Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 69, Issue 8, Pages 1289-1304Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-011-0874-4
Keywords
Type 2 diabetes; Obesity; beta-cell mass; mTOR; TSC; Rheb; S6K; PKB; AMPK; RICTOR
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Funding
- CONACYT by Mexican government [206710]
- Welcome Trust [WT081268MA]
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Type-2 diabetes mellitus (T2DM) is a disorder that is characterized by high blood glucose concentration in the context of insulin resistance and/or relative insulin deficiency. It causes metabolic changes that lead to the damage and functional impairment of organs and tissues resulting in increased morbidity and mortality. It is this form of diabetes whose prevalence is increasing at an alarming rate due to the 'obesity epidemic', as obesity is a key risk factor in the development of insulin resistance. However, the majority of individuals who have insulin resistance do not develop diabetes due to a compensatory increase in insulin secretion in response to an increase in insulin demand. This adaptive response is sustained by an increase in both beta-cell function and mass. Importantly, there is increasing evidence that the Serine/Threonine kinase mammalian target of rapamycin (mTOR) plays a key role in the regulation of beta-cell mass and therefore likely plays a critical role in beta-cell adaptation. Therefore, the primary focus of this review is to summarize our current understanding of the role of mTOR in stimulating pancreatic beta-cell mass and thus, in the prevention of type-2 diabetes.
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