Aims: Liraglutide is a long-acting glucagon-like peptide 1 (GLP-1) receptor agonist used as an anti-hyperglycemic agent in type 2 diabetes treatment and recently approved for obesity management. Weight loss is attributed to appetite suppression, but therapy may also increase energy expenditure. To further investigate the effect of GLP-1 signaling in thermogenic fat, we assessed adipose tissue oxygen consumption and type 2 deiodinase (D2) activity in mice treated with liraglutide, both basally and after β3-adrenergic treatment.
Methods: Male C57BL/6J mice were randomly assigned to receive liraglutide (400 μg/kg, n=12) or vehicle (n=12). After 16 days, mice in each group were co-treated with the selective β3-adrenergic agonist CL316,243 (1 mg/kg, n=6) or vehicle (n=6) for 5 days. Adipose tissue depots were assessed for gene and protein expression, oxygen consumption, and D2 activity.
Results: Liraglutide increased interscapular brown adipose tissue (iBAT) oxygen consumption and enhanced β3-adrenergic-induced oxygen consumption in iBAT and inguinal white adipose tissue (ingWAT). These effects were accompanied by upregulation of UCP-1 protein levels in iBAT and ingWAT. Notably, liraglutide increased D2 activity without significantly upregulating its mRNA levels in iBAT and exhibited additive effects to β3-adrenergic stimulation in inducing D2 activity in ingWAT.
Conclusions: Liraglutide exhibits additive effects to those of β3-adrenergic stimulation in thermogenic fat and increases D2 activity in BAT, implying that it may activate this adipose tissue depot by increasing intracellular thyroid activation, adding to the currently known mechanisms of GLP-1A-induced weight loss.
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http://dx.doi.org/10.3389/fendo.2021.803363 | DOI Listing |
Sci Adv
January 2025
Institute for Diabetes, Obesity and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Adipocyte lipolysis controls systemic energy levels and metabolic homeostasis. Lipolysis is regulated by posttranslational modifications of key lipolytic enzymes. However, less is known about the transcriptional mechanisms that regulate lipolysis.
View Article and Find Full Text PDFWith complex pathogenesis, Alzheimer's disease (AD) is a neurological illness that has worsened over time. Inter-organ crosstalk, which is essential for coordinating organ function and maintaining homeostasis, is involved in multiple physiological and pathological events. Increasing evidence suggests that AD is closely associated with multiple diseases of peripheral organs, including the gut, adipose tissue, liver, and bone.
View Article and Find Full Text PDFFASEB J
January 2025
Department of Clinical Biochemistry, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Cholesterol is vital for nerve processes. Changes in cholesterol homeostasis lead to neurodegeneration and Alzheimer's disease (AD). In recent years, extensive research has confirmed the influential role of adipose tissue mesenchymal stem cells (MSCs) in managing AD.
View Article and Find Full Text PDFAm J Sports Med
January 2025
Orthopaedic Surgery, Weill Medical College of Cornell University, New York, New York, USA.
Background: Microfragmented adipose tissue has been proposed for intra-articular treatment of knee osteoarthritis. There are little data comparing the outcomes of treatment between microfragmented adipose tissue and other biological treatments.
Purpose: To perform a systematic review and meta-analysis comparing microfragmented aspirated fat injections to other orthobiologics, hyaluronic acid, and corticosteroid injections for symptomatic knee osteoarthritis.
Alzheimers Dement
December 2024
Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio De Janeiro, Rio de Janeiro, Brazil.
Background: Age-related decrease glucose utilization, coupled with insulin resistance, are key features of AD, resulting in reduced glucose utilization/catabolism and oxidative stress generation. Irisin, an exercise-induced hormone promoting mitochondrial biogenesis in adipocytes via PGC-1α, stimulates thermogenic pathways, increases energy expenditure and induces browning of adipose tissue. Further, irisin expression was shown to trigger neuroprotection in AD models.
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