Fructose Flashcards

1
Q

Fructose rapidly converts to…

A

glucose, glycogen, lactate, fat

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2
Q

Fructose glycemic index is____ but high consumption causes

A

low, insulin resistance, obesity, type 2 diabetes, dyslipidemia, oxidative stress

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3
Q

GLUT 5

A

transports fructose into the enterocyte, doesn’t require ATP

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4
Q

GLUT 2

A

fructose diffuses into blood vessels at basolaterol pole, and can go into liver

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5
Q

How does fructose metabolism in liver differ from glucose?

A
  1. nearly complete hepatic extraction
  2. fructokinase and fructose -1-P for initial steps
  3. massive uptake and phosphorylation of fructose can lead to degradation of ATP to AMP and uric acid
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6
Q

What controls glucose under glycolysis?

A
  • hexokinase, or glucokinase which have a high Km for glucose
  • Phosphofructokinase (inhibited by ATP and citrate, feedback regulation based on energy of the cell)
  • insulin (stimulates glucokinase gene expression and activates glycolytic enzymes)
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7
Q

Fructose metabolism regulation

A

fructose conversion occurs independent of insulin, is a rapid process because fructokinase has a low Km for fructose, and no feedback system from ATP or citrate

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8
Q

What is a problem with lack of fructose regulation?

A

depletion of free phosphate and a decrease in ATP in liver cells (need ATP for conversion)

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9
Q

What happens to the fructose thats converted to glucose?

A

it’s stored as glycogen or released as plasma glucose

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10
Q

What happens to fructose converted to lactate

A

occurs in liver and enterocyte, leads to lactacidemia

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11
Q

What happens to fructose converted to fatty acid?

A

only a small portion, but could lead to steatosis (fatty liver)

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12
Q

Fructose intake increases hepatic glycogen _____ than an equivalent dose of glucose

A

more

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13
Q

Problems with fructose-induced hyperlactatemia

A

leads to increased adipocytes because it prevents lipolysis from being suppressed

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14
Q

Problems with fructose having a low glycemic index

A
  • doesn’t suppress ghrelin (hunger signal) as well as glucose
  • hinders leptin increase (satiety signal), causes leptin resistance by increasing cytokine 3 (suppressor of leptin) and decreasing serine/theonine phosphorylation of key proteins which could lead to fatty liver
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15
Q

Effect of high-fructose diet compared to same level of glucose

A

increases VLDL (converts to LDL), increase triglyceride production, decrease TG clearance, very lipogenic (supplied triosephosphate, a fatty acid synthesis precursor), hepatic de novo synthesis is stimulated by providing both the glycerol and the fatty-acyl parts of VLDL-triglycerides

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16
Q

How does fructose increase hepatic de novo lipogensis?

A

trioses-P and acetyl-CoA, increased expression of lipogenic genes
-inhibits insulin signaling by reducing phosphorylation of IRS proteins, activates c-Jun terminal kinase (JNK) and increases oxidative stress