Sirtuin 1

From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history

Sirtuin 1 or SIRT1 refers to an enzyme or the gene encoded by the enzyme from the silent information regulator (Sir2)-like family.[1] Levels of SIRT1 expression may be associated with ME/CFS.

Other names[edit | edit source]

Sirtuin 1 is also known as

  • SIR2L1
  • NAD-Dependent Protein Deacetylase Sirtuin-1
  • NAD-Dependent Protein Deacylase Sirtuin-1
  • HSIRT1
  • HSIR2

Function[edit | edit source]

Sirtuins or silent information regulator (Sir2)-like family deacetylases are a group of enzymes found in the cytoplasm, mitochondria or nucleus of the cell and are ubiquitously expressed, and are closely related to histone deacetylases.[2] Their purpose in human disease is not well understood.[1]

ME/CFS[edit | edit source]

Notable studies[edit | edit source]

  • 2018, PO-132 Exogenous VD3 alleviates chronic fatigue syndrome by activating MEKs/ERKs-SIRT1 signaling pathway in skeletal muscle[3] - Conference proceedings (Abstract)
This refers to mice exhausted by excessive activity, which is an exclusion for chronic fatigue syndrome.
Results Compared with C group, CFS group appeared serious damage caused by fighting, and the concentration of serum testosterone decreased significantly (p<0.01 or p<0.05) while cortisol concentration increased significantly (p<0.01 or p<0.05). Regarding antioxidant stress system indexes, the expression of MDA, T-SOD and GSH-PX significantly increased (p<0.05). The concentration of MEK and SIRT3 decreased significantly (p<0.01 or p<0.05). Compared with CFS group, VD intervention group (bVD, mVD and aVD) showed less damage caused by fighting and significantly lighter body weight (p<0.05), and the concentration of serum testosterone increased significantly (p<0.05) while that of cortisol decreased significantly (p<0.01 or p<0.05). The expression of MDA decreased significantly (p<0.05), on the countrary, T-AOC, T-SOD and GSH-PX increased significantly (p<0.05). The expressions of MEK, p-ERK/ERK, SIRT1 and SIRT3 were significantly upregulated (p<0.01 or p<0.05).
  • 2016, Gene expression factor analysis to differentiate pathways linked to fibromyalgia, chronic fatigue syndrome, and depression in a diverse patient sample[4] (Full text)
  • 2015, Novel Associations of F2-Isoprostanes, F3- Isoprostanes and Isofurans in Older Adults with Chronic Fatigue Syndrome: An Exploratory Study[5] - (Full Text)
  • 2011, Increased HDAC in association with decreased plasma cortisol in older adults with chronic fatigue syndrome[6] (Full text)

See also[edit | edit source]

Learn more[edit | edit source]

References[edit | edit source]

  1. 1.0 1.1 "SIRT1 gene". Gene cards. Retrieved March 18, 2022.
  2. "Class III HDACs (Sirtuins)". TOCRIS. Retrieved March 18, 2022.
  3. Wu, Fangnan; Huder, Chaolu; Tian, Zhenjun (October 4, 2018). "PO-132 Exogenous VD3 alleviates chronic fatigue syndrome by activating MEKs/ERKs-SIRT1 signaling pathway in skeletal muscle:". Exercise Biochemistry Review. 1 (4). doi:10.14428/ebr.v1i4.10353. ISSN 2593-7588.
  4. Iacob, E; Light, AR; Donaldson, GW; Okifuji, A; Hughen, RW; White, AT; Light, K (2016). "Gene expression factor analysis to differentiate pathways linked to fibromyalgia, chronic fatigue syndrome, and depression in a diverse patient sample". Arthritis Care and Research. 68 (1): 132-40. doi:10.1002/acr.22639. PMC 4684820. PMID 26097208.
  5. Kubow, Stan; Sorenson, Matthew; Alkazemi, Dalal; Roberts, Jackson L II; Adamski, Katherine Naselli; Jason, Leonard (2015). "Novel Associations of F2-Isoprostanes, F3- Isoprostanes and Isofurans in Older Adults with Chronic Fatigue Syndrome: An Exploratory Study" (PDF). Clinical Research: Open Access. 1: 1–4. doi:10.16966/clroa.103.
  6. Jason, Leonard; Sorenson, Matthew; Sebally, Kebba; Alkazemi, Dalal; Lerch, Athena; Porter, Nicole; Kubow, Stan (November 1, 2011). "Increased HDAC in association with decreased plasma cortisol in older adults with chronic fatigue syndrome". Brain, Behavior, and Immunity. 25 (8): 1544–1547. doi:10.1016/j.bbi.2011.04.007. ISSN 0889-1591.