Sex differences in metabolic regulation by Gi/o-coupled receptor modulation of exocytosis

BackgroundPresynaptic Gi/o coupled GPCRs can act as negative feedback regulators of neurotransmitter release via Gβγ effector modulation through two mechanisms: decreased calcium influx and direct inhibition of membrane fusion by soluble N-ethylmaleimide—sensitive factor attachment protein (SNAP) re...

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Main Authors: Montana Young, Ryan P. Ceddia, Analisa Thompson-Gray, David Reyes, Jackson B. Cassada, Julio E. Ayala, Owen P. McGuinness, Sheila Collins, Heidi E. Hamm
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-03-01
Series:Frontiers in Pharmacology
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Online Access:https://www.frontiersin.org/articles/10.3389/fphar.2025.1544456/full
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author Montana Young
Ryan P. Ceddia
Analisa Thompson-Gray
David Reyes
Jackson B. Cassada
Julio E. Ayala
Owen P. McGuinness
Sheila Collins
Sheila Collins
Heidi E. Hamm
author_facet Montana Young
Ryan P. Ceddia
Analisa Thompson-Gray
David Reyes
Jackson B. Cassada
Julio E. Ayala
Owen P. McGuinness
Sheila Collins
Sheila Collins
Heidi E. Hamm
author_sort Montana Young
collection DOAJ
description BackgroundPresynaptic Gi/o coupled GPCRs can act as negative feedback regulators of neurotransmitter release via Gβγ effector modulation through two mechanisms: decreased calcium influx and direct inhibition of membrane fusion by soluble N-ethylmaleimide—sensitive factor attachment protein (SNAP) receptor (SNARE). Previously, we discovered that truncation of the last three C-terminal amino acids of SNAP25 (SNAP25Δ3) prevents Gβγ-SNARE interaction, effectively removing the braking mechanism on neurotransmitter release. We have demonstrated enhanced metabolic protection in male SNAP25Δ3/Δ3 mice housed at room temperature (22°C), including increased adipose tissue beiging and glucose uptake and enhanced insulin sensitivity, rendering them resistant to diet-induced obesity (DIO). When male SNAP25Δ3/Δ3 mice were housed at thermoneutrality (30°C), all metabolic protection was abolished, suggesting sympathetic tone is important for the phenotypes.MethodsWe housed male and female mice at either standard room temperature (21°C) or at thermoneutrality (30°C) and fed them a high fat diet (HFD) for 8 weeks. Glucose tolerance tests were performed before and after the 8 weeks of HFD along with body composition analyses. Organs were then dissected for mass analysis as well as immunohistochemistry. Additionally, we ovariectomized female mice to investigate the role of sex hormones in our phenotypes. Finally, we housed mice in Sable Promethion chambers at various environmental temperatures to investigate the effect of environmental temperature on basal metabolic rates.ResultsWe found SNAP25Δ3/Δ3 female mice exhibited the same metabolic protection at RT (22°C) and displayed enhanced metabolic protection from DIO compared to standard chow just as males did. However, female SNAP25Δ3/Δ3 mice display persistent metabolic protection even when housed at thermoneutrality. In this study, we investigate the mechanisms behind this sex dependent persistent phenotype. Thermoneutral set point did not differ between sexes nor genotype, suggesting that metabolic protection is not due to a difference in hypothalamic temperature regulation. Metabolic protection in SNAP25Δ3/Δ3 persisted in ovariectomized mice despite increased weight gain compared to mice receiving sham operations.ConclusionThis study has identified that there is not a sex-dependent difference for thermoneutral set point in mice. Additionally, there is a sex hormone independent mechanism driving the persistent metabolic protection of female SNAP25Δ3/Δ3 mice housed in thermoneutrality.
