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Interactions between diabetic and hypertensive drugs: a pharmacogenetics approach

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Abstract

Diabetes is known to increase susceptibility to hypertension due to increase in inflammation, oxidative stress, and endothelial dysfunction, leading to vascular stiffness. The polytherapy might lead to several drug–drug interactions (DDIs), which cause certain life-threatening complications such as diabetic nephropathy and hypoglycaemia. So, in this review we focused on drug–drug interactions and impact of genetic factors on drug responses for better disease management. Drug–drug interactions (DDIs) may act either synergistically or antagonistically. For instance, a combination of metformin with angiotensin II receptor antagonist or angiotensin-converting enzyme inhibitors (ACEIs) synergistically improves glucose absorption, whereas the same hypertensive drug combination with sulphonylurea might cause severe hypoglycaemia sometimes. Thiazolidinediones (TDZs) can cause fluid retention and heart failure when taken alone, but a combination of angiotensin II receptor antagonist with TZDs prevents these side effects. Interindividual genetic variation affects the DDI response. We found two prominent genes, GLUT4 and PPAR-γ, which are common targets for most of the drug. So, all of these findings established a connection between drug–drug interaction and genetics, which might be used for effective disease management.

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Data availability

The data that support the findings of this study are openly available in pubmed, google scholar, reference number [reference Abdul-Ghani et al. 2011 to Zou et al. 2017].

Abbreviations

T2DM:

Type 2 diabetes mellitus

HTN:

Hypertension

DDIs:

Drug–drug interactions

IDF:

International Diabetes Federation

RAAS:

Renin–angiotensin–aldosterone system

ADA:

American Diabetes Association

ACEIs:

Angiotensin-converting enzyme inhibitors

ARBs:

Angiotensin receptor blockers

PPIs:

Proton pump inhibitors

AMPK:

AMP-activated protein kinase

OCT1:

Organic cation transporter 1

OCT2:

Organic cation transporter 2

ATP:

Adenosine triphosphate

CAMKK2:

Calmodulin kinase kinase 2

GLUT 4:

Glucose transporter-4

PPARγ:

Peroxisome proliferator-activated receptor gamma

IRS-1:

Insulin receptor substrate-1

PI3K:

Phosphoinositide 3 kinase

SUR1:

Sulphonylurea receptor

IR:

Insulin receptor

AT1:

Angiotensin II type 1

AT2:

Angiotensin II type 2

TDZs:

Thiazolidinediones

PPRE:

PPARγ response elements

RXR:

Retinoid X receptor

PAX6:

Paired box protein-6

HDL:

High-density lipoprotein

SGLT2:

Sodium–glucose co-transporter-2

SGLT2Is:

Sodium–glucose co-transporter-2 inhibitors

NKCC2:

Sodium–potassium–chloride co-transporters

CCB:

Calcium channel blockers

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Acknowledgements

We are cordially grateful to ERA’s Lucknow Medical College and Hospital, ERA University, for providing intramural funding support (ELMC&H/RCell/2022/81) and laboratory space for this study.

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Authors and Affiliations

  1. Department of Personalized and Molecular Medicine, Era University, Lucknow, Uttar Pradesh, 226003, India

    Asma Imran Ansari, Aliya Abbas Rizvi, Shrikant Verma, Mohammad Abbas, Sushma Verma & Farzana Mahdi

  2. Department of Microbiology, Era University, Lucknow, Uttar Pradesh, 226003, India

    Mohammad Abbas

  3. Department of Biochemistry, Eras Lucknow Medical College and Hospital, Era University, Lucknow, Uttar Pradesh, 226003, India

    Syed Tasleem Raza

  4. Department of Medicine, Eras Lucknow Medical College and Hospital, Era University, Lucknow, Uttar Pradesh, 226003, India

    Zeba Siddiqi & Divakar Mishra

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Ansari, A.I., Rizvi, A.A., Verma, S. et al. Interactions between diabetic and hypertensive drugs: a pharmacogenetics approach. Mol Genet Genomics 298, 803–812 (2023). https://doi.org/10.1007/s00438-023-02011-7

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  • DOI: https://doi.org/10.1007/s00438-023-02011-7

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