Liraglutide improves carotid intima-media thickness in patients with type 2 diabetes and non-alcoholic fatty liver disease: an 8-month prospective pilot study

Rizvi, Ali A.; Patti, Angelo Maria; Giglio, Rosaria Vincenza; Nikolić, Dragana; Amato, Antonella; Al-Busaidi, Noor; Al-Rasadi, Khalid; Soresi, Maurizio; Banach, Maciej; Montalto, Giuseppe; Rizzo, Manfredi

doi:10.1517/14712598.2015.1067299

Cited by 43 publications

(26 citation statements)

References 37 publications

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“…They are considered a second-line treatment for T2DM [33]. Apart from their glucose-lowering effect, they have further positive consequences such as cardio-protective effects [70,71] and an induction of weight loss which is very beneficial in patients with NAFLD [72].…”

Section: Glucagon-like Peptide 1 Receptor (Glp-1 R) Agonistsmentioning

confidence: 99%

The effect of antidiabetic medications on non-alcoholic fatty liver disease (NAFLD)

Prat

Tsochatzis

2018

Hormones

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Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome and is prevalent in more than 50% of patients with type II diabetes. At present, there is no approved therapy for NASH. Until now, the only proven effective interventions in improving biochemical and histological features of NASH, including fibrosis, are weight loss and physical activity even without weight loss. Because of the common epidemiological and pathophysiological features between NAFLD and T2DM, many antidiabetics drugs have been tested in patients with NAFLD over the years. Among these, pioglitazone and liraglutide seem to improve some histological features of NASH but have no clear effect on fibrosis. Metformin has been largely studied in the past years without convincing evidence of improving NAFLD. Data on other compounds such as DDP-4 and SGLT-2 inhibitors are limited. The rational and results of such studies are discussed in the present review.

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Section: Glucagon-like Peptide 1 Receptor (Glp-1 R) Agonistsmentioning

confidence: 99%

The effect of antidiabetic medications on non-alcoholic fatty liver disease (NAFLD)

Prat

Tsochatzis

2018

Hormones

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“…In VSMC, incretins are able to prevent vascular remodeling [42–46]. Exendin-4 and GLP-1 prevent the progression of atherosclerosis in apoE −/− mice, without major effects on metabolic parameters, and markedly reduced the accumulation of monocytes/macrophages in the vascular wall [43, 45].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, in Zucker fatty rats and C57BL/6 mice, exenatide caused a significant reduction in intimal hyperplasia in balloon catheter injured carotid arteries and endothelial denudation injury of the femoral artery, respectively [42, 44]. Furthermore, the GLP-1 receptor analogue liraglutide significantly reduced carotid intima-media thickness, a surrogate marker of atherosclerosis, independently of glucometabolic changes, in diabetic subjects with non-alcoholic fatty liver disease [46]. These data clearly show a direct effect of GLP-1 and its analogs on the vasculature, suggesting a therapeutical role of these peptides on vascular diseases.…”

Section: Discussionmentioning

confidence: 99%

Glucagon-like peptide-1 inhibits vascular smooth muscle cell dedifferentiation through mitochondrial dynamics regulation

Torres

Morales

García-Miguel

et al. 2016

Biochemical Pharmacology

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Glucagon-like peptide-1 (GLP-1) is a neuroendocrine hormone produced by gastrointestinal tract in response to food ingestion. GLP-1 plays a very important role in the glucose homeostasis by stimulating glucose-dependent insulin secretion, inhibiting glucagon secretion, inhibiting gastric emptying, reducing appetite and food intake. Because of these actions, the GLP-1 peptide-mimetic exenatide is one of the most promising new medicine for the treatment of type 2 diabetes. In vivo treatments with GLP-1 or exenatide prevent neo-intima layer formation in response to endothelial damage and atherosclerotic lesion formation in aortic tissue. Whether GLP-1 modulates vascular smooth muscle cell (VSMC) migration and proliferation by controlling mitochondrial dynamics is unknown. In this report, we showed that GLP-1 increased mitochondrial fusion and activity in a PKA-dependent manner in the VSMC cell line A7r5. GLP-1 induced a Ser-637 phosphorylation in the mitochondrial fission protein Drp1, and decreased Drp1 mitochondrial localization. GLP-1 inhibited PDGF-BB-induced VSMC migration and proliferation, actions inhibited by overexpressing wild type Drp1 and mimicked by the Drp1 inhibitor Mdivi-1 and by overexpressing dominant negative Drp1. These results show that GLP-1 stimulates mitochondrial fusion, increases mitochondrial activity and decreases PDGF-BB-induced VSMC dedifferentiation by a PKA/Drp1 signaling pathway. Our data suggest that GLP-1 inhibits vascular remodeling through a mitochondrial dynamics-dependent mechanism.

