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Current clinical and laboratory predictors (e.g., body mass index, fasting glucose, and HbA 1c ) can serve as indicators to gauge diabetes risk, however, provide little insight into the aetiology and disease pathogenesis 5,6

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A similar pathway was shown to be involved in the release of insulin in response to TGR5 ligands in pancreatic cells (Kumar et al., Figure 5 Inhibition of OA-induced GLP-1 and PYY release by H 2 S To investigate the regulation of TGR5-mediated GLP-1 and PYY release by H 2 S, cells were incubated with L-cysteine, an activator of endogenous enzymes CSE and CBS, for 10 min and then GLP-1 and PYY release in response to OA was measured