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Dual endothelin receptor antagonism increases resting energy expenditure in people with increased adiposity

American journal of physiology: endocrinology and metabolism, 2022-06, Vol.322 (6), p.E508-E516 [Peer Reviewed Journal]

Copyright American Physiological Society Jun 2022 ;Copyright © 2022 the American Physiological Society. 2022 American Physiological Society ;ISSN: 0193-1849 ;EISSN: 1522-1555 ;DOI: 10.1152/ajpendo.00349.2021 ;PMID: 35373585

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  • Title:
    Dual endothelin receptor antagonism increases resting energy expenditure in people with increased adiposity
  • Author: Derella, Cassandra C ; Blanks, Anson M ; Nguyen, Andy ; Looney, Jacob ; Tucker, Matthew A ; Jeong, Jinhee ; Rodriguez-Miguelez, Paula ; Thomas, Jeffrey ; Lyon, Matthew ; Pollock, David M ; Harris, Ryan A
  • Subjects: Adipose tissue ; Adiposity ; Adult ; Basal Metabolism ; Body weight ; Bosentan ; Calorimetry ; Calorimetry, Indirect ; Carbohydrates ; Cardiovascular Diseases ; Data exchange ; Endothelin 1 ; Endothelins - metabolism ; Energy expenditure ; Energy Metabolism ; Gas exchange ; Health risks ; Heart diseases ; Humans ; Metabolism ; Obesity ; Obesity - metabolism ; Overweight - metabolism ; Placebos ; Receptors ; Receptors, Endothelin - metabolism ; Weight ; Young Adult
  • Is Part Of: American journal of physiology: endocrinology and metabolism, 2022-06, Vol.322 (6), p.E508-E516
  • Description: Increased adiposity is associated with dysregulation of the endothelin system, both of which increase the risk of cardiovascular disease (CVD). Preclinical data indicate that endothelin dysregulation also reduces resting energy expenditure (REE). The objective was to test the hypothesis that endothelin receptor antagonism will increase REE in people with obesity compared with healthy weight individuals. Using a double blind, placebo-controlled, crossover design, 32 participants [healthy weight (HW): = 16, BMI: 21.3 ± 2.8 kg/m , age: 26 ± 7 yr and overweight/obese (OB): = 16, BMI: 33.5 ± 9.5 kg/m , age: 31 ± 6 yr] were randomized to receive either 125 mg of bosentan (ET antagonism) or placebo twice per day for 3 days. Breath-by-breath gas exchange data were collected and REE was assessed by indirect calorimetry. Venous blood samples were analyzed for concentrations of endothelin-1 (ET-1). Treatment with bosentan increased plasma ET-1 in both OB and HW groups. Within the OB group, the changes in absolute REE (PLA: -77.6 ± 127.6 vs. BOS: 72.2 ± 146.6 kcal/day; = 0.046). The change in REE was not different following either treatment in the HW group. Overall, absolute plasma concentrations of ET-1 following treatment with bosentan were significantly associated with kcal/day of fat ( = 0.488, = 0.005), percentage of fat utilization ( = 0.415, = 0.020), and inversely associated with the percentage of carbohydrates ( = -0.419, = 0.019), and respiratory exchange ratio ( = -0.407, = 0.023). Taken together, these results suggest that modulation of the endothelin system may represent a novel therapeutic approach to increase both resting metabolism and caloric expenditure, and reduce CVD risk in people with increased adiposity. Findings from our current translational investigation demonstrate that dual endothelin A/B receptor antagonism increases total REE in overweight/obese individuals. These results suggest that modulation of the endothelin system may represent a novel therapeutic target to increase both resting metabolism and caloric expenditure, enhance weight loss, and reduce CVD risk in seemingly healthy individuals with elevated adiposity.
  • Publisher: United States: American Physiological Society
  • Language: English
  • Identifier: ISSN: 0193-1849
    EISSN: 1522-1555
    DOI: 10.1152/ajpendo.00349.2021
    PMID: 35373585
  • Source: Geneva Foundation Free Medical Journals at publisher websites
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    Alma/SFX Local Collection
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