With the prevalence of obesity, sedentary body and high calorie diet in the world, the number of type 2 diabetes (T2DM) patients has increased unprecedentedly. As a diabetes focused solution provider, Ace Therapeutics can provide researchers engaged in pathological research of T2DM with more efficient function analysis and overall services.
The development of T2DM is caused by a combination of lifestyle and genetic factors. While some of these factors are under personal control, such as diet and obesity, other factors are not, such as increasing age, female sex, and genetics.
BMI and T2DM (Elli Polemiti, et al., 2021)
Long-term complications from high blood sugar include heart disease, strokes, diabetic retinopathy which can result in blindness, kidney failure, and poor blood flow in the limbs which may lead to amputations. The sudden onset of hyperosmolar hyperglycemic state may occur.
The organs involved in T2DM development include the pancreas (β-cells and α-cells), liver, skeletal muscle, kidneys, brain, small intestine, and adipose tissue. The incretin effect, changes in the colon and microbiome, immune dysregulation, and inflammation have emerged as important pathophysiological factors and are either established or have the potential to be therapeutic targets.
| Targets | Pathophysiological Defect | Glucose-lowering Therapy |
|---|---|---|
| Pancreatic β-cell | Loss of cell mass and function; impaired insulin secretion | Sulfonylureas; meglitinides |
| Pancreatic α-cell | Dysregulated glucagon secretion; increased glucagon concentration | GLP-1 receptor agonist |
| Incretin | Diminished incretin response | GLP-1 receptor agonist; DPP-IV inhibitors |
| Inflammation | Immune dysregulation | GLP-1 receptor agonist; DPP-IV inhibitors |
| Liver | Increased hepatic glucose output | Metformin; pioglitazone |
| Muscle | Reduced peripheral glucose uptake; insulin resistance | Metformin; pioglitazone |
| Adipose tissue | Reduced peripheral glucose uptake; insulin resistance | Metformin; pioglitazone |
| Kidney | Increased glucose reabsorption caused by upregulation of SGLT-2 receptors | SGLT-2 inhibitors |
| Brain | Increased appetite; lack of satiety | GLP-1 receptor agonist |
| Stomach or intestine | Increased rate of glucose absorption | GLP-1 receptor agonist; DPP-IV inhibitors; alpha-glucosidase inhibitors; pramlintide |
| Colon (microbiome) | Abnormal gut microbiota | Metformin; GLP-1 receptor agonist; DPP-IV inhibitors |
T2DM is associated with insulin resistance and islet β-cells dysfunction, but the specific mechanisms of its etiology and development are still not fully understood. It is generally believed that it is caused by the relatively insufficient insulin related to obesity and the tissue is not sensitive to insulin (insulin resistance).
Mechanisms of T2DM (Wei, J., et al. Journal of Diabetes Research, 2022.)
Other potentially important mechanisms associated with T2DM and insulin resistance including increased breakdown of lipids within fat cells, resistance to and lack of incretin, high glucagon levels in the blood, increased retention of salt and water by the kidneys, and inappropriate regulation of metabolism by the central nervous system.
With years of experience in translational medicine research and drug development, Ace Therapeutics is able to provide pathological research services related to T2DM and carry out integration and systematic analysis. Our services include but not limited to the followings.
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Ace Therapeutics offers cost-effect and high-quality research services related to T2DM for our clients worldwide. Our assays are developed and processed with the highest standard and the results are delivered on time without compromising quality. Please feel free to contact us.
