Positions
- Instructor
-
Medicine
Endocrinology, Diabetes, and Metabolism
Baylor College of Medicine
Houston, TX US
Education
- Postdoctoral Training at Baylor College of Medicine
- 12/2019 - Housotn, Texas United States
- Neuroscience and Metabolism
- Postdoctoral Training at UT MD Anderson Cancer Center
- 11/2014 - Houston, Texas United States
- Neuropathic Pain and Mood Disorder
- Postdoctoral Training at University of Alabama at Birmingham
- 11/2011 - Birmingham, Alabama United States
- Mood Disorder
- PhD from University of Shizuoka
- 03/2009 - Shizuoka City, Shizuoka Japan
- Nutritional Neuroscience
Professional Interests
- Type 2 Diabetes
- Neurocognitive Function
- Environmental Stress and Metabolism disorders
Professional Statement
My research is focused on transcriptional regulation of energy metabolism and neurocognition by endocrine factors, environmental factors, and the circadian clock. I am interested in type 2 diabetes, mood disorders, and neurocognitive impairment.Websites
Selected Publications
- Sungguan Hong, Wenjun Zhou, ..., Mitchell A Lazar, Zheng Sun "Dissociation of muscle insulin sensitivity from exercise endurance in mice by HDAC3 depletion." Nat Med. 2017 Feb;23 Pubmed PMID: 27991918
- Wenjun Zhou, Yanlin He, ..., Zheng Sun "Loss of function of NCOR1 and NCOR2 impairs memory through a novel GABAergic hypothalamus-CA3 projection.." Nat Neurosci. 2019 Feb;22 Pubmed PMID: 30664766
- Kong Y, Zhou W, Sun Z "Nuclear receptor corepressors in intellectual disability and autism." Mol Psychiatry. 2020 Feb; Pubmed PMID: 32034290
- Hanneke L D M Willemen, ..., Wenjun Zhou, ..., Niels Eijkelkamp "Identification of FAM173B as a protein methyltransferase promoting chronic pain." PLoS Biol .. 2018 Feb;16 Pubmed PMID: 29444090
- Geoffroy Laumet, Wenjun Zhou, ..., Annemieke Kavelaars "Upregulation of neuronal kynurenine 3-monooxygenase mediates depression-like behavior in a mouse model of neuropathic pain." Brain Behav Immun. 2017 Nov; Pubmed PMID: 28709913
- Wenjun Zhou, Robert Dantzer, Annemieke Kavelaars "Peripheral indoleamine 2,3-dioxygenase 1 is required for comorbid depression-like behavior but does not contribute to neuropathic pain in mice." Brain Behav Immun. 2015 May; Pubmed PMID: 25637485
- Zhou W, Chen L, Yang S, Li F, Li X "Behavioral stress-induced activation of FoxO3a in the cerebral cortex of mice." Biol Psychiatry. 2012 Apr; Pubmed PMID: 21978520
- Guolian Ding #, Xin Li #, Xinguo Hou #, Wenjun Zhou #, Zheng Sun "REV-ERB in GABAergic neurons controls diurnal hepatic insulin sensitivity." Nature. 2021 Apr;592(7856):763-767. Pubmed PMID: 33762728
Memberships
- American Diabetes Association
- Membership (01/2019)
- Society for Neuroscience
- Membership (04/2010)
Funding
- Regulation of hepatic insulin sensitivity by the hypothalamic circadian clock - #ADA 1-19-PDF-012 (01/01/2019 - 12/31/2022) Grant funding from American Diabetes Association
- Many living organisms on earth have evolved a 24h circadian patterns for sleeping, hunting, and eating, which is entrained by sunlight. Industrialized human society has changed our living environment and led to disruption of circadian rhythm by enhan nighttime light, nighttime activity, shiftwork, and social jetlag. And according to the reports from both clinic and animal model, circadian disruption will induce many metabolic disorders, such as glucose intolerance, and insulin resistance. These are highly related with type2 diabetes. This study will identify the pathological reasons of why, and how circadian disruption will cause the symptoms of type2 diabetes. The central clock structure, called suprachiasmatic nucleus (SCN), locates in the ventral part of hypothalamus, a sub-region of the brain. SCN controls and synchronizes the temporal events which should happen in the different peripheral tissues at different time partially depending on the light received by the retina. For these reasons, SCN is an ideal candidate for studying how circadian disruption changes metabolism. Based on the animal models involved in the current study, the molecular and neuronal targets of SCN, which directly regulate blood glucose level, can be identified. It will potentially refresh the insight of how circadian disruption inferring the glucose metabolism and provide a possible new treatment way.
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