Abstract
It is well known that when proteins aggregate, illnesses such as Alzheimer’s disease, Huntington’s disease, and amyotrophic lateral sclerosis arise [1]. Activation of chaperone proteins can suppress diseases associated with protein misfolding [2]. However, the role of chaperone proteins in the treatment of metabolic diseases such as type 2 diabetes (T2D) has been relatively understudied. We [3—5] and others [6] have been studying the role of molecular chaperone proteins in the treatment of T2D. Specifically, we have been studying the role of heat shock protein 72 (HSP72). We have identified an essential role of HSP72 in preventing obesity-induced insulin resistance, using both loss of function and gain of function genetic mouse models and, via the use of small molecule activators of HSP72 currently in human clinical trials for T2D. This lecture will discuss these data and evaluate the clinical utility for molecules that activate molecular chaperone proteins in the treatment of obesity-related diseases.
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