Type 2 Diabetes Clinical Trial
Official title:
Acute Effects of Sodium GlucOse Co-Transporter 2 (SGLT2) Inhibition on Hepatic Glucose and Energy Metabolism
Inhibition of SGLT2 by specific inhibitors has been shown to reduce the renal threshold for
glucose excretion in patients with type 2 diabetes mellitus (T2DM) and control subjects
leading to significant renal glucose loss even in the presence of normal glucose
concentrations. SGLT2 inhibition with canagliflozin induces a 24h urinary glucose loss of
around 70g in healthy subjects.
Recent studies indicate that under fasting and postprandial conditions administration of
SGLT-2 inhibitors leads to increase in endogenous (hepatic) glucose production (EGP)
potentially counteracting the glucose lowering potency of these drugs. Dapagliflozin has
been shown to acutely increase endogenous glucose production (EGP) and plasma glucagon
concentrations under postabsorptive conditions within 2 hours after drug ingestion in
patients with (T2DM). Glucagon binds to receptors in the liver and activates hepatic
gluconeogenesis (GNG) and glycogenolysis, likely contributing to the observed increase in
EGP.
So far the likely interrelation between acute changes in hepatic glucose metabolism and
energy turnover contributing to increased hepatic glucose production induced by SGLT2
inhibition has not been studied. It is known that out of the 80% of oxygen consumption
coupled to ATP synthesis, 7- 10% is used by GNG. However, so far the effects of
dapagliflozin on acute changes in gluconeogenesis (GNG) and ATP turnover in hepatic tissue
and on the time course of hormones involved in hypoglycaemia counter regulation have not
been studied.
n/a
Allocation: Randomized, Endpoint Classification: Pharmacodynamics Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Investigator), Primary Purpose: Basic Science
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