While we continue to debate the incidence and physiology of healthy obesity (i.e. adiposity without any evident health problems), there are ample examples of adiposity in the animal kingdom, where the accumulation of vast amounts of fat tissue are entirely compatible with good health.
One of these fascinating example is the grizzly bear, which accumulates enough fat to last all winter without any apparent ill-effects on its health – indeed, the accumulation of fat to a level that would be considered “morbidly obese” in humans in vital to its survival.
Thus, not only is “healthy” obesity possible in mammals, it may also be an important area of study to better understand healthy obesity (or lack of it) in humans.
Insights into healthy obesity comes from a fascinating study by Lynne Nelson and colleagues from Washington State University, in a paper published in Cell Metabolism.
The researchers studied metabolism in four adult female grizzly bears, trained to “voluntarily” allow blood samples to be drawn for this study (for a video on how exactly this was done click here).
Their study shows that as grizzly bears accumulate fat in preparation for hibernation, they become exquisitely insulin sensitive, only to switch to a state of insulin resistance as they enter hibernation. This process reverses as they emerge from hibernation months later.
While the paper describes in detail the metabolic and hormonal pathways involved in this modulation of insulin sensitivity (via PTEN/AKT signaling in adipose tissue, it suggests that it is the ability to maintain insulin sensitivity in the face of increased adipose tissue that allows these animals to remain metabolically healthy.
As readers may recall, this is akin to the finding in humans that healthy obese individuals also display high levels of insulin sensitivity compared to metabolically unhealthy obese individuals, who display the more typical insulin resistance.
While much of this ability to maintain insulin sensitivity in a state of adiposity may be genetic (as in the rare case of humans with PTEN haploinsufficiency) other factors that enhance insulin sensitivity (e.g. regular aerobic exercise) may also help prevent or alleviate the metabolic consequences of excess fat.
Other factors may well include the actual location of the expanded fat depots, with peripheral accumulation of subcutaneous fat being far less likely to cause metabolic problems (and perhaps even protect against) than visceral or ectopic fat.
Now I guess, we need a study to see how well healthy obese humans do in hibernation.
Hat tip to Susan Jelinski for pointing me to this paper
Nelson OL, Jansen HT, Galbreath E, Morgenstern K, Gehring JL, Rigano KS, Lee J, Gong J, Shaywitz AJ, Vella CA, Robbins CT, & Corbit KC (2014). Grizzly Bears Exhibit Augmented Insulin Sensitivity while Obese Prior to a Reversible Insulin Resistance during Hibernation. Cell metabolism, 20 (2), 376-82 PMID: 25100064