Do artificial sweeteners increase diabetes risk?
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Do artificial sweeteners increase diabetes risk?
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[post_date] => 2024-12-23 18:23:57
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[post_content] => Practice Passage (Question 1-5)
*This passage is the property of Khan Academy and has been reformatted into an AAMC-style interface in their entirety by MedLife Mastery. MedLife Mastery does not endorse and is not an affiliate of Khan Academy.
The effect of non-caloric artificial sweeteners (NAS) on human metabolism is controversial. Some studies suggest that NAS may short-circuit metabolic pathways, resulting in consequences that range from increased obesity rates to higher cancer incidence. Scientists performed three experiments to assess the effects of NAS on blood glucose levels and glycemic index (a number that indicates the total rise in a person's blood glucose after ingesting a particular food) and how the host’s intestinal microbes modulate these effects.
Experiment 1
Scientists supplemented the drinking water of mice with high doses of saccharin, sucralose, or aspartame, all of which are commonly used NAS. Control groups of mice were given water only or water supplemented with glucose or sucrose solutions. After 11 weeks of exposure, glucose tolerance testing was performed on all groups of mice. The results are shown in Figure 1.
Figure 1 Glucose tolerance testing in experimental and control mice: blood glucose levels are shown per 15-30 minute interval following ingestion of oral glucose solution at t = 0; * and ** indicate significantly different results at p < .05 and p < .01, respectively
Experiment 2
Scientists repeated the same experiment, but this time they separated each group of mice into two smaller groups and treated one group with antibiotic A and another with antibiotic B. Results are shown in Figure 2.
Figure 3 Glucose tolerance testing following microbiota transplant from donor mice; blood glucose levels are shown per 15-30 minute interval following ingestion of oral glucose solution at t = 0; * and ** indicate significantly different results at p < .05 and p < .01, respectively.
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[question] => What conclusion can be drawn from the data presented in Experiment 1?
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[answer] => 2
[description] => Reason for Correct Answer:
Figure 1 shows glucose tolerance testing results for groups of rats who have been exposed to either normal drinking water or drinking water supplemented with glucose or fructose (sugars) or non-caloric artificial sweeteners (NAS) saccharin, sucralose, or aspartame.
Glycemic index is defined in paragraph 1 as the effect of a food on blood sugar, so the data in Figure 1 reflect the glycemic index of glucose itself, as it shows blood sugar response to ingesting glucose. A higher glycemic index of glucose would result in higher blood glucose levels during glucose tolerance testing, and this would be a proxy for increased diabetes risk.
Figure 1 shows that rats whose drinking water had been supplemented with NAS, particularly saccharin, had higher blood glucose levels on glucose tolerance testing. This means that long-term saccharin exposure increased the glycemic index of glucose (its effect on blood sugar) in these rats.
Reason for Incorrect Answer:
A. The data show the saccharin exposure group having higher blood glucose levels on glucose tolerance testing, suggesting that saccharin exposure may be a higher risk factor for diabetes.
C. The rats that had been exposed to sucrose or glucose long-term had no change in glucose tolerance testing, compared to the rats that had only been given drinking water.
D. The actual glycemic indexes of the NAS were not tested. The experiment tested the effects of glucose on blood sugar levels in the different groups, after long-term exposure to NAS
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[answers] => Array
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[0] => Array
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[each_answer] => A. Compared to saccharin use, sucralose use is a larger risk factor for diabetes.
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[1] => Array
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[each_answer] => B. Long-term saccharin intake increases the glycemic index of glucose.
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[2] => Array
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[each_answer] => C. Long-term glucose and sucrose intake increase diabetes risk.
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[3] => Array
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[each_answer] => D. Saccharin has a higher glycemic index than glucose.
)
)
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[1] => Array
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[quiz_unique_key] => 1403770772
[question] => Impaired glucose tolerance (IGT) is a pre-diabetic state characterized by hyperglycemia. According to the results of experiments 1 and 2, what can we conclude about the role of antibiotics and NAS on IGT?
[value] => Array
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[answer] => 4
[description] => Reason for Correct Answer:
An increase in IGT in the rats should be indicated by higher blood sugar levels on glucose tolerance testing.
