q

what hormones inhibit transcription of PEPCK?

A

insulin

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16
Q

what hormones stimulate transcription of PEPCK?

A

thyroid hormone, glucagon, glucocorticoids

17
Q

how do glucocorticoids stimulate PEPCK expression?

A

by binding to a specific DNA sequence termed a glucocorticoid response element (GRE)

18
Q

contrast type 1/2 diabetes

A

In type 1 diabetes, pancreatic β-cells are destroyed by immune cells, such as T cells, macrophages, and the cytokines produced by these immune cells, resulting in an absolute deficiency of insulin, leading to hyperglycemia.
In type 2 diabetes, pancreatic β-cells are damaged by hyperglycemia, hyperlipidemia, cytokines, and amyloids. Although pancreatic β-cells produce insulin, the insulin level is insufficient to compensate for insulin resistance, resulting in a relative insulin deficiency, leading to hyperglycemia

19
Q

role of incretins in glucose homeostasis (3)

A

Incretins, gut-derived hormones like GLP-1 and GIP:
1. stimulating insulin secretion in a glucose-dependent manner
2. suppressing glucagon release, both of which lead to lower blood glucose levels
3. also decreased gastric emptying.

20
Q

________ is the first line medication for the treatment of type 2 diabetes. It works by _____

A

Metformin. decreases hepatic gluconeogenesis and intestinal absorption

21
Q

how is DPP-4 inhibition expected to improve blood glucose control?

A

by preventing the breakdown of incretin hormones (GLP-1 and GIP), which leads to increased insulin secretion and reduced glucagon secretion, ultimately lowering blood sugar levels

22
Q

other effects of insulin resistance

A

Endothelial dysfunction, Atherosclerosis, Hypertension, etc.

23
Q

3 major points of regulation of glycolysis - enzymes activated by insulin

A

hexokinase, phosphofructokinase, pyruvate kinase