Background: This retrospective study investigated the effect of adding metformin to pharmacologic insulin dosing in type 1 diabetics on insulin therapy 1 year after treatment compared with patients on insulin therapy alone.
Methods: Twenty-nine adults with type 1 diabetes who had metformin added to their insulin therapy for 12 months were compared with 29 adults with type 1 diabetes who remained on insulin-alone therapy.
Results: Fifty-eight patients with C peptide negative-type 1 diabetics (26 females, mean age: 29.01 ± 7.03 years, BMI: 24.18 ± 3.16 kg/m2) were analyzed. Age, sex, body weight, insulin dose requirement, plasma glucose (PG), blood pressure (BP), and lipids did not differ between groups before treatment (p > 0.05). Metabolic syndrome (44.8 vs 41.4%, p > 0.05) did not differ between the metformin-insulin and insulin alone groups before treatment. Metabolic syndrome was more decreased in the metformin-insulin group than in the insulin alone group after treatment (-8.9 ± 1.3 vs. 2.5 ± 0.6%, p = 0.028). Insulin dose requirement was lower in the metformin-insulin group than in the insulin alone group (-0.03 vs. 0.11 IU/kg/d, p = 0.006). Fasting PG (-26.9 ± 54.2 vs. 0.7 ± 29.5 mg/dL, p = 0.022) and postprandial PG (-43.1 ± 61.8 mg/dL vs. -3.1 ± 40.1 mg/dL, p = 0.010) was more decreased in the metformin-insulin group than in the insulin alone group. Body weight, lipids, and HbA1c did not differ between the groups (p > 0.05).
Conclusions: Metformin decreased glucose concentrations, reduced metabolic syndrome, as well as insulin dose requirement more than insulin therapy alone, 1 year after treatment. These results were independent of blood lipid improvement or weight loss, although on average weight remained decreased with metformin-insulin therapy, whereas the average weight increased with insulin therapy alone.
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http://dx.doi.org/10.1186/s12902-017-0228-9 | DOI Listing |
Am J Manag Care
January 2025
McGovern Medical School at UTHealth Houston, 4513 Teas St, Bellaire, TX 77401.
Objective: To examine the effect of physiologic insulin resensitization (PIR) on the cost of treating patients with diabetes and chronic kidney disease (CKD).
Study Design: The mean 1-year cost of treating 66 Medicare Advantage patients with diabetes and CKD who were receiving PIR was compared with that of treating 1301 Medicare Advantage patients with diabetes and CKD not receiving PIR. Differences in disease severity were compared using mean risk adjustment factor scores.
Health Syst Reform
December 2025
Independent Consultant, Alexandria, VA, USA.
For over 50 years, health systems the world over have failed people with type 2 diabetes mellitus (T2DM). The WHO documents a quadrupling of people with diabetes in a 34-year period to 422 million in 2014, the overwhelming majority of whom were T2DM. This happened despite extensive scientific literature on the causes of, as well as proven treatments for, this disease.
View Article and Find Full Text PDFDiabetologia
January 2025
Department of Chemical and Biological Engineering, Colorado School of Mines, Golden, CO, USA.
Type 1 diabetes is an autoimmune disease characterised by the destruction of pancreatic beta cells, resulting in lifelong insulin dependence. Although exogenous insulin can maintain glycaemic control, this approach does not protect residual or replacement pancreatic beta cells from immune-mediated death. Current therapeutics designed to protect functional beta cell mass or promote beta cell proliferation and regeneration can have off-target effects, resulting in higher dose requirements and adverse side effects.
View Article and Find Full Text PDFProtein Eng Des Sel
January 2025
Pfizer Rare Disease Research Unit, 610 Main Street, Cambridge, MA 02139, United States.
Pompe disease is a tissue glycogen disorder caused by genetic insufficiency of the GAA enzyme. GAA enzyme replacement therapies for Pompe disease have been limited by poor lysosomal trafficking of the recombinant GAA molecule through the native mannose-6-phosphate-mediated pathway. Here, we describe the successful rational engineering of a chimeric GAA enzyme that utilizes the binding affinity of a modified IGF-II moiety to its native receptor to bypass the mannose-6-phosphate-mediated lysosomal trafficking pathway, conferring a significant increase in cellular uptake of the GAA enzyme.
View Article and Find Full Text PDFInfect Dis Rep
January 2025
Royal Brompton Hospital, Part of GSTT NHS Foundation Trust, London SW3 6NP, UK.
Background: Glucagon-like peptide-1 (GLP-1) agonists are an existing treatment option for patients with insulin-resistant states, which elicit further pleiotropic effects related to immune cell recruitment and vascular inflammation. GLP-1 agonists downregulate the cluster of differentiation 147 (CD147) receptor, one of several receptors for the SARS-CoV-2 spike protein that mediate viral infection of host cells.
Methods: We conducted an open-label prospective safety and tolerability study including biomarker responses of the GLP-1 agonist Liraglutide, administered for 5 days as an add-on therapy to the standard of care within 48 h of presentation in a cohort of 13 patients hospitalized with COVID-19 pneumonia.
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