The data in Figure 1 indicates worse glucose tolerance in the groups of rats that were supplemented with NAS.
The data in Figure 2 shows that all the groups of rats, regardless of NAS exposure, had similar glucose tolerance results when antibiotics A or B were administered.
This suggests that antibiotics reset NAS-induced IGT.
)
[answers] => Array
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[0] => Array
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[each_answer] => A. Both antibiotics and NAS reduced IGT.
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[1] => Array
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[each_answer] => B. Antibiotics increased IGT and NAS lowered it.
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[2] => Array
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[each_answer] => C. NAS reset antibiotic-induced IGT.
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[3] => Array
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[each_answer] => D. Antibiotics reset NAS-induced IGT.
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[2] => Array
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[quiz_unique_key] => 1403770772
[question] => What is the rationale for performing Experiments 2 and 3?
[value] => Array
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[answer] => 2
[description] => Reason for Correct Answer:
Consequential is something that happens as a result of something else.
Correlation occurs when two events are linked to each other but do not necessarily imply causation.
Experiment 2 does not show that NAS-induced glucose intolerance is caused by microbiota; it merely shows that NAS-induced glucose intolerance is reversed by antibiotics, indicating that microbiota is likely correlated to glucose tolerance.
The results of transplant of microbiota exposed to saccharin in Experiment 3 show that microbiota is causative in the development of glucose intolerance, as the group of mice received an intestinal microbiota transplant from donor mice that drank saccharin solution inherited that impaired glucose tolerance.
)
[answers] => Array
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[0] => Array
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[each_answer] => A. Experiment 2 suggests that NAS-induced glucose intolerance is correlated with alterations to the intestinal microbiota while Experiment 3 shows that the role of microbiota is consequential.
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[1] => Array
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[each_answer] => B. Experiment 2 suggests that NAS-induced glucose intolerance is correlated with alterations to the intestinal microbiota while Experiment 3 shows that the microbiota role is causal.
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[2] => Array
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[each_answer] => C. Experiment 3 suggests that NAS-induced glucose intolerance is mediated through alterations to the intestinal microbiota while Experiment 2 shows that the microbiota role is consequential.
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[each_answer] => D. Experiment 3 suggests that NAS-induced glucose intolerance is mediated through alterations to the intestinal microbiota while Experiment 2 shows that the microbiota role is causal.
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[quiz_unique_key] => 1403770772
[question] => Which hormones are produced in response to hypoglycemia?
[value] => Array
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[answer] => 1
[description] => Reason for Correct Answer:
Erythropoietin stimulates the production of red blood cells.
Aldosterone increases sodium reabsorption in the kidneys due low blood pressure.
Estrogen is sex hormone, and it is not directly related with blood glucose levels.
Insulin production is increased due to hyperglycemia.
Both glucagon and cortisol production are increased when blood sugar levels are low (in the setting of hypoglycemia).
)
[answers] => Array
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[0] => Array
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[each_answer] => A. Glucagon and cortisol
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[1] => Array
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[each_answer] => B. Glucagon and erythropoietin
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[2] => Array
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[each_answer] => C. Insulin and estrogen
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[3] => Array
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[each_answer] => D. Insulin and aldosterone
)
)
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[4] => Array
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[quiz_unique_key] => 1403770772
[question] => Which graph most closely portrays changes in insulin levels during glucose tolerance testing in normal rats?
[value] => Array
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[answer] => 2
[description] => Reason for Correct Answer:
The figure description states that glucose tolerance testing involves periodic blood glucose measurements after an oral glucose solution is taken at t = 0.
The graphs show that, although the glucose is eaten at t = 0, blood glucose levels don’t rise until around t = 15, as it takes some time for glucose to be absorbed into the bloodstream.
Insulin levels rise in response to blood glucose, as insulin acts to lower blood sugar.
Therefore, insulin should also peak around t = 15 and then go down as blood glucose begins to normalize.
)
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[each_answer] => A.
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[each_answer] => B.
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[each_answer] => C.
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[each_answer] => D.
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Figure 1
Figure 3
