{"id":29089,"date":"2026-10-27T13:47:28","date_gmt":"2026-10-27T11:47:28","guid":{"rendered":"https:\/\/ibsal.es\/?p=29089"},"modified":"2026-10-27T13:52:47","modified_gmt":"2026-10-27T11:52:47","slug":"moderate-oxidation-promotes-glucose-uptake-by-the-muscles","status":"publish","type":"post","link":"https:\/\/ibsal.es\/en\/moderate-oxidation-promotes-glucose-uptake-by-the-muscles\/","title":{"rendered":"Moderate oxidation promotes glucose uptake by the muscles"},"content":{"rendered":"\n

Researchers from USAL, INCyL, and IBSAL provide new evidence on the beneficial role of certain oxidizing molecules in cellular function, challenging the traditional view that associates them primarily with damage and aging<\/strong><\/p>\n\n

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The study, published in the journal *Redox Report*, reinforces the concept of oxidative eustress and opens up new avenues for understanding insulin resistance associated with type 2 diabetes, obesity, and aging, as well as for exploring future therapeutic strategies<\/strong><\/p>\n\n

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Oxidizing molecules do not only cause damage to our bodies. Although they have traditionally been associated with cellular deterioration, disease, and aging, they also perform essential functions necessary for the body\u2019s proper functioning. When produced in moderate and controlled amounts, these substances act as signals that allow cells to communicate and regulate various physiological processes. This phenomenon, known as oxidative eustress, can, among other functions, help muscles take up glucose from the blood\u2014a process that is essential for obtaining energy and maintaining proper blood sugar levels in the body. <\/p>\n\n

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This has been demonstrated by researchers at the University of Salamanca (USAL), the Castile and Le\u00f3n Institute of Neurosciences (INCyL), and the Salamanca Institute for Biomedical Research (IBSAL) in a study that provides new experimental evidence on this mechanism and demonstrates that certain conditions of moderate oxidation promote the activation of cellular signals that facilitate glucose uptake into skeletal muscle. The results reinforce the concept of oxidative eustress and open up new perspectives for understanding the alterations in glucose uptake and insulin resistance associated with diseases such as type 2 diabetes and aging. <\/p>\n\n

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The study, published in the international scientific journal *Redox Report*<\/em> under the title \u201cOxidative eustress is associated with AMPK and AKT activation, GLUT4 translocation, and glucose uptake in skeletal muscle cells and fibers<\/em>,\u201d is authored by Eva Mart\u00edn-Prieto, Leonardo A. Catalano-Iniesta, Escarlata Fern\u00e1ndez-Puente, and Jes\u00fas Palomero.<\/p>\n\n

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\u201cTraditionally, oxidative stress has been associated with harmful effects on the body, such as cellular damage and aging. However, this view is incomplete, since our cells need to maintain certain levels of oxidation to function properly,\u201d explains Jes\u00fas Palomero. That level, he adds, \u201cenables better communication between cells and tissues so they can perform their functions.\u201d <\/p>\n\n

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Graphical abstract of the paper published in Redox Report. The diagram summarizes the relationship between oxidative eustress, AKT\/AMPK activation, GLUT4 translocation, and glucose uptake by skeletal muscle. <\/em><\/figcaption><\/figure>\n\n
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From Oxidative Stress to Distress and Oxidative Eustress<\/strong><\/p>\n\n

For decades, reactive oxygen and nitrogen species (RONS) were associated almost exclusively with so-called oxidative stress, understood as a situation in which excessive production of these molecules causes cellular damage. However, advances in redox biology\u2014which studies oxidation and reduction processes in living organisms\u2014have made it possible to refine this concept and distinguish between two different phenomena. <\/p>\n\n

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On the one hand, oxidative stress occurs when oxidizing molecules reach excessive concentrations or remain unregulated, causing damage to cells and tissues. On the other hand, oxidative eustress occurs when these substances are generated in a moderate, transient, localized, and controlled manner and participate in normal cellular communication and regulation processes. <\/p>\n\n

