Upstream signalling of mTORC1 and its hyperactivation in type 2 diabetes (T2D)

Muhammad Ali, Shazia Anwer Bukhari, Muhammad Ali, Han Woong Lee

Research output: Contribution to journalReview articlepeer-review

16 Citations (Scopus)


Mammalian target of rapamycin complex 1 (mTORC1) plays a major role in cell growth, proliferation, polarity, differentiation, development, and controls transitioning between anabolic and catabolic states of the cell. It collects almost all extracellular and intracellular signals from growth factors, nutrients, and maintains cellular homeostasis, and is involved in several pathological conditions including, neurodegeneration, Type 2 diabetes (T2D), obesity, and cancer. In this review, we summarize current knowledge of upstream signaling of mTORC1 to explain etiology of T2D and hypertriglyceridemia, in which state, the role of telomere attrition is explained. We discuss if chronic inhibition of mTORC1 can reverse adverse effects resulting from hyperactivation. In conclusion, we suggest the regulatory roles of telomerase (TERT) and hexokinase II (HKII) on mTORC1 as possible remedies to treat hyperactivation. The former inhibits mTORC1 under nutrientrich while the latter under starved condition. We provide an idea of TOS (TOR signaling) motifs that can be used for regulation of mTORC1.

Original languageEnglish
Pages (from-to)601-609
Number of pages9
JournalBMB reports
Issue number12
Publication statusPublished - 2017 Dec 1

Bibliographical note

Funding Information:
The study was supported by HEC, Pakistan and by the National Research Foundation funded by the Korean government (NRF-2015R1A2A1A01003845)

Publisher Copyright:
© 2017 by the The Korean Society for Biochemistry and Molecular Biology.

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology


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