AIM: To investigate the budget implications of treatment with glucagon-like peptide-1 receptor agonists (GLP-1 RAs) versus other glucose-lowering treatment (here termed 'standard of care' [SoC]) during 2012-2019.MATERIALS AND METHODS: GLP-1 RA-naïve adults with type 2 diabetes (T2D) in the IBM MarketScan database with at least one glucose-lowering medication claim within 6 months after their first cardiovascular disease (CVD) hospitalization were included (index date was the date of first claim for a GLP-1 RA for the GLP-1 RA group, and the date of the first claim, independent of medication type, for the SoC group). Monthly healthcare costs and hospitalization risk over 12 months postindex date were compared for those who initiated a GLP-1 RA posthospitalization versus those with a claim for any other glucose-lowering RESULTS: Postindex date, mean observed total costs were lower for patients receiving a GLP-1 RA compared with SoC ($3853 vs. $4288). In adjusted analysis, both groups had similar total healthcare costs (P = 6). This was driven by significantly lower inpatient and outpatient costs and higher drug costs in the GLP-1 RA group compared with SoC (P < 01). Risks of all-cause (adjusted hazard ratio: 05) and CVD-related hospitalization (06) were significantly lower in the GLP-1 RA group compared with SoC (P < 01). Similar results were observed in a subgroup with atherosclerotic CVD.CONCLUSIONS: These findings suggest that, in US patients with T2D and a CVD-related hospitalization, the added medical cost of treatment with GLP-1 RAs is offset by lower inpatient and outpatient care costs, resulting in budget Conflict of interest statement: ME has received honoraria from AstraZeneca, Boehringer Ingelheim and Novo Nordisk. MF, KSM and ASC are employees of Novo Nordisk. PBM is employed as a consultant by Novo Nordisk A/S. SV holds a Tier 1 Canada Research Chair in Cardiovascular Surgery, and has received research grants and/or speaking honoraria from Amarin, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, EOCI Pharmacomm Ltd, HLS Therapeutics, Janssen, Merck, Novartis, Novo Nordisk, Pfizer, PhaseBio, Sanofi, Sun Pharmaceuticals, and the Toronto Knowledge Translation Working Group. He is the President of the Canadian Medical and Surgical Knowledge Translation Research Group, a federally incorporated not‐for‐profit physician organization. Exploiting glipizide used for exerted by lipid nanocapsules in non-alcoholic Advanced Drug Delivery and Biomaterials Group, Avenue Emmanuel Mounier 73, 1200 Metabolism and Nutrition Group, Avenue Emmanuel Mounier 73, 1200 Brussels, Belgium; WELBIO (Walloon Excellence in Life sciences and BIOtechnology), WELBIO Department, WEL Research Institute, Avenue Pasteur, 6, 1300 Wavre, Belgium.Clinical Research, Laboratory of Hepato-Gastroenterology, Avenue Emmanuel Mounier 53, 1200 Brussels, Belgium. Electronic address: Advanced Drug Delivery and Biomaterials Group, Avenue Emmanuel Mounier 73, 1200 Brussels, Belgium; WELBIO (Walloon Excellence in Life sciences and BIOtechnology), WELBIO Department, WEL Research Institute, Avenue Pasteur, 6, Non-alcoholic fatty liver disease (NAFLD) affects approximately 25% of the global adult population and can progress to end-stage liver disease with life-threatening complications; however, no pharmacologic therapy has been approved. Drug delivery systems such as lipid nanocapsules (LNCs) are a very versatile platform, easy to produce, and can induce the secretion of the native glucagon-like peptide 1 (GLP-1) when orally administered. glucagon-like peptide-1 drugs -1 analogs are currently being extensively studied in clinical trials in the context of NAFLD. Our nanosystem provides with increased levels of GLP-1, triggered by the nanocarrier itself, and by the plasmatic absorption of the encapsulated synthetic analog (exenatide). Our goal in this study was to demonstrate a better outcome and a greater impact on the metabolic syndrome and liver disease progression associated with NAFLD with our nanosystem than with the subcutaneous injection of the GLP-1 analog alone. To that end, we studied the effect of chronic administration (one month) of our nanocarriers in two mouse models of early NASH: a genetic model (foz/foz mice fed a high fat diet (HFD)) and a dietary model (C57BL/6J mice fed with a western diet plus fructose (WDF)). Our strategy had a positive impact in promoting the normalization of glucose homeostasis and insulin resistance in both models, mitigating the progression of the disease. In the liver, diverging results were observed between the models, with the foz/foz mice presenting a better outcome. Although a complete resolution of NASH was not achieved in either model, the oral administration of the nanosystem was more efficient at preventing the progression of the disease into more severe states than the subcutaneous injection.
glipizide used for|glucagon-like peptide-1 drugs
