Why Don’t Hummingbirds Get Diabetes?
Astronomically high blood sugar is no problem for these tiny speed demons.
It’s no secret that hummingbirds are sugar fiends. To fuel their energy-intensive hovering flight, a wild hummingbird consumes approximately 2 grams of sugar per day—the equivalent of a person consuming about 90 pounds of the stuff.1 In keeping with their sugar-rich diet, hummingbirds have exceptionally high blood glucose levels, up to 42 mM.2 In humans, levels over 10mM are cause for concern and can lead to diabetes-related cardiovascular disease, nerve damage, and even blindness. Yet hummingbirds appear to weather this hyperglycemic state without ill effects and, in fact, are quite long-lived considering their diminutive size.
According to Kenneth Welch Jr., an ecological physiologist at the University of Toronto Scarborough, hummingbirds’ high metabolisms and intense daily workout regimes likely help counteract some of the negative effects of high sugar consumption. Protein glycation—the binding of sugars to proteins—may also play a role. Excessive protein glycation can result in an abundance of advanced glycation end-products, which are implicated in many of the complications of diabetes.3
Yet hummingbirds seem resistant to this glycation stress. Despite their high blood sugar, hummingbirds have lower levels of glycated hemoglobin (sometimes called HbA1c) than humans with diabetes.2 No one knows exactly how hummingbirds accomplish this, but it’s a question that Welch is currently exploring. In the case of chickens (all birds are relatively hyperglycemic), one protein called albumin has evolved to have fewer exposed lysine residues, which may render it glycation resistant.4
Welch said that it’s currently unclear whether hummingbird physiology research can prompt development of new therapies for metabolic disease in humans. However, he said, “Knowing more about how evolution can produce solutions to these functional problems in metabolic physiology can only help us formulate more creative solutions in the human biomedical context.”
- Powers DR, Nagy KA. Physiol Zoo,1988.
- Beuchat CA, Chong CR. Comp. Biochem. Physiol. Part A Mol. Integr. Physiol. 1998;120(3):409-416.
- Goh SY, Cooper ME. J Clin Endocrinol Metab. 2008;93(4):1143-1152.
- Anthony-Regnitz CM et al. J Mol Evol. 2020;88(8):653-661.