Academic Ageing Seminar - Insulin signalling and its impact on mammalian lifespan
Location: Seminar Room, Wolfson Research Centre, Campus for Ageing and Vitality
Time/Date: 11th February 2010, 12:30 - 13:30
You are invited to attend the Academic Ageing Seminar on Thursday 11 February 2010 in the Wolfson Seminar Room, Institute for Ageing and Health. The seminar will take place at 12.30 pm with sandwiches available from 12 noon.
The speaker is Dr Colin Selman, University of Aberdeen and the title of his talk is 'Insulin signalling and its impact on mammalian lifespan'.
Abstract:
Evidence suggests that alterations in insulin/insulin-like growth factor 1 (IGF1) signaling (IIS) pathway and in nutrient-responsive mTOR (mammalian target of rapamycin) signaling pathway increase life span in multicellular organisms.
My recent research indicates that female, but not male, mice lacking insulin receptor substrate protein (Irs1-/-), a major intracellular effectors of the IIS receptors, are long-lived. In addition, these mice are resistant to a range of age-sensitive markers of aging. These improvements in age-related health were seen despite mild, lifelong insulin resistance and indicate that enhanced insulin sensitivity is not a prerequisite for long-life in IIS mutants.
I will then discuss some of my more recent data demonstrating that female mice carrying a global deletion of ribosomal S6 protein kinase 1 (S6K1), a component of the mTOR signaling pathway, are long-lived and resistant to age-related pathologies, such as bone, immune, and motor dysfunction and loss of insulin sensitivity. Deletion of S6K1 induced gene expression patterns similar to those seen in caloric restriction (CR) and Irs1-/- mice or following pharmacological activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK), a conserved regulator of the metabolic response to CR.
These data demonstrate that IRS1 and S6K1 influence healthy mammalian life-span and may be realistic points of intervention for therapies with the potential to delay age-related disease. In particular, therapeutic manipulation of S6K1 and AMPK might mimic CR and therefore could provide broad protection against diseases of aging.
http://www.abdn.ac.uk/ibes/staff/c.selman
Published: 3rd February 2010
