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      Sodium-glucose cotransporter-2 inhibition and the insulin: Glucagon ratio: Unexplored dimensions

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          Abstract

          The sodium-glucose cotransporter 2 (SGLT-2) inhibitors are a novel class of glucose-lowering drugs which act by inhibiting the reabsorption of filtered glucose from the kidneys. Their effect on insulin and glucagon levels has recently been studied but is not fully explained. This communication proposes various hypotheses: A direct effect of SGLT-2 inhibition on the alpha cell receptors, a paracrine or intra-islet mediated effect on alpha cell sensitivity to glucose, and a calorie restriction mimetic action, to explain the impact of these drugs on the insulin glucagon ratio.

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          SGLT inhibitors in management of diabetes.

          Abd A Tahrani, Anthony H. Barnett, Clifford Bailey (2013)
          The two main sodium-glucose cotransporters (SGLTs), SGLT1 and SGLT2, provide new therapeutic targets to reduce hyperglycaemia in patients with diabetes. SGLT1 enables the small intestine to absorb glucose and contributes to the reabsorption of glucose filtered by the kidney. SGLT2 is responsible for reabsorption of most of the glucose filtered by the kidney. Inhibitors with varying specificities for these transporters (eg, dapagliflozin, canagliflozin, and empagliflozin) can slow the rate of intestinal glucose absorption and increase the renal elimination of glucose into the urine. Results of randomised clinical trials have shown the blood glucose-lowering efficacy of SGLT inhibitors in type 2 diabetes when administered as monotherapy or in addition to other glucose-lowering therapies including insulin. Increased renal glucose elimination also assists weight loss and could help to reduce blood pressure. Effective SGLT2 inhibition needs adequate glomerular filtration and might increase risk of urinary tract and genital infection, and excessive inhibition of SGLT1 can cause gastro-intestinal symptoms. However, the insulin-independent mechanism of action of SGLT inhibitors seems to offer durable glucose-lowering efficacy with low risk of clinically significant hypoglycaemia at any stage in the natural history of type 2 diabetes. SGLT inhibition might also be considered in conjunction with insulin therapy in type 1 diabetes.
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            Glucagon and the insulin: glucagon ratio in diabetes and other catabolic illnesses.

            Nathan Unger (1971)
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              Possible role of alpha-cell insulin resistance in exaggerated glucagon responses to arginine in type 2 diabetes.

              Akiko Shimizu, Hitoshi Ando, Toshinari Takamura … (2007)
              Inappropriate excessive secretion of glucagon, which contributes to postprandial hyperglycemia, is a novel target for the treatment of diabetes. In this study, we sought to determine the factors associated with exaggerated glucagon secretion in response to an arginine challenge in patients with type 1 and type 2 diabetes. Changes in circulating C-peptide immunoreactivity (CPR) and immunoreactive glucagon (IRG) after an arginine challenge were investigated in 35 patients with type 1 diabetes, 130 patients with type 2 diabetes, and 35 nondiabetic control subjects. No significant differences were found in the basal level and the area under the concentration-time curve (AUC) of IRG (AUC(IRG)) among type 1 and type 2 diabetic patients and nondiabetic subjects. However, there was an inverse correlation between the AUC(IRG) and the AUC of CPR (AUC(CPR)) for type 1 (r = -0.388, P = 0.023) and type 2 (r = 0.396, P < 0.0001) diabetic patients, whereas AUC(IRG) was not correlated with AUC(CPR) in nondiabetic subjects (r = -0.079, P = 0.655). In type 1 diabetic patients, the AUC(CPR) decreased and the AUC(IRG) increased with increasing disease duration. In type 2 diabetic patients, both AUC(IRG) and AUC(CPR) increased with increasing BMI, basal CPR level, and homeostasis model assessment of insulin resistance value. Our findings suggest that the pathophysiology of the exaggerated glucagon response differs between type 1 and type 2 diabetes. Intraislet insulin deficiency and alpha-cell insulin resistance may be the primary contributors to this condition in type 1 and type 2 diabetes, respectively.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Indian J Endocrinol Metab
                Journal ID (iso-abbrev): Indian J Endocrinol Metab
                Journal ID (publisher-id): IJEM
                Title: Indian Journal of Endocrinology and Metabolism
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 2230-8210
                ISSN (Electronic): 2230-9500
                Publication date (Print): May-Jun 2015
                Volume: 19
                Issue: 3
                Pages: 426-429
                Affiliations
                [1] Department of Endocrinology, Bharti Hospital and B.R.I.D.E, Karnal, Haryana, India
                [1 ] Department of Medicine, Government Medical College and Hospital, Chandigarh, India
                [2 ] Senior Medical Advisor, Boehringer Ingelheim, Mumbai, India
                Author notes
                Corresponding Author: Dr. Sanjay Kalra, Executive Editor, Indian J Endocrinology and Metabolism, Bharti Hospital and B.R.I.D.E, Karnal - 132 001, Haryana, India. E-mail: brideknl@ 123456gmail.com
                Article
                Publisher ID: IJEM-19-426
                DOI: 10.4103/2230-8210.152793
                PMC ID: 4366786
                PubMed ID: 25932403
                SO-VID: a662c43b-d8e0-4d35-a388-5e594c083e1e
                Copyright © Copyright: © Indian Journal of Endocrinology and Metabolism
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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                Categories
                Subject: Brief Communication

                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: beta cell,canagliflozin,dapagliflozin,diabetes,empagliflozin,glucagon,insulin
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: beta cell, canagliflozin, dapagliflozin, diabetes, empagliflozin, glucagon, insulin

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