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  Table of Contents     
Year : 2017  |  Volume : 63  |  Issue : 4  |  Page : 275

Adenosine monophosphate- activated protein kinase- based classification of diabetes pharmacotherapy

1 Department of Internal Medicine, IPGMER, Kolkata, West Bengal, India
2 Department of Internal Medicine, Mount Sinai St. Luke's, New York, USA
3 Department of Internal Medicine, NMB Diagnostics, Serampore, West Bengal, India

Date of Web Publication11-Oct-2017

Correspondence Address:
A Hajra
Department of Internal Medicine, IPGMER, Kolkata, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jpgm.JPGM_434_17

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How to cite this article:
Hajra A, Bandyopadhyay D, Hajra S K. Adenosine monophosphate- activated protein kinase- based classification of diabetes pharmacotherapy. J Postgrad Med 2017;63:275

How to cite this URL:
Hajra A, Bandyopadhyay D, Hajra S K. Adenosine monophosphate- activated protein kinase- based classification of diabetes pharmacotherapy. J Postgrad Med [serial online] 2017 [cited 2023 Mar 28];63:275. Available from:

The article named “Adenosine monophosphate-activated protein kinase-based classification of diabetes pharmacotherapy” by Dutta et al.[1] published in your journal has enlightened us about the role of adenosine monophosphate-activated protein kinase (AMPK) in pathogenesis and the management of diabetes mellitus. In this article, the interaction between sodium-glucose cotransporter type 1 (SGLT1) and AMPK has also been mentioned.[1] The presence of SGLT1 receptors on human as well as “murine Langendorff perfused hearts” has been well supported by an animal study.[2] This study has also demonstrated that SGLT1 inhibitors may also contribute to the increased risk of ischemia–reperfusion injury of the myocardium. SGLT1 is a high-affinity, low-capacity transporter. For this reason, SGLT1 may have a cardioprotective effect on myocardium during ischemia. It is helpful particularly when the availability of fuel is less.[2] We know that nowadays, SGLT2 inhibitors are emerging as newer antidiabetic drugs. Apart from their glucose lowering effects, they have significant effects on other metabolisms also.[3] The authors have rightly mentioned that link between SGLT1 and AMPK at brain and heart has suggested the urgent need for studies evaluating the link between SGLT2 and AMPK.[1] In this regard, we can see that a recent study has compared the expression of SGLT1 and SGLT2 in human myocardium with either ischemia or hypertrophy. Healthy subjects are taken as control. No expression of SGLT2, at both gene and protein level, in either healthy or ischemic/hypertrophic myocardium has been found. In ischemic/hypertrophic myocardium, phosphorylation/activation of AMPK was also increased along with expression of SGLT1. However, the study could not demonstrate a causative association with SGLT1 upregulation and activation of AMPK. Interestingly, experimental cardiomyopathy induced by a hyperactivating mutation of AMPK in mice is associated with increased expression of SGLT1.[4] Another recent data reveal that cardiotrophin-1 inhibits intestinal sugar absorption by SGLT-1 level reduction. The AMPK pathway contributes to this effect. This finding may explore new targets for therapy in future.[5]

These molecular pathways are still to be clarified and to be made clearer by further studies. We would like to thank the authors of the article mentioned above to highlight these points regarding the role of AMPK. We know that the role of SGLT2 inhibitors on cardiovascular morbidities in diabetic patients is an emerging topic of discussion now. Some of these drugs have some action on the SGLT1 receptors also.[4] We will be glad if we can get the authors' opinion regarding the role of the “gliflozins” drugs in this regard. Can these drugs play a role in this SGLT-AMPK interaction and alter the cardiovascular outcomes?

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 :: References Top

Dutta D, Kalra S, Sharma M. Adenosine monophosphate-activated protein kinase-based classification of diabetes pharmacotherapy. J Postgrad Med 2017;63:114-21.  Back to cited text no. 1
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Kashiwagi Y, Nagoshi T, Yoshino T, Tanaka TD, Ito K, Harada T, et al. Expression of SGLT1 in human hearts and impairment of cardiac glucose uptake by phlorizin during ischemia-reperfusion injury in mice. PLoS One 2015;10:e0130605.  Back to cited text no. 2
Ghosh RK, Bandyopadhyay D, Hajra A, Biswas M, Gupta A. Cardiovascular outcomes of sodium-glucose cotransporter 2 inhibitors: A comprehensive review of clinical and preclinical studies. Int J Cardiol 2016;212:29-36.  Back to cited text no. 3
Di Franco A, Cantini G, Tani A, Coppini R, Zecchi-Orlandini S, Raimondi L, et al. Sodium-dependent glucose transporters (SGLT) in human ischemic heart: A new potential pharmacological target. Int J Cardiol 2017;243:86-90.  Back to cited text no. 4
López-Yoldi M, Castilla-Madrigal R, Lostao MP, Barber A, Prieto J, Martínez JA, et al. Cardiotrophin-1 decreases intestinal sugar uptake in mice and in Caco-2 cells. Acta Physiol (Oxf) 2016;217:217-26.  Back to cited text no. 5


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