Carbohydrate, Fat, and Protein Control Flashcards

(33 cards)

1
Q

What are the types of carbohydrates?

A

monosaccharides (ex. glucose), disaccharide (ex. sucrose), polysaccharides (ex. glycogen)

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2
Q

Define: Glycolysis

A

breakdown of glucose to generate energy

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3
Q

What is normal fasting plasma glucose level?

A

70-110 mg/dL

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4
Q

Define: Glycogenesis

A

glucose –> glycogen, occurs after meals

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5
Q

Define: Glycogenolysis

A

glycogen –> glucose, process done by the liver in the fasted state

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6
Q

Define: Gluconeogenesis

A

amino acids & glycerol –> glucose, process done by the liver in the PROLONGED fasting state

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7
Q

What is secreted by pancreatic alpha cells?

A

glucagon, prolucagon

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8
Q

What is secreted by pancreatic beta cells?

A

make up 75% of pancreatic cells that have endocrine function- insulin, C-peptide, proinsulin, amylin

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9
Q

What is secreted by pancreatic delta cells?

A

somatostatin

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10
Q

What is secreted by pancreatic epsilon cells?

A

ghrelin

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11
Q

What effect does Somatostatin have in regulation of nutrient homeostasis?

A

INHIBIT secretion of insulin and glucagon

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12
Q

What effect does Glucagon have in regulation of nutrient homeostasis?

A

STIMULATE secretion of insulin and somatostatin

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13
Q

What effect does Insulin have in regulation of nutrient homeostasis?

A

INHIBIT secretion of glucagon

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14
Q

Describe the role of Incretins

A

feeding induces release of incretins (insulinotropic peptide) from the gut (GIP= glucose-dependent insulinotropic polypeptide, GLP-1= glucagon-like peptide 1) that is PROPORTIONAL to the nutrient load ingested to regulate the pancreas to INCREASE INSULIN and DECREASE GLUCAGON release

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15
Q

What physiological effects does increased glucagon have?

A

stimulates lipolysis in adipose tissue, glycogenolysis/gluconeogenesis in the liver

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16
Q

In a healthy patient, when is insulin secretion highest?

A

during the early phase of meals

17
Q

What factors increase insulin secretion?

A

-glucose
-amino acids
-high fatty acids
-glucagon
-GLP-1 (glucagon-like peptide 1)
-GIP (glucose-dependent insulinotropic polypeptide)
-acetylcholine (vagus stimulation)
-beta adrenoceptor receptor activation (fight or flight)
-sulfonylurea

18
Q

What factors decrease insulin secretion?

A

-chronically elevated glucose
-low fatty acids
-insulin
-somatostatin
-leptin
-beta blockers
-alpha adrenoceptor activation
-K+ depletion

19
Q

What are the primary target tissue for insulin?

A

liver, muscle, and adipose tissue

20
Q

Describe the insulin receptor

A

tyrosine kinase, alpha subunit has affinity for insulin binding and beta subunit is membrane bound portion which can illicit tyrosine kinase activity- phosphorylates insulin receptor substrate (IRS) –> MAP kinase –> phosphatidylinositol-3 (PI-3) kinase pathways –> further trigger downstream events

21
Q

What downstream events are triggered by activation of the insulin receptor?

A

-translocation of glucose transporter (GLUT4) to the cell member to increase glucose uptake
-increased glycogen synthase activity
-increased protein synthesis lipogenesis

22
Q

What role does GLUT play in insulin action?

A

when activated after insulin binding, GLUT mediate facilitated diffusion of glucose into cells

23
Q

Where is GLUT4 located?

A

muscle, adipose tissue

24
Q

Where is GLUT1 located?

A

all tissues, but especially red blood cells and brain

25
Where is GLUT2 located?
beta cells of the pancreas, liver, kidney, gut
26
What is the function of GLUT2?
regulates insulin release
27
What is the function of GLUT4?
insulin-mediated uptake of glucose
28
What effect does insulin have on adipose tissue?
increase triglyceride storage
29
What effect does insulin have on muscles?
increase glucose transport by GLUT4, glycogen synthesis, and protein synthesis
30
What effect does insulin have on the liver?
-increased glycogenesis, triglyceride synthesis and very low-density lipoprotein (VLDL) formation -decreased glycogenolysis, gluconeogenesis, conversion of fatty acids and amino acids to ketones, conversion of amino acids to glucose
31
Describe catabolism of fatty acids
fatty acids --> acetyl CoA --> acetoacetyl CoA --> CO2 (via citric acid cycle for ATP generation) OR acetoacetate (formed in liver only) --> beta-hydroxybutyrate OR acetone (ketone bodies that are formed outside of the liver and entered into blood circulation)
32
Define: Ketoacidosis
accumulation of ketone bodies that exceed the buffering capacity of the blood
33
What conditions can cause ketoacidosis?
-starvation -high fat, low carbohydrate diet -diabetes mellitus