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The aim of study was to establish the effects of clinical doses of Gla-300 vs Gla-100 on suppression of glucagon, lipolysis and ketogenesis in T1DM. Eighteen persons with T1DM [age 40±12 yrs, diabetes duration 26±12 yrs, BMI 23.4±2 kg/m2, A1C 7.19±0.52 % (55±6 mmol/mol)] were studied after 3 month of titration with Gla-300 and Gla-100 (randomized, crossover design) with a 24 h euglycemic clamp (s.c. injection of individual insulin daily doses used by subjects over previous 2 weeks, Gla-300 0.35±0.08 and Gla-100 0.28±0.07 U/kg). Gla-300 resulted in 1) less increase in insulin concentration over 0-12 h, but greater insulin concentration in 12-24 h (no differences over 24 h); 2) greater glucagon suppression; 3) greater prehepatic insulin-to-glucagon molar ratio, primarily in 12-24 h (ratio 1.78, 90%CIs 1.5;2.1); and 4) lower 24 h FFA (0.81; 90%CI 0.73;0.89), glycerol (0.78; 90%CI 0.65;0.94) and -hydroxybutyrate (0.72; 90%CI 0.58;0.90). Over the 24 h post-injection, as compared to Gla-100, clinical doses of Gla-300 exhibit greater suppressive effects on glucagon, lipolysis and ketogenesis, while the effects on glucose metabolism are equivalent.
This article was published in the following journal.
Name: Diabetes technology & therapeutics
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A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
A recombinant LONG ACTING INSULIN and HYPOGLYCEMIC AGENT that is used to manage BLOOD GLUCOSE in patients with DIABETES MELLITUS.
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A receptor for GLUCAGON-LIKE PEPTIDE 1 (GLP-1) expressed primarily on the surface of beta and ductal exocrine cells of the pancreas, as well as cells of other tissues. GLP-1 acts through GLP-1R to potentiate signaling in pancreatic cells in response to glucose-stimulated insulin secretion (GSIS).
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