Earlier this week, I traveled to England to be interviewed as an applicant to Cambridge University. I took David A. Kessler's book, The End of Overeating, along for the flights and train rides. Interesting side note: in Europe, the book's subtitle isn't "Taking Control of the Insatiable American Appetite", but rather "Taking Control of Our Insatiable Appetite".
Well, my choice of reading material could not have been better, as at the beginning of the second of my two interviews, I was presented with the above photograph comparing lean and obese mice. In his book, Kessler mentions several fascinating studies on mice and rats. Here's an excerpt commenting a study where mice had to poke their noses into a hole in order to get a reward - in this case, Ensure, a liquid "nutritional" drink rich in sugar and fat.
"[Sara Ward] found that mice worked enough in an hour to earn approximately fourteen rewards, the last one requiring seventy-seven nose pokes.
This is scientific confirmation that the combination of fat and sugar is a strong reinforcer. In a conversation with Ward, I asked her how strong it really was. The breaking point at which the animals will no longer work for the reward, she told me, is slightly lower than the breaking point for cocaine. Animals are willing to work almost as hard to get either one."[1]
My main tasks were to theorize what was wrong with the mouse and why, then plan simple experiments to find out which specific condition the mouse had. My initial thought was that the mouse's problem was an increase in energy intake due to supernormal stimuli in the environment - specifically, being given higher concentrations of sucrose than could be found in a natural environment.
If the mice ate the same food, a simple way to determine whether the obese mouse is eating more is simply to measure the amount of food it's eating. The "result" of my experiment? The obese mouse ate three times as much as a normal one. I further theorized that the cause of this could be a problem in the hypothalamus, which is responsible for homeostatic mechanisms in the body.
Additionally, as leptin is one of the hormones that regulate appetite, I discussed the possibility that the mouse could have a problem with either leptin resistance or leptin synthesis. To determine which of those is the case, either of two simple experiments could work - either simply test the mouse's blood levels of leptin (they will be abnormally low or nonexistent if there are problems with leptin synthesis, and likely elevated in leptin resistance) or administer a shot of leptin to the obese mouse. If the mouse is leptin resistant, it will remain weight stable, while if the problem is with leptin synthesis, the mouse will lose weight.
I found a copy of the mouse photograph on a page that conveniently goes into an in-depth discussion of leptin and obesity in mice. Good stuff.
References
1. Kessler, David A. The End of Overeating: Taking Control of Our Insatiable Appetite. London: Penguin, 2009. 31. Print.
