Hibernating Bears (Ursidae)

Metabolic Magicians of Definite Interest for the Nephrologist

Peter Stenvinkel; Alkesh H Jani; Richard J Johnson

Disclosures

Kidney Int. 2013;83(2):207-212. 

In This Article

Why Are Hibernating Bears Protected From Vascular Disease and Thromboembolism?

Despite repeated yearly episodes of immobilization, insulin resistance, and reduced renal function with anuria, bears show no evidence of deterioration in either heart or vascular function. Nelson et al.[49] evaluated cardiac function in six grizzly bears and showed that intrinsic cardiac muscle adaptations during hibernation maintain cardiac function in bradycardic hibernating bears, in contrast to the effects of chronic bradycardia in nonhibernating species. Hibernating brown bears show signs of inflammation, such as elevated levels of haptoglobin and β2-macroglobulin (but not C-reactive protein),[50] as well as hyperlipidemia,[51] during hibernation. As atherosclerosis is associated with hyperlipidemia and inflammation, one might anticipate that bears would be at an increased risk for atherosclerotic complications. However, a recent study showed that despite high levels of plasma lipids (cholesterol ≈425 mg/dl), no atherosclerosis, fatty streaks, foam cell infiltration, or inflammation was observed in arteries of brown bears.[51]

The reason(s) why bears are resistant to atherosclerosis despite multiple risk factors during hibernation, such as obesity, dyslipidemia, immobilization, kidney dysfunction, and slow circulatory flow, deserve further study. It could be hypothesized that the observed season variation of acute-phase reactants is associated with hibernating-specific mechanisms rather than with an acute-phase response. One such protein that increases during hibernation is α2-macroglobulin, which is a protease inhibitor involved in the regulation of coagulation that increases clotting time.[52] Could this be one of the reasons bears do not develop thromboembolic complications despite their prolonged repeated immobilization? Another possible explanation for the lack of thrombosis during hibernation is that platelet function is relatively depressed in bears compared with humans.[53] Clearly, more studies are needed to better understand this interesting paradox.

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