acetylmandarin

2+ Year Member
Oct 20, 2014
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Pre-Health (Field Undecided)
I understand why I got this question wrong: the antibiotic treatment would eliminate gut biota and have the same effect of knocking out the GPCR talked about in the passage, leading to weight gain, and thus an increase in adipocyte size.

I want to make sure I understand insulin sensitivity/resistance. So being insulin resistant is unhealthy (diabetes) because your body produces excess insulin to try and pick up glucose, but glucose uptake does not occur at a high enough rate.

So for this question, choice D would be true if, on the graph shown, the left sub column in the left most main column (GPCR 43 knockout, without acetate), would be lower in value than the WT equivalent in the column next to it, thus showing that the lack of GPCR 43 lowers insulin sensitivity because there is less glucose uptake? And this would be the same effect as in the question stem, which talks about the absence of gut microbiota.
 

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Decreased insulin sensitivity would mean that it doesn't respond properly to insulin. We know from the passage that SCFA's are used to activate GPCRs. From Figure 1, we can see that in WT cells (that have GPCR), adding acetate will lower the amount of glucose uptake, which is the same as saying it will decrease the insulin sensitivity as the cells respond less to insulin. This occurs in the WT cells but no difference is seen in the GPCR43 -/- cells, meaning that GPCR43 likely plays a role in decreasing insulin sensitivity.

Now the question refers to antibiotic treatment which kills the gut microbiota. In the passage it says that the bacteria are used to produce SCFA's. If the bacteria die, the SCFA's cant be produced and therefore there will be no GPCR activation. No GPCR activation is analogous to GPCR43 -/- in which insulin sensitivity is not affected.