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What Happens In Type 2 Diabetes And How The Benefits Of Mscs Could Change How It’s Treated

by | May 23, 2024 | Chronic Diseases, Stem Cell Therapy | 0 comments

In the realm of metabolic disorders, Type 2 Diabetes (T2D) stands out as a prevalent and critical public health concern globally. With an estimated 38 million individuals diagnosed with diabetes, an overwhelming majority, about 90-95%, are battling T2D. This condition not only compromises the quality of life of patients but also significantly impacts their life expectancy due to various complications. Despite the availability of numerous therapeutic drugs, the treatment of T2D remains a challenge. These interventions primarily offer a temporary management of blood glucose levels rather than a definitive cure, highlighting an urgent need for innovative and more effective solutions in the fight against this widespread disease.

What is T2D

Type II diabetes (T2D) poses a significant health risk in older adults, often due to reduced activity and weight gain with age.2 It’s characterized by elevated blood sugar levels caused by insulin resistance. Insulin, a hormone produced by the pancreas, plays a crucial role in managing blood sugar. It acts like a key, allowing glucose – the sugar in your blood – to enter muscle, fat, and liver cells, where it’s used for energy.

In the case of T2D, the body’s cells become less responsive to insulin, impacting their ability to absorb glucose from the blood. This is what is known as insulin resistance. In response, the pancreas compensates by producing more insulin, trying to control the rising blood sugar levels. If things don’t improve, the pancreas eventually runs out of energy, unable to keep up with the demand and exhausts, making blood sugar levels increase further. This sequence of events can lead to a state called prediabetes and, eventually, full-blown Type II Diabetes.

The risk of development of T2D is linked to several factors, including lifestyle choices, genetics, and certain health conditions.4 Leading a sedentary lifestyle and consuming a diet rich in processed foods, fats, and sugars can contribute to weight gain, especially around the belly. This excess belly fat is strongly associated with insulin resistance, T2D, and related heart diseases. Additionally, family history and genetics are important, as specific genetic disorders can increase the risk of T2D by affecting how the pancreas functions. Being aware of your family’s medical history can help you understand your risk and take proactive steps to prevent or manage the disease.

Current treatments

Since there is currently no cure for T2D, treatment focuses on managing the condition and maintaining low blood sugar levels. The cornerstone of T2D management focuses on two critical lifestyle factors: diet and exercise. A healthy diet including regular, balanced meals, smaller portion sizes, and a high fiber fruits and vegetables and limiting highly processed and high sugar foods is essential for controlling blood sugar levels. Complementing this with regular physical activity, including both aerobic exercises and resistance training, is key to reducing and maintaining a healthy weight. Consistent blood sugar monitoring is also important, as it helps maintain sugar levels within the desired range.

However, when lifestyle modifications aren’t enough, medications may be necessary. There are a variety of options, each working in different ways to help your body manage glucose levels. Insulin therapy is usually the last resort for those who don’t respond to diet, exercise or medications. Insulin types vary, ranging from long-acting forms that help regulate blood sugar over extended periods, to short-acting ones used primarily around meal times.5

While these are the standard approaches managing T2D, what if there was a way to help reduce or even eliminate T2D all together? Stem cell therapy is emerging as a potential treatment to do just that.

What are UC-MSCs

Stem cells serve as the body’s cellular foundation. They are like the blueprint for all other cells in our body. Their primary function is to replenish dying cells and repair damaged tissues.6 Among various stem cells, Mesenchymal stem cells (MSCs) stand out for their special capabilities. These cells can differentiate into various types including bone, cartilage, and fat cells, and have self-renewal properties, maintaining their populations over time, which is crucial for therapeutic uses.7

MSCs are primarily found in bone marrow, umbilical cord blood, and adipose tissue. Of these, umbilical cord MSCs (UC-MSCs) have shown superior effectiveness. They multiply faster than other MSC types and can differentiate into the three primary cell layers, playing a significant role in tissue repair.8

UC-MSCs have other advantages, including, they are easily harvested, have a lower infection and tumor risk, can turn into many different cells, and have a low likelihood of triggering immune responses.9 These benefits, along with their ethical acceptability, make UC-MSCs a promising option in various clinical settings

How UC-MSCs can help in diabetes

One of the standout capabilities of UC-MSCs is their ability to reduce inflammation caused by illness in the body. This connection has led researchers to explore UC-MSCs as a potential treatment for T2D, which is often associated with chronic inflammation. Clinical studies have shown promising results; UC-MSC treatments in T2D patients have not only decreased the activation of inflammatory agents but also improved blood sugar levels and beta-cell function. This is crucial since beta-cells are vital for insulin production and blood sugar regulation. 10 In animal models, UC-MSCs have significantly reduced blood glucose and enhanced insulin sensitivity in key tissues like liver, fat, and muscle.11

UC-MSCs have the biggest effect for diabetes through pancreatic function.12 Patients treated with UC-MSC show a re-stabilizing of their blood glucose levels. This effect is partly due to exosomes produced by UC-MSCs, which enhance insulin sensitivity, improving blood sugar control and reducing harm to insulin-producing cells. The cell renewal properties of UC-MSCs also help insulin sensitive tissues like liver, fat and muscle improving glucose absorption.