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The difference is crucial: while excessive oxidation can lead to tissue damage and loss of function, certain levels of oxidation are necessary for the body to function properly. Molecules such as hydrogen peroxide (H\u2082O\u2082) or nitric oxide (NO) can act as cellular messengers and participate in the regulation of numerous signaling pathways. <\/p>\n\n

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In this regard, Palomero warns that it is not simply a matter of eliminating oxidizing substances to avoid their potential harmful effects. \u201cIt has sometimes been thought that the best way to prevent oxidative damage is to reduce oxidation by administering antioxidants. However, excessive reduction can also interfere with the physiological processes that cells need to function properly,\u201d he notes. <\/p>\n\n

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Therefore, the issue is not whether oxidative stress can be good or bad, but rather to distinguish between oxidative distress\u2014associated with cellular damage\u2014and oxidative eustress\u2014related to the physiological signaling necessary for the body to function properly.<\/p>\n\n

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\"Description
Scientific analysis and research conducted in university laboratories.\/USAL Press Release: \u00c1lvaro Ballesteros Villarino<\/em><\/figcaption><\/figure>\n\n
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Skeletal Muscle and Glucose Uptake<\/strong><\/p>\n\n

In this context, the team at the University of Salamanca has focused its research on one of the body\u2019s fundamental metabolic functions: the ability of skeletal muscle to take up glucose from the blood.<\/p>\n\n

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This tissue, which enables voluntary body movements, is one of the main factors responsible for removing glucose from the bloodstream and plays an essential role in maintaining blood glucose levels.<\/p>\n\n

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To take up glucose, muscle cells use, among other mechanisms, a transporter protein called GLUT4, which moves from inside the cell to its membrane. Once it is located on the cell surface, it facilitates the entry of glucose, which the muscle can use as an energy source. <\/p>\n\n

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When muscle tissue becomes less responsive to insulin\u2014a hormone that helps regulate this process\u2014a condition known as insulin resistance develops. This condition reduces the ability of muscle cells to remove glucose from the blood and contributes to hyperglycemia, that is, an increase in blood glucose levels. This is a characteristic feature of type 2 diabetes that can also occur as people age. <\/p>\n\n

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In this context, identifying mechanisms that facilitate the uptake of glucose into muscle cells is particularly important for understanding how metabolism is regulated and which processes may be disrupted in certain diseases.<\/p>\n\n

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The study shows that conditions consistent with oxidative eustress are associated with the activation of two important cellular signaling proteins, AKT and AMPK, with increased transport of GLUT4 to the membrane, and with increased glucose uptake.<\/p>\n\n

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Confocal microscopy images obtained using immunocytochemistry that show the translocation of the GLUT4 glucose transporter to the plasma membrane of C2C12 myotubes.<\/em><\/figcaption><\/figure>\n\n
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To analyze these processes, the researchers used C2C12 muscle cells and individual muscle fibers isolated from mouse skeletal muscle. Among the various stimuli studied, they observed that hydrogen peroxide promoted glucose uptake in a concentration-dependent manner, while certain conditions related to the availability of nitric oxide also increased this uptake. <\/p>\n\n

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The results reinforce findings from previous studies and provide new evidence regarding the role of oxidative signals in muscle metabolism.<\/p>\n\n

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\u201cWhen it comes to skeletal muscle and glucose uptake, we are reinforcing the idea that certain levels of oxidation can promote glucose uptake,\u201d explains Palomero.<\/p>\n\n

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\"Description
Close-up of analytical instruments and samples in the laboratory.\/USAL Press Release by \u00c1lvaro Ballesteros Villarino<\/em><\/figcaption><\/figure>\n\n
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From Combating Oxidants to Understanding Cell Signaling<\/strong><\/p>\n\n

Beyond the specific findings on muscle metabolism, this work is part of a broader conceptual shift within redox biology.<\/p>\n\n

