Regulation of skeletal muscle health with respect to metabolism and insulin sensitivity; role of non-coding RNA

The dysregulated glucose control distinctive of type 2 diabetes is a result of relative insulin deficiency, where insulin producing beta cells are unable to compensate insulin resistance evident in peripheral tissues such as skeletal muscle.

Increased prevalence is partly driven by changes in lifestyle, however, there is a strong genetic component to type 2 diabetes.

The overarching aim of my research is to understand the molecular regulation of the impaired insulin response and altered metabolism in skeletal muscle from people with type 2 diabetes.

I hypothesize that dysregulation of non-coding RNA plays a key role in the regulation of skeletal muscle health with respect to metabolism and insulin sensitivity.

Although all cells in a mammal share the same genome, ~80% of DNA is transcribed in a cell-specific manner, and this is particularly true for regions not coding for protein transcripts.

Several different classes of non-coding RNAs, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), play key roles in skeletal muscle myogenesis including satellite cell activation, proliferation, and differentiation, however only a few transcripts have been studied, particularly in the context of metabolic disease.

Thus, to understand the role of non-coding RNA in regulation of metabolism, and the role played in metabolic disease is the aim of this research programme.