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Biology subjects

Yang, J. C. C.

Publications and source records attributed to Yang, J. C. C..

2 recordsLinked to original sources

Energetic consequences of single and repeated freezing in the intertidal mussel, Mytilus trossulus

The bay mussel, Mytilus trossulus, is a bivalve commonly found in intertidal zones along the west coast of North America which risks freezing during low tides in the winter. Previous work has shown that despite their freeze tolerance, freezing can still cause damage. Yet little is known about the energetic consequences of these freezing events. Here we measured the oxygen consumption of mussels before and after single and repeated freezing exposures across three seasons. We compared these responses to hypoxia exposures as tissues are not perfused while frozen which inhibits gas exchange. In general, we observed that mussels metabolic rates decreased immediately after a single freeze but recovers after 24 hours. By contrast, repeated freeze-thaws caused variable effects of metabolic rate, depending on the season of exposure. Overall, this suggests that the periods of recovery that occur between freeze-thaw cycles may mitigate freezing damage. We also found that hypoxia in general causes an increase in metabolic rate and may be associated with clearing oxygen debt. Therefore, the metabolic consequences after freezing are unlikely to be driven by hypoxia stress. Here we explore the energetic costs of freezing in M. trossulus informing future research directions into the mechanisms behind freeze tolerance.

zoology↗

Insulin receptors in pancreatic acinar cells contribute to KrasG12D-driven cancer initiation in the context of diet-induced obesity

The rising pancreatic cancer incidence due to obesity and type 2 diabetes is closely tied to hyperinsulinemia, an independent cancer risk factor. Previous studies demonstrated reducing insulin production suppressed pancreatic intraepithelial neoplasia (PanIN) pre-cancerous lesions in Kras-mutant mice. However, the pathophysiological and molecular mechanisms remained unknown and in particular it was unclear whether hyperinsulinemia affected PanIN precursor cells directly or indirectly. Here, we demonstrate that insulin receptors (Insr) in KrasG12D-expressing pancreatic acinar cells are dispensable for glucose homeostasis, but necessary for hyperinsulinemia-driven PanIN formation in the context of diet-induced hyperinsulinemia and obesity. Mechanistically, this was attributed to amplified digestive enzyme protein translation, triggering of local inflammation and PanIN metaplasia in vivo. In vitro, insulin dose-dependently increased acinar-to-ductal metaplasia formation in a trypsin- and Insr-dependent manner. Collectively, our data shed light on the mechanisms connecting obesity-driven hyperinsulinemia and pancreatic cancer development.

cancer biology↗