Metabolism Flashcards

1
Q

What causes insulin resistance?

A

Insulin resistance is when the cells don’t respond to insulin as well, causing the pancreas to make more insulin to maintain healthy blood glucose levels

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2
Q

Where is insulin released from

A

pancreatic beta cells

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3
Q

What does insulin do?

A

binds to insulin receptors and induces glucose uptake into the cells

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4
Q

What does increased glucose in the blood do to insulin production?

A

increase in glucose stimulated production of insulin

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5
Q

Estrogen increases or decreases subcutaneous adipose tissue beige-ing?

A

increase

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6
Q

What is the effect of ERa signaling on thermogenesis in brown adipose tissue

A

it enhances it

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7
Q

Does estrogen reduce or increase inflammation in adipocytes?

A

reduce inflammation

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8
Q

what are the effects of estrogen on food intake?

A

decreases food intake via the hypothalamus

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9
Q

How does estrogen affect energy expenditure?

A

increases energy expenditure

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10
Q

How does estrogen affect leptin sensitivity?

A

increases leptin sensitivity

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11
Q

How does estrogen affect insulin synthesis and secretion (pancreas)?

A

increases it

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12
Q

What is the effect of estrogen on mitochondrial activity?

A

increases mitochondrial activity

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13
Q

What is the effect of estrogen on insulin sensitivity?

A

increases sensitivity

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14
Q

What is the effect of diabetes on cerebral blood flow?

A

Elderly people with T2 diabetes have reduced cerebral blood flo

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15
Q

What is the connection between obesity and diabetes?

A

visceral adiposity accelerates atherosclerosis

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16
Q

Why is chronic hyperglycemia damaging?

A

a. Proteins or lipids interact with sugars for extended periods of time to form AGEs
b. It produces advanced glycation end products
c. AGEs are associated with cognitive dysfunction and have been shown to accumulate in the brains of diabetic rats
d. AGEs can contribute to atherosclerosis
e. RAGE receptors become upregulated
f. Can form cross links with molecules in the basement membrane and alter cellular structure and increase vascular stiffness
g. Can induce monocyte migration across an endo monolayer
h. Activation of RAGE can increase leakiness of a monolayer (is this also true in the BBB?)
i. Reduce the bioavailability of NO
i. Potential mechanisms: reduce the half-life of eNOS, deactivation of eNOS, quenching of NO
j. In endothelial cells, AGEs bind to RAGE and this results in the production of ROS

17
Q

What does ERalpha do in pancreatic beta cells?

A

ERα in pancreatic beta cells has been proposed to regulate insulin production in vivo, such that it has an anti-diabetic effect (Le May et al., 2006; Wong et al., 2010).

Consistent with these findings, αERKO mice show impaired glucose tolerance and increased insulin resistance (Ribas et al., 2010).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4024050/pdf/nihms-580925.pdf