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Hao X, Zhu B, Yang P, et al. SNAP25 mutation disrupts metabolic homeostasis, steroid hormone production and central neurobehavior. Biochim Biophys Acta Mol Basis Dis. 2021;1868(2):166304doi: 10.1016/j.bbadis.2021.166304.
Hao, X., Zhu, B., Yang, P., Dong, D., Sahbaie, P., Oliver, P. L., Shen, W. J., Azhar, S., & Kraemer, F. B. (2021). SNAP25 mutation disrupts metabolic homeostasis, steroid hormone production and central neurobehavior. Biochimica et biophysica acta. Molecular basis of disease, 1868(2), 166304. https://doi.org/10.1016/j.bbadis.2021.166304
Hao, Xiao, et al. "SNAP25 mutation disrupts metabolic homeostasis, steroid hormone production and central neurobehavior." Biochimica et biophysica acta. Molecular basis of disease vol. 1868,2 (2021): 166304. doi: https://doi.org/10.1016/j.bbadis.2021.166304
Hao X, Zhu B, Yang P, Dong D, Sahbaie P, Oliver PL, Shen WJ, Azhar S, Kraemer FB. SNAP25 mutation disrupts metabolic homeostasis, steroid hormone production and central neurobehavior. Biochim Biophys Acta Mol Basis Dis. 2021 Nov 24;1868(2):166304. doi: 10.1016/j.bbadis.2021.166304. Epub 2021 Nov 24. PMID: 34826585.
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Biochim Biophys Acta Mol Basis Dis. 2021 Nov 24;1868(2):166304. doi: 10.1016/j.bbadis.2021.166304. Epub 2021 Nov 24.

SNAP25 mutation disrupts metabolic homeostasis, steroid hormone production and central neurobehavior.

Biochimica et biophysica acta. Molecular basis of disease

Xiao Hao, Bing Zhu, Pinglin Yang, Dachuan Dong, Peyman Sahbaie, Peter L Oliver, Wen-Jun Shen, Salman Azhar, Fredric B Kraemer

Affiliations

  1. Division of Endocrinology, Gerontology and Metabolism, Stanford University School of Medicine, Stanford, CA, United States; Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States; Department of Endocrinology, First Affiliated Hospital of the Medical College of Zhengzhou University, Zhengzhou, China.
  2. Division of Endocrinology, Gerontology and Metabolism, Stanford University School of Medicine, Stanford, CA, United States; Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States; Department of Endocrinology and Metabolism, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
  3. Division of Endocrinology, Gerontology and Metabolism, Stanford University School of Medicine, Stanford, CA, United States; Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States; Department of Orthopedics, Second Affiliated Hospital of Xi'an, Jiaotong University, Xi'an, Shaanxi, China.
  4. Division of Endocrinology, Gerontology and Metabolism, Stanford University School of Medicine, Stanford, CA, United States; Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States.
  5. Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States; Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, United States.
  6. Medical Research Council Harwell Institute, Harwell Campus, Oxfordshire, United Kingdom.
  7. Division of Endocrinology, Gerontology and Metabolism, Stanford University School of Medicine, Stanford, CA, United States; Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States. Electronic address: [email protected].
  8. Division of Endocrinology, Gerontology and Metabolism, Stanford University School of Medicine, Stanford, CA, United States; Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States. Electronic address: [email protected].

PMID: 34826585 DOI: 10.1016/j.bbadis.2021.166304

Abstract

OBJECTIVE: SNAP-25 is one of the key proteins involved in formation of soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complexes that are at the core of hormonal secretion and synaptic transmission. Altered expression or function of SNAP-25 can contribute to the development of neuropsychiatric and metabolic disease. A dominant negative (DN) I67T missense mutation in the b-isoform of SNAP-25 (DN-SNAP25mut) mice leads to abnormal interactions within the SNARE complex and impaired exocytotic vesicle recycling, yet the significance of this mutation to any association between the central nervous system and metabolic homeostasis is unknown.

METHODS: Here we explored aspects of metabolism, steroid hormone production and neurobehavior of DN-SNAP25mut mice.

RESULTS: DN-SNAP25mut mice displayed enhanced insulin function through increased Akt phosphorylation, alongside increased adrenal and gonadal hormone production. In addition, increased anxiety behavior and beigeing of white adipose tissue with increased energy expenditure were observed in mutants.

CONCLUSIONS: Our results show that SNAP25 plays an important role in bridging central neurological systems with peripheral metabolic homeostasis, and provide potential insights between metabolic disease and neuropsychiatric disorders in humans.

Copyright © 2021 Elsevier B.V. All rights reserved.

Keywords: Anxiety-like behavior; Beigeing; Brown adipose tissue; Glucose metabolism; Insulin secretion; Neurobehavior; SNAP25; Steroidogenesis; White adipose tissue

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