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“…The trial named Liraglutide Effect and Action in Diabetes: Evaluation of Cardiovascular Outcome Results-A Long Term Evaluation (LEADER; CT. gov identifier: NCT01179048) clearly demonstrated in T2DM patients at elevated CV risk that liraglutide (1.8 mg) significantly reduces the rates of major adverse CV events [15]. In a prospective study performed on subjects with T2DM but without CAD [16], Carotid Intima-Media Thickness (CIMT) decreased independently to the well-known effects of liraglutide on both glucose and lipids [17]. Moreover, further studies demonstrated that liraglutide reduced CIMT also in subjects with metabolic syndrome, highlighting that its prevalence may be significantly reduced of about 26% in these subjects (p < 0.0001) [18].…”

Section: Glucagon Like Peptide-1 Receptor Agonists (Glp-1ras)mentioning

confidence: 99%

Impact of Glucose-Lowering Medications on Cardiovascular and Metabolic Risk in Type 2 Diabetes

Patti

Rizvi

Giglio

et al. 2020

JCM

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Type 2 Diabetes Mellitus (T2DM) is associated with a high risk of atherosclerotic cardiovascular (CV) disease. Among the well-known pathophysiologic factors, crucial roles are played by endothelial dysfunction (caused by oxidative stress and inflammation hyperglycemia-linked), increased activity of nuclear factor kB, altered macrophage polarization, and reduced synthesis of resident endothelial progenitor cells. As consequence, a potentially rapid progression of the atherosclerotic disease with a higher propensity to unstable plaque is arguable, finally leading to significantly increased cardiovascular mortality. Main managements are focused on both prevention and early diagnosis, by targeted treatment of hyperglycemia and vascular complications. Innovative therapeutic approaches for T2DM seek to customize the antidiabetic treatment to each patient in order to optimize glucose-lowering effects, minimize hypoglycemia and adverse effects, and prevent cardiovascular events. The newer drugs (e.g., Glucagon Like Peptide-1 Receptor Agonists, GLP-1 RAs; Sodium GLucose coTransporter-2 inhibitors, SGLT2is; DiPeptidyl Peptidase-4 inhibitors, and DPP4is) impact body weight, lipid parameters, and blood pressure, as well as endothelial (dys)functions, inflammatory markers, biomarkers of both oxidative stress, and subclinical atherosclerosis. The present review summarizes the results of the main trials focused on the cardiovascular safety of these drugs from the CV standpoint.

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Liraglutide improves carotid intima-media thickness in patients with type 2 diabetes and non-alcoholic fatty liver disease: an 8-month prospective pilot study

Abstract: Eight months of liraglutide use in patients with T2DM and NAFLD significantly reduced carotid IMT, a surrogate marker of atherosclerosis, independently of glucometabolic changes.

Cited by 43 publications

References 37 publications

The effect of antidiabetic medications on non-alcoholic fatty liver disease (NAFLD)

The effect of antidiabetic medications on non-alcoholic fatty liver disease (NAFLD)

Glucagon-like peptide-1 inhibits vascular smooth muscle cell dedifferentiation through mitochondrial dynamics regulation

Impact of Glucose-Lowering Medications on Cardiovascular and Metabolic Risk in Type 2 Diabetes

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