T2DM Pathological Research Service

T2DM Pathological Research Service

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.

What Causes T2DM

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.

  • Genetics
    Most cases of diabetes involve many genes, with each being a small contributor to an increased probability of becoming a T2DM. In T2DM over 400 genetic variants have been found, and most genes are related to β-cells function related. The TCF7L2 gene increases the risk of developing diabetes by 1.5 times and is the greatest risk of the common genetic variants. The TCF7L2 gene can affect glucagon-like pep-tide1 (GLP-1) levels, and the GLP-1 has stimulating effects both on insulin secretion and on β-cells growth.
  • Lifestyle
    Lifestyle factors are important to the development of T2DM, including obesity and being overweight (defined by a body mass index of greater than 25), lack of physical activity, poor diet, psychological stress, and urbanization.

BMI and T2DM (Elli Polemiti, et al, 2021)BMI and T2DM (Elli Polemiti, et al., 2021)

Complications of T2DM

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. 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

Pathogenesis of T2DM

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 T2DMMechanisms of T2DM (Wei, J., et al. Journal of Diabetes Research, 2022.)

  • Insulin Resistance
    Insulin resistance is an important cause of T2DM, which mainly refers to the impairment of the body's ability to uptake and metabolize glucose, including decreased insulin sensitivity and responsiveness.
  • Impaired Function of Islet Cells
    Islet β-cell dysfunction is one of the common features of T1DM and T2DM. While in T2DM, the reasons for the decline or death of β-cell function are more complex and are related to oxidative stress, inflammation, etc.

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.

Our Services

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.

  • Discovering Candidate Genes and Targets Related to T2DM
  • Discovering Relationship between T2DM and Its Complications
  • Discovering Mechanisms and Pathways Associated with T2DM and Insulin Resistance
  • Discovering Epigenetic Modifications to Crucial Pathways in the Pathogenesis of T2DM

Features of Our Services

Highly CustomizableHighly Customizable

One-stop ServicesOne-stop Services

High QualitysHigh Quality

Professional TeamProfessional Team

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.

References

  1. Chatterjee, S.; et al. Type 2 diabetes. The lancet. 2017, 389(10085), 2239-2251.
  2. Elli Polemiti, et al., BMI and BMI change following incident type 2 diabetes and risk of microvascular and macrovascular complications: the EPIC-Potsdam study, Diabetologia (2021).
All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.
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