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First of all, I am ONLY analyzing the parts of the article that are included in the AAMC Section Bank! I'm reading the Introduction (all of it) & Results section (but only the parts that relate to what's in the SB which isn't actually all that much)
I would like anyone and everyone's input on this scientific journal article as it relates to the MCAT experimental-based passages format / required skills. I've outlined what I noticed was relevant to the correlating AAMC Section Bank B/B (passage 2). Let me know if you interpreted anything differently and enjoy the practice if you choose to participate!
Source: The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43
Title:
The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43
What’s the big picture
Obesity & diabetes are associated w/ altered GPR43 activity & FA metabolism (ie. our metabolism is storing too much body fat -or- retaining too much glucose in the blood).
Main idea/gist of the article
Gut microbes convert our dietary fat into SCFAs (signaling molecules) which activate adipose GPR43 (an adipose G-protein coupled receptor). This system regulates our metabolism. Any change to this system could lead to obesity or diabetes, depending on what is changed.
Purpose of the study
To determine the true function of adipose GPR43.
To determine the role of adipose GPR43 in the regulation of the energy balance.
The scientific logic/strategy behind each trial or experiment (e.g., Why did they choose those conditions? What variables were they controlling or isolating? What did they hope to clarify?)(the italicized parts are the titles taken straight from the journal article; IV = Independent Variable & DV = Dependent Variable)
Experiment: Gpr43 knockout mice exhibit obesity
Study purpose - to clarify the function of GPR43 in the WAT.
IV’s:
Yes gene or no gene
GPR43 +/+ (WT)
GPR43 -/-
Diet
Standard diet (Std)
High-fat diet (HFD)
DV:
Body weight (g)
Results:
upload my pictures
( ^The legend lists: WT (Std), GPR43 -/- (Std), WT (HFD), GPR43 -/- (HFD) )
^Conclusion:
-Over 16 weeks of growth, the knockout mice (ie. GPR43 -/-) exhibited an inc in Body Weight.
-Differences were enhanced when it came to the HFD mice.
-GPR43 +/+ : less weight gain.
-GPR43 -/- : more weight gain
-GPR43 (gene) prevents weight gain.
Experiment: GPR43 suppresses insulin signalling in adipose tissue
Study purpose:
To further examine the relationship between GPR43 function and insulin sensitivity.
IV’s:
Yes gene or no gene
GPR43 +/+ (WT)
GPR43 -/-
Tx of cells
Insulin yes/no
Acetate yes/no
DV:
Glucose uptake (nmol)(indicates insulin sensitivity)
Results:
how to upload pic
^( the y-axis measures Glucose Uptake)
Conclusion:
-without insulin we don’t expect a high level of glucose uptake. With insulin we expect a higher level of glucose uptake. However, in GPR43 +/+ (WT) mice, Acetate (could be from SCFAs, which come from gut microbes + dietary fat) suppresses glucose uptake (aka decreases insulin sensitivity) when insulin is present.
-GPR43 (gene) causes a decrease in glucose uptake, and therefore a decrease in insulin sensitivity (when acetate (aka SCFAs) is present).
What can be concluded from the results/data?
Gut microbes take our dietary fat and convert it into SCFAs (such as acetate). SCFAs stimulate GPR43. Stimulated GPR43 leads to decreased insulin sensitivity. Decreased insulin sensitivity leads to more glucose remaining in the blood. More glucose remaining in the blood leads to an increased risk of diabetes.
-however-
Without GPR43 there is an increase in insulin sensitivity which leads to an increase in the import of glucose which leads to an increase in FA synthesis which could lead to obesity.
I would like anyone and everyone's input on this scientific journal article as it relates to the MCAT experimental-based passages format / required skills. I've outlined what I noticed was relevant to the correlating AAMC Section Bank B/B (passage 2). Let me know if you interpreted anything differently and enjoy the practice if you choose to participate!
Source: The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43
Title:
The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43
What’s the big picture
Obesity & diabetes are associated w/ altered GPR43 activity & FA metabolism (ie. our metabolism is storing too much body fat -or- retaining too much glucose in the blood).
Main idea/gist of the article
Gut microbes convert our dietary fat into SCFAs (signaling molecules) which activate adipose GPR43 (an adipose G-protein coupled receptor). This system regulates our metabolism. Any change to this system could lead to obesity or diabetes, depending on what is changed.
Purpose of the study
To determine the true function of adipose GPR43.
To determine the role of adipose GPR43 in the regulation of the energy balance.
The scientific logic/strategy behind each trial or experiment (e.g., Why did they choose those conditions? What variables were they controlling or isolating? What did they hope to clarify?)(the italicized parts are the titles taken straight from the journal article; IV = Independent Variable & DV = Dependent Variable)
Experiment: Gpr43 knockout mice exhibit obesity
Study purpose - to clarify the function of GPR43 in the WAT.
IV’s:
Yes gene or no gene
GPR43 +/+ (WT)
GPR43 -/-
Diet
Standard diet (Std)
High-fat diet (HFD)
DV:
Body weight (g)
Results:
upload my pictures
( ^The legend lists: WT (Std), GPR43 -/- (Std), WT (HFD), GPR43 -/- (HFD) )
^Conclusion:
-Over 16 weeks of growth, the knockout mice (ie. GPR43 -/-) exhibited an inc in Body Weight.
-Differences were enhanced when it came to the HFD mice.
-GPR43 +/+ : less weight gain.
-GPR43 -/- : more weight gain
-GPR43 (gene) prevents weight gain.
Experiment: GPR43 suppresses insulin signalling in adipose tissue
Study purpose:
To further examine the relationship between GPR43 function and insulin sensitivity.
IV’s:
Yes gene or no gene
GPR43 +/+ (WT)
GPR43 -/-
Tx of cells
Insulin yes/no
Acetate yes/no
DV:
Glucose uptake (nmol)(indicates insulin sensitivity)
Results:
how to upload pic
^( the y-axis measures Glucose Uptake)
Conclusion:
-without insulin we don’t expect a high level of glucose uptake. With insulin we expect a higher level of glucose uptake. However, in GPR43 +/+ (WT) mice, Acetate (could be from SCFAs, which come from gut microbes + dietary fat) suppresses glucose uptake (aka decreases insulin sensitivity) when insulin is present.
-GPR43 (gene) causes a decrease in glucose uptake, and therefore a decrease in insulin sensitivity (when acetate (aka SCFAs) is present).
What can be concluded from the results/data?
Gut microbes take our dietary fat and convert it into SCFAs (such as acetate). SCFAs stimulate GPR43. Stimulated GPR43 leads to decreased insulin sensitivity. Decreased insulin sensitivity leads to more glucose remaining in the blood. More glucose remaining in the blood leads to an increased risk of diabetes.
-however-
Without GPR43 there is an increase in insulin sensitivity which leads to an increase in the import of glucose which leads to an increase in FA synthesis which could lead to obesity.
