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- W4207025762 startingPage "4013" @default.
- W4207025762 abstract "Accumulating molecular evidence suggests that insulin resistance, rather than SARS-CoV-2- provoked beta-cell impairment, plays a major role in the observed rapid metabolic deterioration in diabetes, or new-onset hyperglycemia, during the COVID-19 clinical course. In order to clarify the underlying complexity of COVID-19 and diabetes mellitus interactions, we propose the imaginary diabetes-COVID-19 molecular tetrahedron with four lateral faces consisting of SARS-CoV-2 entry via ACE2 (lateral face 1), the viral hijacking and replication (lateral face 2), acute inflammatory responses (lateral face 3), and the resulting insulin resistance (lateral face 4). The entrance of SARS-CoV-2 using ACE2 receptor triggers an array of multiple molecular signaling beyond that of the angiotensin II/ACE2-Ang-(1-7) axis, such as down-regulation of PGC-1 α/irisin, increased SREBP-1c activity, upregulation of CD36 and Sirt1 inhibition leading to insulin resistance. In another arm of the molecular cascade, the SARS-CoV-2 hijacking and replication induces a series of molecular events in the host cell metabolic machinery, including upregulation of SREBP-2, decrement in Sirt1 expression, dysregulation in PPAR-ɣ, and LPI resulting in insulin resistance. The COVID-19-diabetes molecular tetrahedron may suggest novel targets for therapeutic interventions to overcome insulin resistance that underlies the pathophysiology of worsening metabolic control in patients with diabetes mellitus or the new-onset of hyperglycemia in COVID-19." @default.
- W4207025762 created "2022-01-26" @default.
- W4207025762 creator A5021669782 @default.
- W4207025762 creator A5057462120 @default.
- W4207025762 creator A5059467256 @default.
- W4207025762 creator A5086739030 @default.
- W4207025762 date "2022-01-24" @default.
- W4207025762 modified "2023-10-16" @default.
- W4207025762 title "The COVID-19-diabetes mellitus molecular tetrahedron" @default.
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