Recent reporting suggests that red blood cells may influence glycemic control under low-oxygen (hypoxic) conditions. In a study described as investigating mice exposed to high-altitude–like hypoxia, researchers observed rapid decreases in blood glucose and improved glucose tolerance. They propose a “glucose sink” mechanism in which RBCs adapt to hypoxia by increasing glucose uptake and metabolism. Two mechanisms are highlighted: first, chronic hypoxia elevates red blood cell numbers, expanding total glucose-consuming capacity. Second, individual RBCs from hypoxic environments display higher glucose uptake per cell, linked to increased GLUT1 transporter levels. Additionally, hypoxic RBCs reportedly metabolize glucose more quickly to produce 2,3-DPG, which facilitates oxygen release to tissues. The authors suggest that reduced circulating glucose under hypoxia could contribute to the observed lower diabetes risk in high-altitude populations, though the exact contribution of RBC-mediated glucose disposal versus other tissues remains uncertain. Caveats: the primary data derive from animal models with hypoxic exposure, and translational relevance to humans and routine clinical diabetes management is not yet established. Further studies are needed to define applicability and safety.
Blood sugar management, or glycemic control, is a central component of diabetes care . The primary goal is to maintain blood glucose (sugar) levels within a recommended, personalized target range to prevent complications .
It is a comprehensive, daily effort that combines monitoring, lifestyle adjustments, and when necessary, medication .
Physical activity can be a useful strategy to manage blood glucose levels. It works by increasing insulin sensitivity , allowing cells to use available insulin to take up glucose in the bloodstream during and after activity.
Similarly, some diabetes medications help to manage blood glucose levels by improving insulin sensitivity, or increasing insulin production.
Now, research is suggesting that another component present in the blood my also play a role in regulating blood sugar levels, by acting as a “glucose sponge” and soaking up sugar from the bloodstream.
A recent study, published in Cell Metabolism , reports that red blood cells can dramatically increase their uptake of glucose in low-oxygen environments, which may offer a potential explanation for the reduced diabetes risk seen at high elevations.
Previous observational research has shown that individuals living at higher elevations typically have a lower incidence of type 2 diabetes .
The biological mechanism behind this protective effect was unclear, but the study led by scientists from the Gladstone Institutes may offer an answer.
Previous research led by the team found that mice breathing low-oxygen air had dramatically lower blood glucose levels than normal.
Exploring this observation further, the researchers identified that when oxygen is scarce, red blood cells adapt by pulling more glucose out of the bloodstream.
This “glucose sink” effect not only fuels the cells’ own energy needs, but also reduces circulating blood sugar levels.
Senior author of the study, Isha Jain , PhD, an associate investigator at Gladstone Institutes, and an associate [rofessor at UCSF highlighted the findings from the study to Medical News Today .
“We identified two mechanisms. First, red blood cell numbers increase in chronic hypoxia, thereby increasing total glucose-consuming capacity. Second, individual RBCs from hypoxic environments take up more glucose per cell due to higher glucose transporter type 1 (GLUT1) transporter levels,” said Jain.
“We identified two mechanisms. First, red blood cell numbers increase in chronic hypoxia, thereby increasing total glucose-consuming capacity. Second, individual RBCs from hypoxic environments take up more glucose per cell due to higher glucose transporter type 1 (GLUT1) transporter levels.” – Isha Jain, PhD
“We also found that hypoxic red blood cells metabolize glucose faster to produce 2,3-diphosphoglycerate (2,3-DPG), a molecule that helps hemoglobin release oxygen to tissues,” she added.
“The mechanism involves deoxygenated hemoglobin displacing glyceraldehyde-3-phosphate dehydrogenase (GAPDH) from the cell membrane, removing a brake on glycolysis,” the researcher detailed.
In the study, the researchers exposed mice to conditions that mimicked high-altitude hypoxia . This describes when body tissues are deprived of adequate oxygen.
The team observed that blood glucose levels dropped rapidly, better glucose tolerance developed, and traditional glucose-consuming tissues, such as muscles, the brain , and the liver , did not fully explain where the sugar was going.