Diabetes Gene Testing Panel | Personalized Genetic Testing

DIABETES PANEL
Genetic Testing for Diabetes Medications

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Personalized Genetic Testing provides an invaluable service to physicians and patients throughout the U.S.

Thousands of Tests Performed

Providing doctors with the information needed to determine the best medicines and treatments for each of their patients.

20+ Years Experience

Experience in biotechnology, pharmaceutical, hematology, flow cytometry, clinical molecular biology, immunology, and chemistry industries.

Fast 5-Day Turnaround

Using the latest technologies from the leaders in the industry, our process is 3 times faster than competitor’s analysis methods.

Accurate Reporting

Through Coriell Institute, backed by over 60 years of research experience providing the quality control required for validation in pharmacogenetics testing.

The PGT Diabetes Panel supports doctors in determining the appropriate pain medications and doses that are best suited for a patient’s genetic profile.

PGT Diabetes Panel provides genetic results for:

Type 2 diabetes mellitus (T2DM) is an extremely predominant metabolic disorder, categorized by chronic hyperglycemia. It outcomes from an interface of environmental as well as genetic factors. Numerous genes have been related to disease development and therapeutic results. T2DM is a multifactorial disease with Inter-individual variations genetic in which particular candidate genes affect with the handling of glycemic control in the body. interindividual variability is primarily verified by single nucleotide polymorphisms (SNPs). Precisely an applicable segment of the genetic variability detected in T2D patients has been discovered in genes directly (or indirectly correlated to the activity (or to the metabolism) of oral antidiabetic drugs. Hence the detection of genetic variants linked to altered drug reaction is an important fact in diabetes research, subsequently, it is projected to improve the therapeutic style in a tailor-made way.

 

PGT Metformin Panel provides results for: SLC22A1, SLC47A1, SLC22A2 , ATM

SLC22A1: SLC22A1 gene encodes the OCT1 which is expressed in hepatocytes and mediates the electrogenic transport of drugs. OCT1 helps in transport of metformin into the liver (hepatocytes) and subsequent activity. It has been hypothesized that highly polymorphic SLCC22A1 gene will influence the therapeutic success of rate of metformin. Researchers reported that one variant of SLC22A1 was significantly associated with efficacy of metformin.

SLC22A2: Solute carrier family 22 member 2 (SLC22A2) gene encodes the OCT2. OCT2 is a drug transporter and expressed in renal tubular cells thought to be responsible for their elimination. In several studies, the SLC22A2 gene has been reported as highly polymorphic in nature. It was found that SLC22A2 variant 808G > T (270Ala > Ser) significantly transforms the uptake of drugs. In healthy subjects, rs316019 (A270S) variant appeared responsible for decreased renal clearance of Metformin. A recent randomized cohort study performed in T2DM patients with one-year follow-up demonstrated that efficacy of metformin was also influenced by SLC22A2 variant, rs316019 (808G > T).

SLC47A1 Solute carrier family 47 member 1 (SLC47A1) gene encodes the multidrug toxin extrusion receptor 1 expressed on apical domain of proximal and distal renal tubular cells and serves as an electroneutral organic cation/H+ exchanger. Since genetic polymorphisms in SLC47A1 associated with altered transport/excretion function might have great influence on metformin disposition, it is important to identify them in various ethnic populations and correlate in terms of therapeutic response

ATM Genotyping: Ataxia telangiectasia mutated (ATM) gene

Recently a novel variant in ataxia telangiectasia mutated (ATM) gene (rs11212617) is strongly implicated in affecting the glycemic response of metformin. It has been this gene associated with two successful treatment outcomes: (1) the ability to achieve HbA1c values ≤7% (53 mmol/mol); (2) lower HbA1c when analyzed as a quantitative trait.

PGT Sulfonylureas Panel: KCNJ11, ABCC8, KCNQ1, CYP2C9

Glibenclamide, gliclazide, glipizide, and glimepiride are the main Sulphonylureas (SUs)  currently used for T2D treatment S. Regardless of the extensive usage of these drugs in the clinical practice, diverse side effects, such as weight gain and increased risk of hypoglycemia, have been often.

Nucleotide variations in genes encoding KATP channel proteins, such as potassium channel inwardly rectifying subfamily J member 11 (KCNJ11) and ATP-binding cassette, subfamily C, member 8 (ABCC8), are associated with the onset of neonatal diabetes mellitus. Studies on SUs revealed that these drugs might effectively act in response to the defect induced by KCNJ11 and ABCC8 mutations in T2D patients.

Sulphonylureas are metabolized in the liver by the cytochrome P450 isoenzyme 2C9, encoded by CYP2C9 gene  Consequently it is clear that some allelic variants in CYP2C9 are likely to be associated with T2D susceptibility and/or altered drug responsiveness to SUs. The major risk alleles so far described for this gene are CYP2C9*2 (rs1799853, C/T, Arg144Cys) and CYP2C9*3 (rs1057910, C/T, Ile359Leu).

PGT Thiazolidinediones Panel: PPARG, Cytochrome P450 2C8 (CYP2C8)                    

In the last era PPARG polymorphisms—both in coding and regulatory regions—have been mostly studied for their possible connotation to pathologic phenotypes, such as T2D. One of the most investigated polymorphisms is Pro12Ala (rs1801282), often related to clinical significances and changes of the physiological metabolic status.

Cytochrome P450 2C8. Both pioglitazone and rosiglitazone are metabolized by the cytochrome P450 2C8 isoenzyme. The CYP2C83 and 11 polymorphisms, coding for a reduced functioning CYP2C8 enzyme, have been studied in relation to the pharmacokinetics of these drugs. Only in the study including patients with type 2 diabetes treated by rosiglitazone from the South Danish Diabetes Study cohort ( = 187), the association between 2 83 variant and change HbA1c was studied. The authors found a reduced therapeutic response and a lower risk for developing edemas in 2 83 carriers. In this study, rosiglitazone was added to the previous insulin treatment and it was allowed to change the insulin dose during the treatment which could have influenced the observed study results

References:

Pharmacogenomics of Drug Response in Type Diabetes: Toward the Definition of Tailored Therapies? PPAR Research Volume 2015, Article ID 415149, 10 pages

Pharmacogenetic studies update in type 2 diabetes mellitus World J Diabetes 2016 August 10; 7(15): 302-315