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PDA 1 > Carbohydrate, Fat, and Protein Control > Flashcards

Carbohydrate, Fat, and Protein Control Flashcards

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
Q

Where is GLUT2 located?

A

beta cells of the pancreas, liver, kidney, gut

26
Q

What is the function of GLUT2?

A

regulates insulin release

27
Q

What is the function of GLUT4?

A

insulin-mediated uptake of glucose

28
Q

What effect does insulin have on adipose tissue?

A

increase triglyceride storage

29
Q

What effect does insulin have on muscles?

A

increase glucose transport by GLUT4, glycogen synthesis, and protein synthesis

30
Q

What effect does insulin have on the liver?

A

-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
Q

Describe catabolism of fatty acids

A

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
Q

Define: Ketoacidosis

A

accumulation of ketone bodies that exceed the buffering capacity of the blood

33
Q

What conditions can cause ketoacidosis?

A

-starvation
-high fat, low carbohydrate diet
-diabetes mellitus

PDA 1 (10 decks)

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