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spelling doaj-art-e2b5154231fa47a5968990e75713dba92025-08-20T03:42:37ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122025-03-011610.3389/fphar.2025.15444561544456Sex differences in metabolic regulation by Gi/o-coupled receptor modulation of exocytosisMontana Young0Ryan P. Ceddia1Analisa Thompson-Gray2David Reyes3Jackson B. Cassada4Julio E. Ayala5Owen P. McGuinness6Sheila Collins7Sheila Collins8Heidi E. Hamm9Department of Pharmacology, School of Medicine, Vanderbilt University, Nashville, TN, United StatesDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, United StatesDepartment of Pharmacology, School of Medicine, Vanderbilt University, Nashville, TN, United StatesDepartment of Pharmacology, School of Medicine, Vanderbilt University, Nashville, TN, United StatesDepartment of Pharmacology, School of Medicine, Vanderbilt University, Nashville, TN, United StatesDepartment of Molecular Physiology and Biophysics, School of Medicine, Vanderbilt University, Nashville, IN, United StatesDepartment of Molecular Physiology and Biophysics, School of Medicine, Vanderbilt University, Nashville, IN, United StatesDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, United StatesDepartment of Molecular Physiology and Biophysics, School of Medicine, Vanderbilt University, Nashville, IN, United StatesDepartment of Pharmacology, School of Medicine, Vanderbilt University, Nashville, TN, United StatesBackgroundPresynaptic Gi/o coupled GPCRs can act as negative feedback regulators of neurotransmitter release via Gβγ effector modulation through two mechanisms: decreased calcium influx and direct inhibition of membrane fusion by soluble N-ethylmaleimide—sensitive factor attachment protein (SNAP) receptor (SNARE). Previously, we discovered that truncation of the last three C-terminal amino acids of SNAP25 (SNAP25Δ3) prevents Gβγ-SNARE interaction, effectively removing the braking mechanism on neurotransmitter release. We have demonstrated enhanced metabolic protection in male SNAP25Δ3/Δ3 mice housed at room temperature (22°C), including increased adipose tissue beiging and glucose uptake and enhanced insulin sensitivity, rendering them resistant to diet-induced obesity (DIO). When male SNAP25Δ3/Δ3 mice were housed at thermoneutrality (30°C), all metabolic protection was abolished, suggesting sympathetic tone is important for the phenotypes.MethodsWe housed male and female mice at either standard room temperature (21°C) or at thermoneutrality (30°C) and fed them a high fat diet (HFD) for 8 weeks. Glucose tolerance tests were performed before and after the 8 weeks of HFD along with body composition analyses. Organs were then dissected for mass analysis as well as immunohistochemistry. Additionally, we ovariectomized female mice to investigate the role of sex hormones in our phenotypes. Finally, we housed mice in Sable Promethion chambers at various environmental temperatures to investigate the effect of environmental temperature on basal metabolic rates.ResultsWe found SNAP25Δ3/Δ3 female mice exhibited the same metabolic protection at RT (22°C) and displayed enhanced metabolic protection from DIO compared to standard chow just as males did. However, female SNAP25Δ3/Δ3 mice display persistent metabolic protection even when housed at thermoneutrality. In this study, we investigate the mechanisms behind this sex dependent persistent phenotype. Thermoneutral set point did not differ between sexes nor genotype, suggesting that metabolic protection is not due to a difference in hypothalamic temperature regulation. Metabolic protection in SNAP25Δ3/Δ3 persisted in ovariectomized mice despite increased weight gain compared to mice receiving sham operations.ConclusionThis study has identified that there is not a sex-dependent difference for thermoneutral set point in mice. Additionally, there is a sex hormone independent mechanism driving the persistent metabolic protection of female SNAP25Δ3/Δ3 mice housed in thermoneutrality.https://www.frontiersin.org/articles/10.3389/fphar.2025.1544456/fullg protein coupled receptor (GPCR)sex hormonemetabolismnorepinephrenediet induced obesity (DIO)exocytosis
spellingShingle Montana Young
Ryan P. Ceddia
Analisa Thompson-Gray
David Reyes
Jackson B. Cassada
Julio E. Ayala
Owen P. McGuinness
Sheila Collins
Sheila Collins
Heidi E. Hamm
Sex differences in metabolic regulation by Gi/o-coupled receptor modulation of exocytosis
Frontiers in Pharmacology
g protein coupled receptor (GPCR)
sex hormone
metabolism
norepinephrene
diet induced obesity (DIO)
exocytosis
title Sex differences in metabolic regulation by Gi/o-coupled receptor modulation of exocytosis
title_full Sex differences in metabolic regulation by Gi/o-coupled receptor modulation of exocytosis
title_fullStr Sex differences in metabolic regulation by Gi/o-coupled receptor modulation of exocytosis
title_full_unstemmed Sex differences in metabolic regulation by Gi/o-coupled receptor modulation of exocytosis
title_short Sex differences in metabolic regulation by Gi/o-coupled receptor modulation of exocytosis
title_sort sex differences in metabolic regulation by gi o coupled receptor modulation of exocytosis
topic g protein coupled receptor (GPCR)
sex hormone
metabolism
norepinephrene
diet induced obesity (DIO)
exocytosis
url https://www.frontiersin.org/articles/10.3389/fphar.2025.1544456/full
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