Beta cells are essential for insulin production and managing blood sugar. In T2D, these cells function poorly, leading to lower insulin levels. UC-MSCs target these impaired beta cells, aiding in their regeneration and restoring their function.13 This process enhances the body’s insulin sensitivity, helping to regulate and lower blood sugar levels. Additionally, UC-MSCs reduce inflammation, which is known to impact beta cell and pancreatic function in T2D.

What this all means

As the number of cases of T2D continues to increase, so does the need for an effective, long-lasting treatment. The potential for UC-MSC treatment in managing T2D is an exciting topic in medical research. With their ability to regenerate and repair key cells in the pancreas and other key organs along with their benefits they have to beta- cells and reducing inflammation, UC-MSCs could be a powerful advancement in the realm of this disease. While ongoing research continues to unlock their full potential, the hope they offer for millions battling Type 2 Diabetes is a testament to the incredible possibilities of regenerative medicine.

References

  1. https://www.cdc.gov/diabetes/basics/type2.html#:~:text=Healthy%20eating%20is%20your%20recipe,adults%20are%20also%20developing%20it
  2. Type 2 Diabetes—NIDDK. (n.d.). National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved December 26, 2023, from https://www.niddk.nih.gov/health-information/diabetes/overview/what-is-diabetes/type-2-diabetes
  3. Insulin Resistance & Prediabetes—NIDDK. (n.d.). National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved December 26, 2023, from https://www.niddk.nih.gov/health-information/diabetes/overview/what-is-diabetes/prediabetes-insulin-resistance
  4. Symptoms and Causes of Diabetes- NINNK. (n.d.) National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved February 7, 2024, from https://www.niddk.nih.gov/health-information/diabetes/overview/symptoms-causes#type2
  5. https://www.mayoclinic.org/diseases-conditions/type-2-diabetes/diagnosis-treatment/drc-20351199
  6. Jones D, Wagers A. 2008. No place like home: anatomy and function of the stem cell niche. Nat Rev Mol Cell Biol 9, 11–21. https://www.nature.com/articles/nrm2319
  7. Stem Cell Basics | STEM Cell Information. National Institutes of Health. https://stemcells.nih.gov/info/basics/stc-basics
  8. Stem Cells: Types, What They Are & What They Do. Cleveland Clinic. https://my.clevelandclinic.org/health/body/24892-stem-cells
  9. Stem Cell Biology. NIH Intramural Research Program. National Institutes of Health. https://irp.nih.gov/our-research/scientific-focus-areas/stem-cell-biology#
  10. Lian, X. F., Lu, D. H., Liu, H. L., Liu, Y. J., Han, X. Q., Yang, Y., Lin, Y., Zeng, Q. X., Huang, Z. J., Xie, F., Huang, C. H., Wu, H. M., Long, A. M., Deng, L. P., & Zhang, F. (2022). Effectiveness and safety of human umbilical cord-mesenchymal stem cells for treating type 2 diabetes mellitus. World journal of diabetes, 13(10), 877–887. https://doi.org/10.4239/wjd.v13.i10.877
  11. Sun, X., Hao, H., Han, Q., Song, X., Liu, J., Dong, L., Han, W., & Mu, Y. (2017). Human umbilical cord-derived mesenchymal stem cells ameliorate insulin resistance by suppressing NLRP3 inflammasome-mediated inflammation in type 2 diabetes rats. Stem cell research & therapy, 8(1), 241. https://doi.org/10.1186/s13287-017-0668-1
  12. Gomes, A., Coelho, P., Soares, R., & Costa, R. (2021). Human umbilical cord mesenchymal stem cells in type 2 diabetes mellitus: the emerging therapeutic approach. Cell and Tissue Research, 385(3), 497-518. https://doi.org/10.1007/s00441-021-03461-4
  13. Wang, L., Liu, T., Liang, R., Wang, G., Liu, Y., Zou, J., Liu, N., Zhang, B., Liu, Y., Ding, X., Cai, X., Wang, Z., Xu, X., Ricordi, C., Wang, S., & Shen, Z. (2020). Mesenchymal stem cells ameliorate β cell dysfunction of human type 2 diabetic islets by reversing β cell dedifferentiation. EBioMedicine, 51, 102615. https://doi.org/10.1016/j.ebiom.2019.102615

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