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As the researchers explain, contrary to the old view based on a simple dichotomy between \u201cbad oxidants\u201d and \u201cgood antioxidants,\u201d we now know that reactive oxygen and nitrogen species are part of a genuine cellular language. Their effect depends on their nature, concentration, location, and duration. <\/p>\n\n

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Thus, the goal of the research can no longer be limited to eliminating oxidizing molecules; it must also include understanding how these signals are generated and transmitted, what functions they regulate, and under what circumstances a state of oxidative eustress can turn into oxidative distress.<\/p>\n\n

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\u201cOur cells need an appropriate level of oxidation to perform their functions\u2014for example, glucose uptake, which we have addressed in this study. It is important to maintain this \u2018eustress\u2019 and prevent \u2018distress\u2019\u2014the excess oxidation that causes damage,\u201d Palomero emphasizes.<\/p>\n\n

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This perspective is driving the development of what is known as \u201cRedox Biomedicine,\u201d a field of research that aims to apply knowledge of oxidative signaling mechanisms to the understanding of diseases and, in the long term, to the identification of new preventive or therapeutic strategies.<\/p>\n\n

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New Perspectives on Diabetes and Aging<\/strong><\/p>\n\n

Type 2 diabetes, obesity, and aging have traditionally been linked to increased oxidative damage\u2014that is, to states of oxidative stress. However, in addition to an excess or dysregulation of these molecules, there may also be an alteration in the physiological signals that normally contribute to maintaining cellular balance. <\/p>\n\n

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From this perspective, the study\u2019s findings suggest that modulating signals related to oxidative eustress may, in the future, help improve glucose uptake in cases of insulin resistance.<\/p>\n\n

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However, the researchers caution that the current study does not demonstrate that eustress reverses this resistance. To determine whether it can do so, at least partially, specific studies will be needed in models exhibiting this alteration. <\/p>\n\n

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\u201cFrom a therapeutic standpoint, we are seeing that these moderate levels of oxidation promote glucose uptake, which is very interesting in diseases such as diabetes, where insulin resistance occurs and cells have difficulty taking up glucose,\u201d explains Palomero. The researcher notes that the next step will be to test whether these mechanisms can help overcome this difficulty in experimental models of the disease. <\/p>\n\n

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In this regard, the team aims to gain a deeper understanding of the mechanisms that regulate oxidative eustress and to study its potential future applications. \u201cIf we understand these mechanisms well, we could identify pharmacological targets to act upon or design new drugs to activate an enzyme or channel that promotes eustress and prevents distress,\u201d he notes. <\/p>\n\n

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The significance of these findings, therefore, lies not in administering oxidizing agents, but in identifying and understanding the physiological signaling pathways that facilitate glucose uptake and investigating whether they can be selectively modulated in pathological conditions.<\/p>\n\n

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This line of research takes a broader perspective on redox biomedicine in metabolism, neurodegeneration, and aging, with the aim of understanding how these signals play a role in both normal cellular function and the changes associated with disease and aging.<\/p>\n\n

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Overall, the study helps to update the traditional view of oxidative stress: oxidizing molecules are not only potential agents of damage, but also part of the language that cells use to regulate their functions. Understanding the difference between oxidative eustress and distress and learning how to modulate these signals is one of the current challenges in biomedical research. <\/p>\n\n

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Reference article:<\/strong><\/p>\n\n

Mart\u00edn-Prieto, E., Catalano-Iniesta, L. A., Fern\u00e1ndez-Puente, E., & Palomero, J. (2026). Oxidative eustress is associated with AMPK and AKT activation, GLUT4 translocation, and glucose uptake in skeletal muscle cells and fibers. Redox Report, 31(1). https:\/\/doi.org\/10.1080\/13510002.2026.2721882<\/p>\n\n

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Contact:<\/p>\n\n

Dr. Jes\u00fas Palomero, full professor in the Department of Physiology and Pharmacology at the School of Medicine, University of Salamanca. <\/p>\n\n

Phone: 63030 6666 1493<\/p>\n\n

jespala@usal.es<\/p>\n\n

<\/p>\n","protected":false},"excerpt":{"rendered":"

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