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

Muhammad Ali1, Shazia Anwer Bukhari1, Muhammad Ali2

  • 1Departments of Biochemistry, Government College University, Faisalabad, 38000 Pakistan.

BMB Reports
|December 1, 2017
PubMed

Insights

Mammalian target of rapamycin complex 1 (mTORC1) is crucial for cell functions and linked to diseases like Type 2 diabetes. This review explores mTORC1 signaling, telomere attrition, and potential therapeutic targets like TERT and HKII.

Area of Science:

  • Cellular Biology
  • Metabolic Diseases
  • Molecular Signaling

Background:

  • Mammalian target of rapamycin complex 1 (mTORC1) is a central regulator of cell growth, proliferation, and metabolism.
  • mTORC1 integrates extracellular and intracellular signals to maintain cellular homeostasis.
  • Dysregulation of mTORC1 signaling is implicated in various pathologies, including neurodegeneration, Type 2 diabetes (T2D), obesity, and cancer.

Purpose of the Study:

  • To review upstream signaling pathways of mTORC1.
  • To elucidate the etiology of T2D and hypertriglyceridemia in relation to mTORC1.
  • To explore the role of telomere attrition in mTORC1-related conditions and discuss therapeutic interventions.

Main Methods:

  • Literature review of current knowledge on mTORC1 signaling.
  • Analysis of the connection between mTORC1, telomere attrition, T2D, and hypertriglyceridemia.
  • Discussion of potential regulatory mechanisms and therapeutic strategies.

Main Results:

  • mTORC1 signaling is a key factor in the development of T2D and hypertriglyceridemia.
  • Telomere attrition plays a role in the pathological states associated with mTORC1 dysregulation.
  • Chronic inhibition of mTORC1 may reverse adverse effects of its hyperactivation.

Conclusions:

  • Telomerase (TERT) and hexokinase II (HKII) show regulatory roles on mTORC1, offering potential therapeutic avenues.
  • TERT inhibits mTORC1 under nutrient-rich conditions, while HKII inhibits it under starved conditions.
  • TOR signaling (TOS) motifs are proposed as tools for mTORC1 regulation.

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