scholarly journals SGLT2 Inhibition Increases Fasting Glucagon but Does Not Restore the Counterregulatory Hormone Response to Hypoglycemia in Participants with Type 1 Diabetes

Diabetes ◽  
2021 ◽  
pp. db210769
Author(s):  
Schafer C. Boeder ◽  
Justin M. Gregory ◽  
Erin R. Giovannetti ◽  
Jeremy H. Pettus
Keyword(s):  
Type 1 Diabetes ◽  
Hormone Response ◽  
Sglt2 Inhibition

scholarly journals SGLT2 Inhibition Increases Fasting Glucagon but Does Not Restore the Counterregulatory Hormone Response to Hypoglycemia in Participants with Type 1 Diabetes

2021 ◽  
Author(s):  
Schafer C. Boeder ◽  
Justin M. Gregory ◽  
Erin R. Giovannetti ◽  
Jeremy H. Pettus
Keyword(s):  
Type 1 Diabetes ◽  
Cell Function ◽  
Sglt2 Inhibitor ◽  
Treatment Phase ◽  
Glycemic Variability ◽  
Hormone Response ◽  
Double Blind ◽  
Sodium Glucose Cotransporter ◽  
Sglt2 Inhibition

Individuals with type 1 diabetes have an impaired glucagon counterregulatory response to hypoglycemia. Sodium-glucose cotransporter (SGLT) inhibitors increase glucagon concentrations. We evaluated whether SGLT inhibition restores the glucagon counterregulatory hormone response to hypoglycemia. Adults with type 1 diabetes (<i>n</i> = 22) were treated with the SGLT2 inhibitor dapagliflozin (5 mg daily) or placebo for 4 weeks in a randomized, double-blind, crossover study. After each treatment phase, participants underwent a hyperinsulinemic hypoglycemic clamp. Basal glucagon concentrations were 32% higher following dapagliflozin versus placebo, with a median within-participant difference of 2.75 pg/mL (95% CI 1.38-12.6). However, increased basal glucagon levels did not correlate with decreased rates of hypoglycemia, and thus do not appear to be protective in avoiding hypoglycemia. During hypoglycemic clamp, SGLT2 inhibition did not change counterregulatory hormone concentrations, time to recovery from hypoglycemia, hypoglycemia symptoms, or cognitive function. Thus, despite raising basal glucagon concentrations, SGLT inhibitor treatment did not restore the impaired glucagon response to hypoglycemia. We propose that clinical reduction in hypoglycemia associated with these agents is a result of changes in diabetes care (e.g., lower insulin doses or improved glycemic variability) as opposed to a direct, physiologic effect of these medications on alpha cell function.

scholarly journals SGLT2 Inhibition Increases Fasting Glucagon but Does Not Restore the Counterregulatory Hormone Response to Hypoglycemia in Participants with Type 1 Diabetes

2021 ◽  
Author(s):  
Schafer C. Boeder ◽  
Justin M. Gregory ◽  
Erin R. Giovannetti ◽  
Jeremy H. Pettus
Keyword(s):  
Type 1 Diabetes ◽  
Cell Function ◽  
Sglt2 Inhibitor ◽  
Treatment Phase ◽  
Glycemic Variability ◽  
Hormone Response ◽  
Double Blind ◽  
Sodium Glucose Cotransporter ◽  
Sglt2 Inhibition

Individuals with type 1 diabetes have an impaired glucagon counterregulatory response to hypoglycemia. Sodium-glucose cotransporter (SGLT) inhibitors increase glucagon concentrations. We evaluated whether SGLT inhibition restores the glucagon counterregulatory hormone response to hypoglycemia. Adults with type 1 diabetes (<i>n</i> = 22) were treated with the SGLT2 inhibitor dapagliflozin (5 mg daily) or placebo for 4 weeks in a randomized, double-blind, crossover study. After each treatment phase, participants underwent a hyperinsulinemic hypoglycemic clamp. Basal glucagon concentrations were 32% higher following dapagliflozin versus placebo, with a median within-participant difference of 2.75 pg/mL (95% CI 1.38-12.6). However, increased basal glucagon levels did not correlate with decreased rates of hypoglycemia, and thus do not appear to be protective in avoiding hypoglycemia. During hypoglycemic clamp, SGLT2 inhibition did not change counterregulatory hormone concentrations, time to recovery from hypoglycemia, hypoglycemia symptoms, or cognitive function. Thus, despite raising basal glucagon concentrations, SGLT inhibitor treatment did not restore the impaired glucagon response to hypoglycemia. We propose that clinical reduction in hypoglycemia associated with these agents is a result of changes in diabetes care (e.g., lower insulin doses or improved glycemic variability) as opposed to a direct, physiologic effect of these medications on alpha cell function.

scholarly journals Erratum to: Characterisation of glomerular haemodynamic responses to SGLT2 inhibition in patients with type 1 diabetes and renal hyperfiltration

Diabetologia ◽  
2017 ◽  
Vol 60 (6) ◽  
pp. 1159-1160
Author(s):  
Marko Škrtić ◽  
Gary K. Yang ◽  
Bruce A. Perkins ◽  
Nima Soleymanlou ◽  
Yuliya Lytvyn ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Renal Hyperfiltration ◽  
Sglt2 Inhibition

The Effect of SGLT2 Inhibition on Urinary Adenosine Excretion in Patients with Type 1 Diabetes

2016 ◽  
Vol 40 (5) ◽  
pp. S64
Author(s):  
Harindra Rajasekeran ◽  
Yuliya Lytvyn ◽  
Michelle Hladunewich ◽  
Daniel Cattran ◽  
Andrea Bozovic ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Sglt2 Inhibition

SGLT2 Inhibition by Dapagliflozin Attenuates Diabetic Ketoacidosis in Mice with Type-1 Diabetes

2021 ◽  
Author(s):  
Huan Chen ◽  
Yochai Birnbaum ◽  
Regina Ye ◽  
Hsiu-Chiung Yang ◽  
Mandeep Bajaj ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Diabetic Ketoacidosis ◽  
Sglt2 Inhibition

scholarly journals SGLT2 inhibition increases serum copeptin in young adults with type 1 diabetes

2020 ◽  
Vol 46 (3) ◽  
pp. 203-209 ◽  
Author(s):  
Y. Lytvyn ◽  
P. Bjornstad ◽  
A. Katz ◽  
S.K. Singh ◽  
L.C. Godoy ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Young Adults ◽  
Sglt2 Inhibition

Acute SGLT2 Inhibition and the Pressure Natriuresis Response in Rats with Type 1 Diabetes

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Matthew A Bailey ◽  
Hannah M Costello ◽  
Kevin Stewart ◽  
David Binnie ◽  
Geoffrey C Culshaw ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Sglt2 Inhibition ◽  
Pressure Natriuresis
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