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EcoPhysioMichelle is a graduate student in organismal biology. Her thesis research is on the ecophysiology of epidermal lipids and water homeostasis in house sparrows, and she is a graduate teaching associate for an introductory human physiology class for non-majors. She blogs about human physiology, weird animal biology, and the interface of science and culture on her blog C6-H12-O6. You can follow her on Twitter (@physilology).
Hypoadiponectinemia is a long word that simply describes the state of having too little of a certain endocrine called adiponectin. Adiponectin is a major metabolic endocrine, and is responsible for regulating things like glucose uptake and lipolysis (the breakdown of fat stores). Having hypoadiponectinemia, or too little adiponectin, is a risk factor for both Type II Diabetes and metabolic syndrome (a syndrome principally characterized by central obesity, or an overly large waist circumference, among other things).
Plasma adiponectin concentration (or how much of the endocrine is present in your blood) is inversely correlated with the amount of body fat you have. The more body fat you have, the less adiponectin in your blood, and that results in less fat being broken down. Sounds like a deleterious positive feedback loop, doesn't it? How do you break the cycle? Well, you need to start losing fat. How do you start losing fat? Increase your adiponectin levels. How do you increase adiponectin levels when high levels of body fat are inhibiting its expression?
This may be a case where correlation doesn't equal causation (let's be honest: it rarely does). Instead of body fat itself influencing adiponectin levels in the body, it could be that diet plays a more important role in adiponectin expression. Specifically, high calorie or high fat diets (which lead to obesity) may cause adiponectin levels to plummet.
Researchers at UC San Diego recently designed an experiment to determine the relative influence of high calorie diets, high fat diets, and actual body fat on the expression of adiponectin in mice. They found a lot of really cool stuff, but a lot of it is complicated genetics stuff. I'm going to skip over some of that and just show you the most interesting results. First of all, they set up feeding regiments for the mice. We're going to focus on four of them:
HF-AL: high fat, ad libitum. These mice were fed a diet high in fat and were allowed to eat as much as they wanted.
LF-AL: low fat, ad libitum. They ate a low fat diet, but as much of it as they wanted.
HF-CR: high fat, calorie restricted. They ate a diet high in fat, but were restricted to a certain number of calories per day. They ate 60% of the calories that the LF-AL group ate.
LF-CR: low fat, calorie restricted. These mice ate the same number of calories per day as HF-CR, but their diet was lower in fat.
Now, let's look at what adiponectin is doing in these four groups:
In the top half of the figure, you can see that the calorie restricted mice (the ones on a "diet") had more circulating adiponectin than the ad-libitum mice. Not only that, but the two calorie restricted groups did not differ in circulating adiponectin. This suggests that total calorie intake is more important than the relative amount of dietary fat in influencing adiponectin levels. In addition, the calorie restricted groups did not gain as much weight as the ad libitum groups as you can see in the bottom half of the figure. This is not surprising. Less energy coming in will pretty much always equal less fat being stored when all other things are equal.
What does this mean for people with hypoadiponectinemia who are at risk for other diseases? The good news is that your already accumulated fat may not be a major inherent barrier to increasing your adiponectin levels. Decreasing your caloric intake (already a major staple of most diet programs) will likely go a long way towards stabilizing your adiponectin levels, which in turn will help you burn the fat you already have. As with most disorders related to obesity, the old standby of exercise and cutting calories remains the gold standard!
Citation: Liping Qiao, Bonggi Lee, Brice Kinney, Hyung sun Yoo, and Jianhua Shao. 2011. Energy intake and adiponectin gene expression. AJP - Endo. vol. 300 no. 5 E809-E816.
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The traditional HF diet of mice is also a diet high in sucrose. Was that the case here?
And I don't agree with the 'gold standard' you've proposed. :-)
Was this standard rat chow? If so, in addition to being high in sugars, it's also high in vegetable oils. Nasty stuff. It would be nice if you could delve more into the macronutrient breakdown and the types of fat in the HF and LF diets.